title: scRNA-seq of endocrine pancreatic lineages in Isl1CKO mouse model

status: Public on Feb 07 2026

city: Vestec

first: Valéria

last: Fabríciová

address: Průmyslová 595

country: Czech Republic

institute: Institute of biotechnology CAS

summary: To understand the pathophysiology of diabetes and to develop more effective treatments, we need to unravel how pancreatic endocrine lineages are generated. ISL1 transcription factor has important role in differentiation, maturation and maintenace of endocrine cells.  Eliminating ISL1 in mouse pancreatic endocrine progenitors leads to the diabetic phenotype with altered islet architecture. To evaluate effects of lacking transcription factor on molecular level we performed single cell transcriptomics.

overall_design: We created conditional knockout mouse model using Cre-loxP system. Isl1CKO mutants carry genotype Neurod1 Cre/+; Isl1 f/f and mice with genotype Neurod1 Cre/+; Isl1f/+ do not show any phenotype and are used as controls. TdTomato fluorescent protein is used as reporter. 9 days old (P9) pups were sacrificed and pancreases were dissected. 6 samples from each genotype were pooled together. FACSed tdTomato+ cells were loaded to 10x Chromium Next GEM Single cell 3' Reagents kit v.3.1.

first: Pavel

last: Abbafy

first: Valeria

last: Fabriciova

first: Romana

last: Bohuslavova

first: Eva

last: Rohlova

first: Zuzana

last: Berkova

first: Frantisek

last: Saudek

first: Gabriela

last: Pavlinkova


title: miRNA-18a screened based on CRISPR can regulate targeted therapy resistance and T-cell killing in melanoma

status: Public on Feb 06 2026

city: Tianjin

first: Wanyi

last: Xiao

address: West Huan-Hu Rd, Ti Yuan Bei, Hexi District Tianjin

country: China

institute: Tianjin Medical University Cancer Institute and Hospital

summary: In melanoma, the knockout of miR-18a not only leads to resistance to monotherapy with BRAF inhibitors but also to combined therapy with BRAF and MEK inhibitors. This resistance is achieved by promoting the expression of YAP in the Hippo pathway. Additionally, the knockout of miR-18a results in high expression of THBS1-CD47, which causes T cell tolerance. miR-18a is regulated by hnRNPA1, and patients with low expression of miR-18a and hnRNPA1 have poorer Event-Free Survival (EFS).

overall_design: A pooled CRISPR-Cas9 knockout screen targeting human miRNAs was performed in A375 melanoma cells to identify regulators of vemurafenib resistance and CD8+ T cell–mediated cytotoxicity. Cells stably expressing Cas9 were transduced with a lentiviral sgRNA library at low MOI and selected with puromycin. Genomic DNA was collected at baseline (Day 0) and after drug treatment or T cell co-culture, followed by PCR amplification and next-generation sequencing of sgRNA cassettes. Biological replicates were included for each condition.


title: Transcriptomic profiling of miR-18a CRISPR knockout melanoma identifies genes associated with therapy resistance and T cell killing

type: Expression profiling by high throughput sequencing

overall_design: Bulk RNA sequencing was performed to compare transcriptomic changes between wild-type and miR-18a knockout melanoma cells under vemurafenib treatment or CD8+ T cell co-culture. Biological replicates were included for each experimental condition.


title: Single-cell transcriptomic profiling reveals the heterogeneity of miR-18a-mediated resistance to targeted therapy and immunotherapy in melanoma

overall_design: Single-cell RNA sequencing was performed on miR-18a knockout, vemurafenib-resistant, and CD8+ T cell–resistant melanoma cells to characterize transcriptional heterogeneity and cell state changes. Cells were processed using the 10x Genomics platform, and biological replicates were included.


title: Targeting SAGA/ATAC disrupts chromatin regulation and cholesterol metabolism in diffuse midline glioma [CUT&Run]

status: Public on Feb 05 2026

city: Houston

first: Jamie

middle: N.

last: Anastas

state: TX

address: 1 Baylor Plaza

department: Neurosurgery

country: USA

institute: Baylor College of Medicine

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Diffuse midline gliomas (DMG) are aggressive pediatric brain tumors characterized by chromatin and transcriptional dysregulation induced by H3K27M mutations with a median survival of 11-15 months. We identified multiple components of the SAGA and ATAC chromatin regulatory complexes as DMG genetic dependencies and found that genetic or pharmacological inhibition of the SAGA/ATAC-associated chromatin reader SGF29 reduces DMG proliferation. Small molecules targeting SAGA/ATAC-associated histone acetylation, ubiquitination, and methylation similarly suppress DMG growth. Chromatin profiling and RNA‑seq analyses reveal that SGF29 regulates H3K9ac and H3K4me3 deposition at both H3K27M‑bound and H3K27M‑independent loci controlling proliferation, differentiation, and metabolic programs. We further show that inhibition of the SAGA/ATAC histone acetyltransferases KAT2A/2B reduces DMG viability by repressing cholesterol‑metabolism gene expression, and that combined cholesterol‑pathway and KAT2A/2B inhibition synergistically suppresses DMG growth in vitro and decreases proliferation in a xenograft model. Together, these findings define a functional link between SAGA/ATAC‑dependent chromatin modulation and transcriptional and metabolic dysregulation underlying DMG malignancy.

overall_design: For CUT&RUN, a single cell suspension of 5x105 of control of SGF29KO SU-DIPGXIII+Cas9 cells were immobilized on ConA beads, permeabilized with 0.01% Digitonin, incubated with primary antibodies, and then cut with pAG-MNase to release DNA fragments as previously described. The following antibodies were used in CUT&RUN analyses: rabbit IgG (cat# C15410206, Diagenode), H3K4me3 (cat# C15410003, Diagenode), H3K9ac (cat# 9649, Cell Signaling Technology), and H3K27me3 (cat#C15410195, Diagenode). Yeast spike-in DNA (S. cerevisiae; Cell Signaling Technology) was added at 0.5% to each reaction following chromatin digestion.

first: Richard

last: Rosemary

first: Akdes

last: Serin-Harmanci

middle: N


title: Mapping convergent regulators of melanoma drug resistance by PerturbFate

city: New York

first: Zihan

last: Xu

state: NY

address: 1230 York Ave

institute: The Rockefeller University

summary: High-throughput genomic studies have uncovered associations between diverse genetic alterations and disease phenotypes; however, elucidating how perturbations in functionally disparate genes give rise to convergent cellular states remains challenging. Here, we present PerturbFate, a high-throughput, cost-effective, combinatorial-indexing single-cell platform that enables systematic interrogation of massively parallel CRISPR interference (CRISPRi) perturbations across the full spectrum of gene regulation, from chromatin remodeling and nascent transcription to steady-state transcriptomic phenotypes. Using PerturbFate, we profiled over 300,000 cultured melanoma cells to characterize multi-modal phenotypic and gene regulatory responses to perturbations in more than 140 Vemurafenib resistance-associated genes. We uncovered a shared dedifferentiated cell state marked by convergent cooperative transcription factor (TF) activities across diverse genetic perturbations. We further dissected phenotypic responses to perturbations in Mediator Complex components, linking module-specific biochemical properties to convergent transcriptional activations. Together, we reveal common regulatory nodes that drive similar phenotypic outcomes across distinct genetic perturbations. We also delineate how perturbations in functionally unrelated genes reshape cell state. PerturbFate thus establishes a versatile platform for identifying key molecular regulators by anchoring multi-modal regulatory dynamics to disease-relevant phenotypes.

overall_design: Single-cell and parallel bulk CRISPR screen including 143 gRNA pairs targeting 143 genes and no-target with either DMSO or Vemurafenib treatment

first: Ziyu

last: Lu

first: Aileen

last: Ugurbil

first: Abdulraouf

last: Abdulraouf

first: Andrew

last: Liao

first: Jianxiang

last: Zhang

first: Wei

last: Zhou

first: Junyue

last: Cao


title: HR3/RORα-mediated cholesterol sensing regulates TOR signaling

city: København Ø

first: Kim

last: Rewitz

state: Capital region

address: Universitetsparken 15, Building 3.3.401

country: Denmark

institute: University of Copenhagen

summary: Cells and organisms adjust their growth based on the availability of cholesterol, which is essential for cellular functions. However, the mechanisms by which cells sense cholesterol levels and translate these into growth signals are not fully understood. We report that cholesterol rapidly activates the master growth-regulatory TOR pathway in Drosophila tissues. We identify the nuclear receptor HR3, an ortholog of mammalian RORα, as an essential factor in cholesterol-induced TOR activation. We demonstrate that HR3 binds cholesterol and promotes TOR pathway activation through a non-genomic mechanism acting upstream of the Rag GTPases. Similarly, we find that RORα is necessary for cholesterol-mediated TOR activation in human cells, suggesting that HR3/RORα represents a conserved mechanism for cholesterol sensing that couples cholesterol availability to TOR-pathway activity. These findings advance our understanding of how cholesterol influences cell growth, with implications for cholesterol-related diseases and cancer.

overall_design: To determine the biological effects of dietary cholesterol replenishment, and to assess which effects require HR3 or TOR, we performed RNAseq on whole larvae expressing no RNAi, Hr3-RNAi, or Tor-RNAi throughout the body (using ubiquitous driver Tub-GAL80TS; Tub-GAL4), after the animals had been stimulated with dietary cholesterol or not. Thus there are three genotypes x two feeding conditions, with five replicates each. Each replicate contains five late-third-instar larvae.

first: Mette

last: Lassen

first: Michael

last: Texada


title: Toosendanin Suppresses Acute Myeloid Leukemia by Targeting DDX5/c-Myc Axis to inhibit Protein Synthesis

status: Public on Feb 03 2026

city: Guiyang

first: Xianchao

last: He

state: Guizhou

address: Huaxi

institute: Guizhou University

summary: The treatment of acute myeloid leukemia (AML) continues to be challenged by relapse and resistance, necessitating the development of novel therapeutic strategies. Toosendanin (TSN), a natural product derived from traditional Chinese medicine, exhibits antitumor activity in solid tumors; however, its mechanism of action and direct molecular targets in AML remain undefined. Here, we demonstrate that TSN potently inhibits AML cell proliferation, induces dual G0/G1 and G2/M phase arrest, and triggers caspase-dependent apoptosis at nanomolar concentrations. Using an integrated approach, including affinity pull-down, cellular thermal shift assay (CETSA), and molecular docking, we identified RNA helicase DDX5 as a direct target of TSN. TSN binding promotes DDX5 degradation via both proteasomal and lysosomal pathways. Transcriptomic and functional analyses revealed that TSN downregulates the c-Myc transcriptional network via DDX5 targeting, leading to the suppression of ribosome biogenesis. Rescue experiments confirmed that DDX5 is the central mediator of this pathway. In an MLL-AF9-driven AML mouse model, TSN treatment significantly prolonged survival, without observable toxicity. Collectively, our study delineates a novel anti-leukemic mechanism wherein TSN targets DDX5 for degradation and consequently inhibits c-Myc signaling, providing a rationale for therapeutic targeting of the DDX5/c-Myc axis and further development of TSN in AML.

overall_design: MOLM-13 cells were treated with 20 nM TSN or DMSO for 48 h (n=3 biological replicates). Total RNA was extracted, and libraries were constructed and sequenced using the NovaSeq™ X Plus platform. Differential gene expression analysis was performed using DESeq2 v1.26.0 (FDR < 0.05, |log₂FC| > 0.584). Gene Set Enrichment Analysis (GSEA) was conducted using the MSigDB Hallmark 2023 gene set (FDR < 0.25), and the analysis was performed on the OmicShare platform v6.2.

first: Jing

last: Luo

first: Hongru

last: Chen

first: Yu

last: Hou

first: Dan

last: Liu

first: Yuanyuan


title: Integrative transcriptomic analysis uncovers the miRNA-centric regulation of Japanese encephalitis virus infection in porcine trophoblast cells.

status: Public on Feb 01 2026

city: Yangzhou

first: Juan

last: Yang

address: 大学南路88号

department: College of Veterinary Medicine

institute: Yangzhou University

type: Non-coding RNA profiling by high throughput sequencing

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Expansion of outer cortical layer Cux2+ neurons required selective adaptations for DNA repair

status: Public on Feb 02 2026

city: Los Angeles

first: Riki

last: Kawaguchi

state: CA

address: 760 Westwood Plaza, Room 37-420

department: Department of Psychiatry and Neurology Department of Psychiatry

institute: University of California, Los Angeles

summary: During mammalian evolution, upper cortical layer 2/3 excitatory neurons have shown a disproportionate expansion compared to other layers. Replicative expansion of cortical neural progenitors is associated with significant oxidative DNA damage. Here we show that Activating Transcription Factor 4 (Atf4) has new roles as a critical regulator of the DNA Damage Response, directly activating components of double stranded DNA repair, including CIRBP, Uba52 and Ebf1. Strikingly, pan-cortical knockout (Emx1cre, Atf4fl/fl) demonstrates that Atf4 is specifically required for development of upper layer 2/3 neurons, marked by expression of CUT-homeodomain protein, Cux2.  Atf4 functions to repair DNA damage and attenuate cell death of embryonic radial glial progenitors in a p53-dependent manner.  In particular, we show that Cold-Inducible RNA-Binding Protein (Cirbp) is a transcriptional target of Atf4 that is required for the normal phosphorylation of the key double strand DNA repair factor Ataxia-Telangiectasia Mutated (ATM). These findings establish that Atf4 is an essential regulator of the DNA Damage Response. They further indicate extraordinary requirements for DNA repair post-replicative stress in Cux2+ neurons during mammalian brain development.

overall_design: We collected the E11.5 embryonic cortex from timed-pregnant mice, and after the genotyping been done, three same genotype cortex been pool together as one to get enough sample for snRNA sequencing, Atf4 fl/fl as control and Emx1-Cre, Atf4 fl/fl as knockout group


title: Study on the mechanism of action of NUDT21 in acute T-lymphocytic leukemia [eCLIP-seq]

city: suzhou

first: yang

last: yang

address: zhongnan road

institute: soochow university

summary: Alternative polyadenylation (APA) is a widespread post-transcriptional mechanism that regulates transcript stability, localization, and translation. While dysregulated APA has been implicated in multiple cancers, its role in T-cell acute lymphoblastic leukemia (T-ALL) remains poorly understood. Here, we identify NUDT21, a core subunit of the APA machinery, as an essential oncogenic regulator in T-ALL. NUDT21 is significantly upregulated in T-ALL patient samples and associated with poor prognosis. Functional assays demonstrate that NUDT21 knockdown inhibits T-ALL cell proliferation, induces apoptosis, and suppresses leukemia progression in vivo. Integrative PAS-seq and RNA-seq analysis reveals that NUDT21 maintains distal polyadenylation site usage of oncogenic transcripts, including UBE2D3, whose 3′UTR shortening upon NUDT21 loss leads to decreased expression and impaired leukemic cell growth. In addition to its APA role, NUDT21 occupies gene regulatory regions and directly activates transcriptional programs enriched for MYC and E2F targets, promoting cell cycle progression and ribosome biogenesis. Pharmacological suppression of NUDT21 using ouabain, a cardiac glycoside, downregulates UBE2D3 and E2F/MYC effectors, resulting in robust anti-leukemic effects.Our findings reveal a dual regulatory role of NUDT21 in T-ALL, functioning through both APA-dependent and APA-independent mechanisms to sustain leukemic proliferation. Targeting NUDT21 or its downstream programs represents a promising therapeutic strategy for T-ALL.

overall_design: eCLIP profiles of J-Gamma1 cells NUDT21 were generated by eCLIP sequencing, using DNBSEQ-T7.

first: Yang

first: Shuiyan

last: Wu


title: Study on the mechanism of action of NUDT21 in acute T-lymphocytic leukemia [CUT&Tag]

overall_design: CUT&Tag profiles of J.gamma1 cells NUDT21 were generated by CUT&Tag sequencing, in double, using Illumina NovaSeq X plus.


title: Study on the mechanism of action of NUDT21 in acute T-lymphocytic leukemia [PAS-seq]

overall_design: PAS-seq profiles of J-Gammal cells treated with short hairpin RNAs (shRNAs) targeting NUDT21 or negative control (shNC) were generated by PAS-seq, in double, using Illumina NovaSeq X plus.


title: Study on the mechanism of action of NUDT21 in acute T-lymphocytic leukemia [RNA-Seq]

overall_design: mRNA profiles of J-Gammal cells treated with short hairpin RNAs (shRNAs) targeting NUDT21 or negative control (shNC) were generated by RNA sequencing, in double, using Illumina NovaSeq X plus.


title: FaRIF at the Core of Strawberry Fruit Ripening: Deciphering its Targets and Interaction Networks

status: Public on Jan 31 2026

city: Madrid

first: Jose M.

last: Franco-Zorrilla

state: Madrid

address: Darwin, 3

department: Plant Molecular Genetics

country: Spain

institute: Centro Nacinal de Biotecnologia-CSIC

summary: Ripening Inducing Factor (RIF) is a key NAC transcription factor regulating strawberry fruit ripening. Previous studies using RIF-RNAi and overexpression lines in Fragaria × ananassa and CRISPR knock-out lines in F. vesca have established the role of RIF in controlling ABA biosynthesis and signaling, cell wall remodeling, and secondary metabolism. In this study, we deciphered FaRIF’s transcriptional regulatory network by combining ChIP-seq-based identification of its direct targets with an analysis of FaRIF-RNAi transcriptome data. These analyses revealed FaRIF’s direct role in multiple aspects of strawberry fruit ripening, including the regulation of ripening-related transcription factors, phytohormone content and signaling, primary and secondary metabolism, and cell wall degradation. Additionally, using the TurboID-based proximity labeling approach, we have identified FaRIF interactors, including proteins involved in mRNA and protein homeostasis, as well as several NAC transcription factors. Among these, FaNAC034 was found to synergistically enhance FaRIF’s transcriptional activity. This integrative analysis, combining transcriptome analysis, in vivo ChIP-seq, and proximity labeling, broadens our knowledge of FaRIF-mediated transcriptional networks and interaction partners, providing valuable insights into the molecular mechanisms underlying strawberry fruit ripening regulation by this transcription factor.

overall_design: ChIP-seq of FaRIF from leaves of 35Spro:FaRIF-GFP plants, two biological replicates

first: Carmen

last: Martín-Pizarro

first: María Florencia

last: Perotti

first: Jose M

first: Rosa

last: Lozano-Durán

first: Guozheng

last: Qin

first: David

last: Posé


title: Depot-Specific Differences and heterogeneity of Adipose-Derived Stem Cells in Diet-Induced Obesity

city: Jinan

first: Honglin

last: Guo

state: Shandong

address: No. 324, Jingwu Road

department: Department of Pathology, Department of Endocrinology

institute: Shandong University, Shandong Provincial Hospital

summary: Obesity is a global health concern. Studying the heterogeneity of ADSCs play pivotal roles in understanding metabolic disorders such as obesity. Using Mass cytometry, we discerned the spatial heterogeneity of ADSCs and their alterations at the single cell level in a diet-induced-obesity (DIO) model treated with Liraglutide. We characterized the relationship of ADSCs markers and found that CD26 and CD142 are capable of identifying the most representative heterogeneous ADSCs in Subcutaneous Adipose Tissue (SAT) and Visceral Adipose Tissue (VAT). Specifically, CD26+CD142- and CD26+CD142+ADSCs were exclusive to SAT and VAT, respectively, while CD26-CD142+ADSCs were present in both.  To acquire more robust examination of the expression variances for a range of functional markers within these depot-specific heterogeneous subpopulations, transcriptomic sequencing was performed on the Fluorescence-activated cell sorting (FACS) sorted CD26+CD142-, CD26+CD142+ and CD26-CD142+ ADSCs from SAT and VAT of chow diet mice. In the VAT of DIO mice, we observed significant down-regulation of CD26+CD142+ ADSCs and up-regulation of CD26-CD142+ ADSCs, both of which could be mitigated by Liraglutide. Our research illuminates the spatial heterogeneity of ADSCs and their alterations under DIO, which can be potentially reversed by Liraglutide treatment. This study contributes new insights for identifying more specific ADSCs subgroups to explore the etiology for metabolic-related diseases.

overall_design: FACS was performed on SVFs from SAT and VAT of 30 chow diet mice (12-14 weeks old) to obtain ADSCs subclusters with different expression pattern of CD26 and CD142. A total of 5 samples were obtained from FACS sorting, which included a single sample for SAT_CD142+, SAT_CD26+CD142-, VAT_CD26+CD142+ ADSCs, and two samples for VAT_CD142+ ADSCs.  Transcriptomic sequencing was performed on these FACS sorted ADSCs subpopulations.

first: Xu

first: Ailing

last: Sheng


title: miRNA Profiling shows shared Signatures in Pediatric Asthma, Obesity and their comorbidity

city: Doha

first: Mohamed Nadhir

last: Djekidel

state: Doha

address: Gharafa

department: Translational Medicine Department

country: Qatar

institute: Sidra Medicine

summary: Obesity is considered as a significant contributor of childhood asthma. Concerningly, obesity and asthma comorbity is found to be  associated with increased asthma symptoms and reduced response to corticosteroid therapy. In this study we investigate how the co-existence of obesity in children with asthma alter their molecular characteristics.

overall_design: We aimed to identify microRNA (miRNA) signatures associated with pediatric asthma-obesity comorbidity. We compared miRNA profiles in the RNA extracted from peripheral blood between four groups: normal weight with asthma (NW-A, n = 11), overweight/obesity with asthma (OO-A, n = 10), overweight/obesity with no asthma (OO, n = 10), and normal weight with no asthma (NW, n = 12). Downstream analysis of differentially expressed miRNAs were conducted using different bioinformatic tools. Finally, correlation of differentially expressed miRNAs with different clinical parameters and plasma cytokines were assessed using Pearson’s correlation analysis.

first: Harshita

last: Hailesh

first: Safa

last: Noor

first: Lena

last: Hayati

first: Stefan

last: Worgall

first: Ibrahim

last: Janahi


title: Spatial transcriptomic analysis of CLDN6-positive solid and small cluster areas in human ovarian cancer

status: Public on Jan 30 2026

city: Yokohama

first: Shinichi

last: Onishi

state: Kanagawa

address: 216,Totsuka-cho, Totsuka-ku

country: Japan

institute: Chugai pharmaceutical co., Ltd.

summary: To investigate the intratumoral heterogeneity of CLDN6 expression in epithelial ovarian cancer (EOC), we performed spatial transcriptomic analysis on clinical specimens. CLDN6-positive cells were observed to form two morphologically distinct patterns: solid tumor areas and dispersed small tumor cell clusters. Using the NanoString GeoMx Digital Spatial Profiler, we compared the gene expression profiles of these two areas within the same tumors. The analysis revealed that small cluster areas showed higher expression of genes related to epithelial-mesenchymal transition (EMT) and extracellular matrix (ECM) remodeling compared to solid areas. These findings suggest that morphologically distinct CLDN6-positive areas represent cell populations with different molecular characteristics, highlighting the plasticity of EOC.

overall_design: Formalin-fixed, paraffin-embedded (FFPE) tissue sections from two patients with ovarian serous adenocarcinoma were analyzed by spatial transcriptomics using the NanoString GeoMx Digital Spatial Profiler. Regions of interest (ROIs) were selected from CLDN6-positive/Pan-CK-positive areas, categorized as either 'solid tumor areas' or 'dispersed small tumor cell clusters'. Gene expression profiles of Pan-CK-segmented areas within these ROIs were compared to characterize the molecular differences between the two morphological patterns.

first: Chie

last: Kato

first: Etsuko

last: Fujii

first: Nami

last: Yabuki

first: Hitomichi

last: Terashima

first: Atsuhiko


title: Gene expression in NIH:OVCAR-3 xenograft tumor treated with vehicle or carboplatin

first: Naoki

last: Kimura

address: 216 Totsukacho, Totsuka-ku, Chugai Life Science Park Yokohama

institute: Chugai Pharmaceutical Co.,ltd

summary: Gene expression differences in OVCAR3 xenograft tumors after vehicle or carboplatin treatment were successfully identified

overall_design: NIH:OVCAR-3 tumor bearing HuNOG mice were administrated saline (vehicle) or carboplatin (30 mg/kg) and used for gene expression analysis


title: Gene expression in NIH:OVCAR-3 xenograft tumor treated with vehicle or carboplatin [Progression]


title: Gene expression in NIH:OVCAR-3 cells treated with chemotherapeutic drugs

summary: Difference of gene expression in NIH:OVCAR-3 cells after treatment of chemotherapies

overall_design: NIH:OVCAR-3 cells treated with chemotherapeutic drugs were harvested and used for gene expression analysis


title: Impact of NPAS2 on mPFC dopamine synthesis and nap behavior

status: Public on Jan 28 2026

city: GuangZhou

first: Haobin

last: CEN

address: 232 Outer Ring East Road, University Town, Panyu District, Guangzhou City

institute: Guangzhou University of Chinese Medicine

summary: The biological basis of afternoon nap, a widespread yet poorly understood phenomenon, has remained elusive. Here we identify NPAS2, among core circadian regulators, as a sex-independent determinant of the nap behavior in mice. Specifically, medial prefrontal cortex (mPFC)-expressed NPAS2 orchestrates nap regulation through circadian modulation of local dopaminergic activity. We demonstrate that tyrosine hydroxylase-positive (TH+) neurons in mPFC exhibit time-of-day dependent wake-promoting activity, showing minimal excitation precisely during nap hours. Mechanistically, NPAS2 achieves this circadian suppression through a POU2F2-TH regulatory pathway: 1) transcriptional activation of the transcription repressor POU2F2, and 2) consequent downregulation of TH expression (a rate-limiting enzyme for dopamine synthesis) and dopamine production in mPFC TH+ neurons. These findings establish an endogenous circadian mechanism where mPFC NPAS2 periodically inhibits wake-promoting dopaminergic activity to drive nap behavior, providing fundamental insights into the neural and molecular regulation of nap biology.

overall_design: To elucidate the molecular mechanisms by which mPFC NPAS2 regulates sleep-wake cycles and nap behavior, we performed a comparative single-nucleus transcriptomic analysis using Npas2 KO mice and wild-type littermate controls. Medial prefrontal cortex (mPFC) tissues were harvested from four mice per genotype at circadian time ZT20 (the peak of nap behavior) and pooled by genotype to ensure robust biological representation. Nuclei were isolated using the Shbio Cell Nuclear Isolation Kit (52009-10) in combination with NP-40 lysis buffer to obtain high-quality single-nucleus suspensions. Single-nucleus libraries were then constructed using the 10x Genomics Chromium Next GEM Single Cell 3' Reagent Kit v3.1, followed by high-depth sequencing on the Illumina NovaSeq 6000 platform with a paired-end 150 bp (PE150) configuration.

first: Lianxia

last: Cen

first: Yuwei

last: Huang

first: Zanjin

last: Li

first: Kengran

last: Zeng

first: Zicong

last: Wu

first: Jiaxian

last: Weng

first: Xiaocao

first: Di

last: He

first: Xinyu

last: Liu

first: Zhehan

last: Yang

first: Haiman

last: Xu

first: Tingying

last: Hao

first: Binbin

last: Wei

first: Xingxing

last: Diao

first: Baojian


title: Gene expression in NIH:OVCAR-3 cells cultured in different cell density conditions

first: Naoki

summary: Difference of gene expression in different cell culture condition was successfully identified

overall_design: NIH:OVCAR-3 cells were cultured under low density, medium density, and high density. After one week of culture, cells were harvested and used for gene expression analysis


title: Omacetaxine reduces c-Myc expression and demonstrates antitumor effects in osteosarcoma

city: Fort Collins

first: Sunetra

last: Das

state: CO

address: 300 W Drake Rd

department: Clinical Sciences

institute: Colorado State University

summary: Omacetaxine mepesuccinate (OMX), formerly known as homoharringtonine, is a protein translation inhibitor approved for use in human chronic myeloid leukemia.  Recent studies suggest that OMX may be effective against other cancer types, and may be successful against protein targets that are otherwise difficult to inhibit by reducing their translation rates.  Using canine, human, and mouse osteosarcoma (OS) cell lines, we investigated the antineoplastic effects of OMX against OS by evaluating growth inhibition, migration and invasion, apoptosis, expression of c-Myc, changes in gene expression, and in vivo efficacy.  OMX induced dose-dependent growth inhibition and apoptosis of OS cells with IC50 values in the low nanomolar range.  OMX also reduced migration and Matrigel invasion.  Strikingly, levels of c-Myc protein were reduced in most canine, human, and mouse OS cell lines after OMX exposure, and Myc target RNA transcripts were also reduced with treatment. OMX significantly inhibited tumor growth in and metastasis in two separate orthotopic mouse OS models.  OMX is a promising candidate for treatment of OS in both dogs and humans, and potentially other c-Myc-driven cancers.

sample_organism:
Canis lupus familiaris
Mus musculus

platform_organism:
Canis lupus familiaris
Mus musculus

overall_design: RNA-seq profiling of DLM8 and Gracie cells with 6 hours of 50 nM omacetaxine exposure and untreated control cells.

first: Kristen

middle: B

last: Farrell


title: MNK3 cells with CRISPR interference or activation at the CLN3 gene

city: London

first: Mikhail

last: Spivakov

address: Du Cane Road

country: United Kingdom

institute: MRC London Institute of Medical Sciences

summary: This RNA-seq data in MNK3 cells with CRISPRi/a at CLN3 accompanies the manuscript: "High-resolution promoter interaction analysis implicates genes involved in activation of type 3 innate lymphoid cells in immune disease risk" (Malysheva/Ray-Jones/Lakes et al., Nat Gen 2026)

overall_design: RNA-seq of MNK3 cells with CLN3 gene perturbed with either CRISPRi or CRISPRa approach, and their respective scramble controls. Cells were either unstimulated or stimulated with IL-23 and IL1B. Each condition has three replicates.

first: Rachel

last: Green

first: Gene

last: Oltz

first: Helen

last: Ray-Jones

first: Valeriya

last: Malysheva


title: RNA sequencing of HSkM myotubes deficient in DMD, full-length dystrophin (DP427) and utrophin reveals common transcriptomic alterations

status: Public on Jan 27 2026

city: Poznań

first: Paulina

last: Kościelniak-Wawro

address: Uniwersytetu Poznańskiego 6

department: Faculty of Biology, Institute of Human Biology and Evolution

country: Poland

institute: Adam Mickiewicz University

summary: iRNA approaches were used to knock down the expression of dystrophin (DMD), including its full-length isoform DP427, and utrophin (UTRN) genes. Specifically, iRNA-mediated knockdown of both DMD (full-length dystrophin DP427) and UTRN was performed in HSkM myotubes. It is known that the shorter dystrophin isoform DP71 compensates for full-length dystrophin DP427 in the early stages of myofiber differentiation in cell models of Duchenne muscular dystrophy. Accordingly, DP427-deficient and DP71/DP427-deficient HSkM myotubes exhibit distinct changes in the expression of genes involved in membrane integrity and cytoskeletal functions. RNA-sequencing analyses revealed overlapping transcriptomic alterations in these HSkM cell lines, which corresponded to observed phenotypic abnormalities such as increased membrane permeability and intracellular calcium levels, mitochondrial aggregation, elevated reactive oxygen species (ROS), enhanced cyto- and genotoxicity, and induction of apoptosis.

overall_design: RNA-seq profiling of HSkM myotubes after siCtrl delivery and wild-type HSkM myotubes after siDMD, siDP427 and UTRN delivery. Myotubes were obtained after 12 days of differentiation.

first: Patryk

last: Konieczny

first: Sylwia

last: Szwec


title: Latent cytomegalovirus disrupts NK cell responses to P. falciparum and impairs parasite control

city: Brisbane

first: Zuleima

last: Pava Imitola

state: Queensland

address: 300 Herston road

country: Australia

institute: QIMR Berghofer

summary:
NK cells are major innate and adaptive responders to malaria, with multiple roles in protection. Function of NK cells is heterogeneous, underpinned by expression of a diversity of receptors.  One driver of NK cell heterogeneity is latent CMV infection, which drives the expansion of memory-like NK cells. We have recently reported that latent CMV infection can negatively impact the adaptive immune response to malaria, but whether CMV-mediated changes to the NK cell compartment also impact responses to malaria is unknown.

Methods: We investigated the impact of latent CMV infection on NK cell response to the malaria parasite Plasmodium falciparum in vitro, and in CMV seronegative and seropositive individuals during controlled human malaria infection. We analysed NK cell activation, cytotoxicity and NK cell receptor expression. Additionally, we investigated the impact of CMV serostatus on cytokine production in response to TLR stimulation in the myeloid cell compartment. The impact of CMV and NK cell responses on malaria symptoms and parasite control and symptoms of malaria was investigated.

Results: NK cells from CMV seropositive individuals had reduced responsiveness to P. falciparum parasites in vitro and had reduced activation during controlled human infection. Reduced activation was not restricted to NK subsets modulated by CMV but occurred across the entire NK cell compartment. Consistent with global NK cell attenuation, IL-12 production from myeloid cells, a response that supports NK cell activation on exposure to P. falciparum parasites, was lower in CMV infected individuals. Linking NK cell activation to clinical outcomes, NK cells expressing perforin were strongly associated with parasite control in CMV seronegative individuals.

Conclusion: CMV infection modulates NK cell responses during malaria by disruption of IL-12, leading to reduced parasite control.

overall_design: PBMCs were co-cultured at 37 °C, 5% CO2 in a 96-well U-bottom plate for 4 hours at a 1:1 cell ratio with 1x106 mature trophozoite stage pRBCs. After incubation NK cells subsets were FACS sorted using the BD FACSAria™ III Cell Sorter. RNA was extracted from isolated cell population lysates using the QIAGEN PicoPureTM RNA isolation kit (Applied Biosystems™, KIT0204), and RNA quality confirmed with the 2200 TapeStation system (G2964AA) by High Sensitivity RNA ScreenTape (5067- 5579). RNA sequencing libraries were constructed using the NEBNext® Single Cell/Low Input RNA Library Prep Kit for Illumina® (E6420S) and NEBNext® Multiplex Oligos for Illumina® (96 Unique Dual Index Primer Pairs) (E6440S). The libraries were sequenced using a NetSeq 550 system

first: Reena

last: Mukhiya

first: Jessica

middle: R

last: Loughland

first: Nick

middle: L

last: Dooley

last: Pava

first: Damian

last: Oyong

first: Dean

middle: W

last: Andrew

first: Julian

last: Hamelink

first: Kiana

last: Berry

first: James

middle: S

last: McCarthy

first: Bridget

middle: E

last: Barber

first: J. Alejandro

last: Lopez

first: Christian

last: Engwerda

first: Michelle

middle: J

last: Boyle


title: Exercise-Derived Exosomal miR-151-3p: An Innovative Anti-inflammatory and Antioxidant Exerkine for Spinal Cord Injury

status: Public on Jan 26 2026

city: Shanghai

first: Tiansheng

last: Xu

state: Shanghai

address: Shanghai

institute: OE

summary: Exercise (Exe) training serves as the hub of the multimodal treatment system for spinal cord (SC) injury (SCI), with well-established efficacy. However, the forms in which it exerts its effects and the potential key mechanisms still require in-depth research. Exosomes (Exos) have demonstrated great potential in disease treatment and the elucidation of disease mechanisms. This experiment aims to investigate the functions and action targets of Exe-derived Exos (Exe-Exos) in SCI, providing a theoretical foundation for developing treatment strategies targeting Exos pathways post-SCI. Circulating blood Exos were extracted from normal Sprague-Dawley (SD) rats after 4-week treadmill Exe and from the control group (Sed). Hydrogel (Hyd) microneedles were employed to target and deliver the Exos to the T10 segment of the SC in rats with SCI. By constructing corresponding in vitro and in vivo cell and SCI animal models, we found that Exe-derived Exo miR-151-3p (Exe-Exos-miR-151-3p) mediated functional repair following SCI in rats. Furthermore, Exos were found to carry protective signals, with Exo-miR-151-3p as the key molecule. For the first time, we discovered that Exo-miR-151-3p produced anti-inflammatory (NF-kB signaling pathway), anti-apoptotic (Caspase3 and JNK), and anti- oxidative stress (Oxs)oxidative (Nrf2 and HO-1) effects by inhibiting the mitochondrial membrane gene ROMO1.

overall_design: Then, we analyzed the gene expression profiles of RNA-seq from serum exosomes of 20 rats in Exercise group and 20 rats in Sedentary group.

first: Xinwang

last: Ying

first: Jiamen

last: Shen

first: Yanfang

last: Zhao

first: Tiantaixi

last: Tu

first: Yi

last: Jiang

first: Zhiyang

last: Huang

first: Qingfeng

last: Xie


title: Generalization of negative memories drives the development of  psychological distress-related behaviors

city: Guangzhou

first: Xin

last: Cheng

address: 74 Zhongshaner Rd

institute: Sun Yat-sen University

summary: To investigate the molecular mechanism of unpredictable aversive stress induced commobidity between fear generalization and depression, mice were treated by different training paterns (1xTr, 2xTr-same and 2xTr-altered). Therefore, mPFC were dissected to perform immunoprecipitation and RNA seq.

overall_design:
Translating profiles of the BNST-projecting mPFC neurons and transcriptomic profiles of the mPFC in mice after 1xTr, 2xTr-same and 2xTr-altered CFC trainings.
Comparative gene expression profiling analysis of RNA-seq data for BNST-projecting mPFC neurons or mPFC tissues under different treatment (1xTr, 2xTr-same, 2xTr-altered).
Immunoprecipitation was performed using GFP Recombinant Rabbit Monoclonal Antibody (Invitrogen G10362, Lot2306774).

first: Yubo

last: Hu

first: Yan

first: Panwu

first: Jiale

last: Chen

first: Xiaomeng

last: Bai

first: Deshan

last: Kong

first: Chuan

last: Xiao

first: Youhua

first: Shuyu

last: Zheng

first: Yuena

first: Yumeng

last: Wang

first: Hu

first: Yanni

last: Zeng

first: Wei-Jye

last: Lin

first: Xiaojing

last: Ye


title: Smyd5 mediates IL-4 epigenetic control of macrophage antigen presentation to drive cooperative T cell-mediated tumor suppression [RNA-Seq]

city: Xiamen

first: dang

last: buyun

state: Fujian

address: Xiang 'an District Xiang Annan Road

institute: xiamen university

summary: IL-4 is classically associated with “M2” macrophages considered tumor-immunosuppressive, yet marker-based labels poorly reflect macrophage function in tumors. Reports of a non-canonical, IL-4–imprinted macrophage state (M2inf) with trained-immunity features prompted us to test whether such imprinting contributes to antitumor immunity in vivo. Here we show that, in B16F10 melanoma, IL-4 programs macrophages through the lysine methyltransferase Smyd5 to deposit promoter-proximal H3K36me3, increase MHC class II, and potentiate T cell activation. Myeloid Il4ra deletion increased tumor burden and reduced MHC class II and intratumoral T cell activation, whereas co-transfer of IL-4–primed macrophages suppressed tumors and expanded activated CD4 and CD8 T cells. Antitumor benefit required adaptive lymphocytes and macrophage-intrinsic MHC class II, as Rag1 deficiency or macrophage Rfx5 deletion abrogated tumor suppression. These findings identify a non-canonical, IL-4–imprinted macrophage program that enables antigen presentation and cooperative T cell immunity in this tumor context.

overall_design:
The BMDM macrophages of WT or Smyd5 KO were treated with IL-4 for 24 hours and then RNA library construction was performed

UPDATE: [Apr-28-2026] The GSM9426189_Mix_pool_library_RNA-seq.counts.txt file was updated.

first: Buyun

last: Dang

first: Yuling

last: Hong

first: Qingxiang

last: Gao

first: Shih-Chin


title: The deacetylase Sir2 is the primary sensor driving transcriptional changes in response to low NAD+ in the yeast Kluyveromyces lactis

status: Public on Jan 22 2026

city: Buffalo

first: Charikleia

last: Karageorgiou

address: 109 Cooke Hall, Mary Talbert Way

department: Department of Biological Sciences

institute: University at Buffalo

summary: The coenzyme NAD+ (nicotinamide adenine dinucleotide) is a critical electron carrier in central metabolism and is required for cellular health. It is proposed that cells sense intracellular NAD+ levels using sirtuin deacetylases, which require NAD+ for their enzymatic activity.  We tested this hypothesis by examining how intracellular NAD+ levels affect expression of Sir2-repressed genes in the yeast Kluyveromyces lactis. Because K. lactis cannot synthesize NAD+, we could create a gradient of intracellular NAD+ levels by growing cells in varying concentrations of the precursor nicotinic acid. We found that as NAD+ levels decreased, acetylation of histones at target promoters increased, as did expression of these genes. RNA-Seq analysis revealed that genes induced in low nicotinic acid include some that would restore NAD+ levels, such as the high-affinity nicotinic acid transporter TNA1, and some that would enable long term survival, such as genes promoting sporulation. Most genes induced in low nicotinic acid (100 of 114 or 88%) were also induced in the absence of Sir2. Moreover, in sir2Δ cells, few transcriptional changes occurred in response to low nicotinic acid. Thus, Sir2 is the primary sensor responsible for the transcriptional response to low NAD+ in K. lactis. In addition, the degree of induction varied across NAD+ levels, suggesting that Sir2 behaves as a rheostat, tuning gene expression to NAD+ availability.

overall_design: Kluyveromyces lactis wild-type (WT; CBS2359) and sir2Δ strains were grown in yeast nitrogen base supplemented with nicotinic acid (NA) at four concentrations, 15 to 400 μg/L, to create a gradient of intracellular NAD⁺. Cultures were harvested at mid-log phase (OD₆₀₀ ≈ 1.0). For each strain × condition combination, two independent biological replicates were collected (17 total RNA-seq libraries).

first: Mahasweta

last: Acharjee

first: Kristen

last: Humphrey

first: Vincent

last: Lactaoen

first: Omer

last: Gokcumen

first: Laura

last: Rusche


title: High Resolution Spatial Mapping of Microbiome-Host Interactions via in situ Polyadenylation and Spatial RNA Sequencing [bulk RNA-Seq]

status: Public on Jan 21 2026

city: New York

first: Joao

last: Xavier

state: New York

address: 430 E 67th St

department: Computational and Systems Biology Program

institute: Sloan Kettering Institute

summary: Inter-microbial and host–microbial interactions are thought to be critical for the functioning of the gut microbiome, but few substantive tools are available to measure these interactions. Here, we report a method for unbiased spatial sampling of microbiome-host interactions in the gut at high spatial resolution. This method combines enzymatic in situ polyadenylation of both bacterial and host transcripts with spatial RNA-sequencing. Application of this method revealed the biogeography of the mouse gut microbiome as function of location in the intestine, short-range intermicrobial interaction, local shaping of the microbiome by the host, and tumor-associated changes in the architecture of the host-microbiome interface. This method is compatible with broadly available commercial platforms for spatial RNA-sequencing, and can therefore be readily adopted to broadly study the role of short-range, bidirectional host-microbe interactions in microbiome health and disease.

overall_design: bulk RNA-Seq of intestinal tissue for host gene expression and microbiome composition analysis

first: Ioannis

last: Ntekas

first: David

last: McKellar

first: Lena

last: Takayasu

first: Iwijn

last: De Vlaminck


title: High Resolution Spatial Mapping of Microbiome-Host Interactions via in situ Polyadenylation and Spatial RNA Sequencing (Stereoseq)

overall_design: Spatial transcriptomics (Stereoseq)


title: Aldosterone stimulation of fibroblasts affects gene expression and function relevant to muscle injury and disease

city: Columbus

first: Jill

last: Rafael-Fortney

state: OH

address: 460 W. 12th Ave

department: Physiology & Cell Biology

institute: The Ohio State University

summary: Here, we report the RNA sequencing of fibroblasts isolated from wild-type (C57BL/10) neonatal hindlimb skeletal muscle. The fibroblasts were directly treated with the MR agonist aldosterone, the MR antagonist spironolactone, or vehicle control (DMSO). We find that aldosterone treatment increased expression of genes involved in fibrosis, muscle function, and metabolism, and that aldosterone treatment decreased expression of genes involved in cell migration and cytokine receptor binding. This data suggests that MR signaling can directly affect fibroblasts and contribute to pathology in skeletal muscle.

overall_design: RNA-seq profiling of wild-type (C57/BL 10) neonatal mouse hindlimb skeletal muscle fibroblasts, treated for 48h with either 1 uM aldosterone, 1 uM spironolactone, or vehicle control (DMSO).

first: Chetan

middle: K

last: Gomatam

first: Swathy

last: Krishna

first: Jeovanna

last: Lowe

first: Esther

last: Silver

first: Christoph

last: Lepper

middle: A


title: High Resolution Spatial Mapping of Microbiome-Host Interactions via in situ Polyadenylation and Spatial RNA Sequencing [Ileum, without in situ Polyadenylation]

overall_design: Spatial transcriptomics: Ileum, without in situ Polyadenylation


title: Gene expression analysis and proximity labeling reveal posttranscriptional functions of the yeast RNA Polymerase II regulator Def1

city: University Park

first: Oluwasegun

middle: Tosin

last: Akinniyi

state: PA

address: 463 North Frear

department: Biochemistry and Molecular Biology

institute: Pennsylvania State University

summary: Def1 is a yeast protein that promotes transcription elongation and regulates the degradation of RNA polymerase II during transcription stress. Although Def1 is localized in the cytoplasm, its functions in this cellular compartment are not yet understood. Despite its well-established roles in transcription, a comprehensive genome-wide analysis of its impact on gene expression has not been conducted. Here, we performed RNA sequencing (RNA-seq) analysis on cells lacking DEF1 and surprisingly found that only a few hundred genes exhibited altered expression, both upregulated and downregulated. To evaluate mRNA synthesis and decay rates in these DEF1-deficient cells, we used a nascent transcription metabolic labeling technique called RATE-seq. As expected, we observed reduced synthesis rates across the genome in these cells. Additionally, a global decrease in mRNA decay rates was observed, suggesting that Def1 plays a role in the post-transcriptional regulation of mRNAs. The changes in synthesis and decay rates showed a strong correlation, indicating that this compensation helps buffer steady-state mRNA levels. To gain further insight into Def1's functions, we conducted proximity labeling experiments to identify its protein binding partners within the cells. Our findings revealed that Def1 primarily interacts with cytoplasmic regulators involved in post-transcriptional processes, including proteins responsible for deadenylation, decapping, and translation regulation. Using an mRNA decay reporter assay, we demonstrated that recruiting Def1 to mRNA reduces its expression and accelerates its turnover. In summary, we have identified a novel cytoplasmic function for Def1, establishing it as a key regulator of gene expression in both transcription and mRNA decay.

overall_design:
The role of Def1 in translation and in the regulation of RNA was studied by using RNA-seq, RNA metabolic labeling, and Ribo-seq
Wild type (W303) and def1△ strains were grown to log phase (OD~0.8-1) and then treated with 5mM 4-thiouracil
For metabolic labeling, cells were labeled for different times, then harvested, followed by RNA isolation and pull-down.
For Ribo-seq, RNA was isolated from monosomes
For steady-state RNA-seq, RNA was isolated at log phase
Libraries were prepared and sequenced. Analysis was carried out.

first: Aswathy

last: Sebastian

first: Joseph

middle: C

last: Reese


title: High Resolution Spatial Mapping of Microbiome-Host Interactions via in situ Polyadenylation and Spatial RNA Sequencing [Ileum, with in situ Polyadenylation]

overall_design: Spatial transcriptomics: Ileum, with in situ Polyadenylation


title: High Resolution Spatial Mapping of Microbiome-Host Interactions via in situ Polyadenylation and Spatial RNA Sequencing

overall_design: Spatial transcriptomics


title: Total RNA-seq of C2C12 myotubes treated with agrin or MuSK antibodies

status: Public on Jan 20 2026

city: Leiden

first: Hailiang

last: Mei

address: Einthovenweg 20

department: Sequencing Analysis Support Core

country: Netherlands

institute: Leiden University Medical Center

summary: Total RNA-seq was performed to investigate if MuSK antibody binding directly affects (NMJ) gene expression in muscle cells. C2C12 differentiated myotubes were treated for 16 hours with bivalent MuSK antibodies (activating MuSK signaling) or functionally monovalent MuSK antibodies (inhibiting agrin-induced MuSK signaling) derived from B-cell receptor sequences from a MuSK myasthenia gravis patient. The total RNA transcriptome was compared to treatment with agrin (the natural activator of MuSK) or a negative control antibody targeting a protein not present in myotubes.

overall_design: RNA-seq profiling of C2C12 differentiated myotubes treated with bivalent MuSK antibodies (13-3B5) or agrin + monovalent MuSK antibodies (13-3B5xb12 or 11-3F6xb12). For each condition 4 biological replicates were generated and used for statistical analysis.

first: Dana

last: Vergoossen

first: Maartje

middle: G

last: Huijbers


title: TL1A-activated Tcells as upstream regulators of perianal fistulizing disease-associated changes in the rectum of Crohn's Disease patients.

city: Barcelona

first: Azucena

last: Salas

address: Rosselló, 149-153

department: Gastroenterology

institute: IDIBAPS

summary: Single-cell RNA sequencing revealed the increased abundance of some cell types, such as intestinal fibroblasts, in the CD-PFD rectal mucosa relative to CD. Within the stromal subset, the lamina propria S1 fibroblasts showed the highest number of differentially expressed genes (DEGs) between CD and CD-PFD patients, including an upregulation of TFPI2 and a downregulation of the TGFβ-responding gene CTGF. These changes were validated by bulk RNA analysis, where we also observed overexpression of the previously described PFD target genes MMP1 and MMP3. In vitro studies with intestinal fibroblasts confirmed the negative regulation by TGFβ of the PFD-signature, thus ruling out TGFβ as a driver of the PFD-associated fibroblast signature. Next, we investigated DEGs in the lymphoid compartment and identified lymphotoxin beta (LTB) as being upregulated in CD-PFD intestinal CD4+ T cells. LTB interacts with its receptor LTBR, which is expressed in stromal, epithelial and myeloid cells. Interestingly, LTB-LTBR interactions were increased in the CD-PFD group. In vitro studies in primary fibroblasts showed that LTB upregulates TFPI2, while it downregulates CTGF, thus reproducing the PFD-associated signature. Finally, we submitted the top 50 genes overexpressed by CD-PFD CD4+ T cells to the immune dictionary1, which identified TL1A as its most likely driver. In line with this, the TL1A receptor TNFRSF25 was overexpressed in CD-PFD CD4+ T cells. As a link between TL1A and LTB is not described in the literature, we stimulated anti-CD3-activated peripheral T cells with TL1A and observed the significant upregulation of LTa1b2, the functional form of LTB. Intriguingly, we also observed that while TNF can drive the PFD-associated signature in fibroblasts, it cannot induce LTa1b2 in T cells, suggesting that TNF and TL1A/LTB signalling are two independent but potentially complementary pathways in PFD. In summary, we propose a previously unrecognized TL1A-LTB axis as being responsible for inducing PFD-associated alterations in the rectal mucosa, and we hypothesise that inhibition of TL1A might be worth exploring in the context of perianal disease.

overall_design: Rectum biopsies from patients with Crohn's Disease (CD) with and without perianal fistulizing disease (PFD) were digested and processed for scRNA-seq analysis (10x Genomics). A total of 31 patients were included, with distinct clinical characteristics (active inflammation, remission, or uninvolved tissue).

first: Victoria

last: Gudiño

first: Jae-won

last: Cho

first: Berta

last: Caballol

first: Angela

last: Sanzo-Machuca

first: Ana

last: Corraliza

first: Marisol

last: Veny

first: Livia

last: Genaro

first: Elisa

last: Melón-Ardanaz

first: Carme

middle: M

last: Casademunt

first: Miriam

last: Esteller

first: Agnes

last: Fernández-Clotet

first: Ingrid

last: Ordàs

first: Raquel

last: Franco-Leal

first: Elena

last: Ricart

first: Julia

last: Panes

first: Martin

last: Hemberg


title: Codonopsis pilosula polysaccharides mitigates Brucella abortus outer membrane protein 19-induced uterine damage via macrophage adhesion and calcium signaling

status: Public on Jan 19 2026

city: Hohhot

first: xuxu

last: wang

address: Jinshan Campus, Inner Mongolia Medical University, Jinshan Economic and Technological Development Zone, Tumed Left Banner

department: School of Public Health

institute: Inner Mongolia Medical University

summary: Brucellosis is a zoonotic disease caused by the Brucella species. Its pathogenesis is closely linked to bacterial evasion of macrophage-mediated killing, induction of a pro-inflammatory cytokine storm, and immune-mediated pathological damage. Accumulating evidence indicates that Codonopsis pilosula polysaccharides (CPPS) inhibits inflammatory signaling, enhances macrophage phagocytosis, and exerts immunomodulatory effects across multiple organs. However, the therapeutic potential of CPPS against brucellosis remains largely unexplored.

overall_design:
This study aimed to explore the effects of CPPS on inflammatory response induced by Brucella outer membrane protein 19 (OMP19). In vivo, CPPS significantly alleviated tissue damage and HMGB1 expression in the mouse uterus induced by OMP19. In vitro, CPPS inhibited the SYK/FAK/AKT phosphorylation, PKC activation, and Wnt-1 signaling pathway transduction. Additionally, CPPS also modulated the cytokine profile, downregulating pro-inflammatory cytokines (TNF-α, IL-6) while increasing anti-inflammatory IL-10 levels. Furthermore, CPPS decreased the levels of paxillin and E-cadherin, and reduced the intracellular calcium ion (Ca²⁺) concentration. Collectively, these findings indicate that CPPS mitigates OMP19-triggered uterine damage by regulating macrophage adhesion and calcium-dependent signaling, highlighting its potential as a therapeutic agent against brucellosis.
Control: Untreated (mouse primary peritoneal macrophages)
CPPS+OMP: Stimulated with CPPS and OMP19 (mouse primary peritoneal macrophages)
OMP: Stimulated with OMP19 (mouse primary peritoneal macrophages)


title: TL1A-activated Tcells as upstream regulators of perianal fistulizing disease-associated changes in the rectum of Crohn's Disease patients [scRNA-seq]

first: Azucena

last: Salas

first: Victoria

last: Gudiño

first: Jae-Won

first: Carme M

last: Masamunt

first: Agnès

first: Julià

last: Panés


title: Mechanism of SETX-BRCA1-BARD1 complex in resolution of R-loops and transcription-replication conflicts

status: Public on Jan 16 2026

city: San Antonio

first: Hanzhou

last: Wang

address: 8403 Floyd Curl Drive, MSC 7784

institute: UT Health at San Antonio

summary: Senataxin (SETX), a RNA-DNA helicase, is recruited to transcription pause sites via the tumor suppressor BRCA1. Here, we define the mechanism by which SETX-BRCA1 resolves transcription-associated R-loops to prevent deleterious outcomes. Specifically, we show that SETX unwinds R-loops, and that the complex of BRCA1 and its obligatory partner BARD1 binds R-loops and stimulates R-loop unwinding by SETX. Importantly, BRCA1-BARD1 alleviates the inhibitory effect of RAD52 on SETX-mediated R-loop unwinding. We also demonstrate that phosphorylation of Ser642 in SETX promotes its interaction with BRCA1 via the tandem BRCT domain of the latter. Accordingly, mutations in the catalytic domain or Ser642 in SETX lead to R-loop accumulation, transcription-replication conflicts, replication fork stalling, and DNA double strand breaks in human cells. Our results thus establish the molecular basis for functional synergy between SETX and BRCA1-BARD1 in R-loop resolution and the mitigation of transcription-replication conflicts to preserve genome integrity.

overall_design: DRIP-seq (DNA-RNA Immunoprecipitation sequencing) was performed to detect R-loops in HAP1 WT and SETX KO cells. Each condition was analyzed in triplicate. RNase H-treated samples served as negative controls to confirm R-loop specificity.

first: Lai

last: Zhao

first: Chen

last: Yidong


title: tRNA-derived RNA processing in sperm transmits non-genetically inherited phenotypes to offspring in C. elegans

status: Public on Feb 04 2026

city: Philadelphia

first: Colin

last: Conine

state: Pennsylvania

address: 421 Curie Blvd BRB 1213

department: Genetics and Neonatology

institute: UPenn Perelman SOM and CHOP

summary: The environment encountered by an organism can modulate epigenetic information in the gametes to transmit non-genetically inherited phenotypes to offspring. In mouse models, the diet of males regulates specific tRNA-derived RNAs (tDRs) in sperm. After fertilization, tDRs regulate embryonic gene expression and generate metabolic phenotypes in adult offspring through uncharacterized changes during development. Here we demonstrate that in C. elegans tDRs also accumulate in sperm and can similarly transmit epigenetically inherited phenotypes to offspring. We identify the RNaseT2 enzyme, rnst-2, as a regulator of C. elegans’ tDR accumulation. RNST-2 processes or degrades tRNA-halves, leading to the accumulation of shorter <30 nt fragments. This rnst-2 dependent regulation of tDR length distribution modulates specific tDRs in sperm which, after fertilization, regulate early embryonic and developmental gene expression, leading to adaptive phenotypes in progeny. Our findings establish tDRs as a deeply conserved carrier of intergenerational epigenetic information and position the worm as a model for dissecting paternal non-genetic inheritance mechanistically.

overall_design: Small RNA-seq on adult C. elegans males and females, as well as sperm. mRNA-seq on adult C. elegans males and females. Single embryo RNA-seq on C.elegans 2- and 8-cell embryos.

first: Nicholas

last: Galambos


title: Single-cell multiomics of neuronal activation reveals context dependent genetic controls of brain disorders

status: Public on Jan 15 2026

city: Evanston

first: Christina

last: Thapa

state: Illinois

address: 1001 University Place

department: Center for Psychiatric Genetics (CPG)

institute: Endeavor Health

summary: Despite hundreds of genetic risk loci identified for neuropsychiatric disorders (NPD), most causal variants/genes remain unknown. A major hurdle is that disease risk variants may act in specific biological contexts, e.g., during neuronal activation, which is difficult to study in vivo at the population level. Here, we conducted a single-cell multiomics study of neuronal activation (stimulation) in human iPSC-induced excitatory and inhibitory neurons from 100 donors, and uncovered abundant neuronal stimulation-specific causal variants/genes for NPD. We surveyed NPD-relevant transcriptomic and epigenomic landscape of neuronal activation and identified thousands of genetic variants associated with activity-dependent gene expression (i.e., eQTL) and chromatin accessibility (i.e., caQTL). These caQTL explained considerably larger proportions of NPD heritability than the eQTL. Integrating the multiomic data with GWAS further revealed NPD risk variants/genes whose effects were only detected upon stimulation. Interestingly, multiple lines of evidence support a role of activity-dependent cholesterol metabolism in NPD. Our work highlights the power of cell stimulation to reveal context-dependent “hidden” genetic effects. This dataset aims to validate the cell type-specific transcriptomic effects of the key transcription factors (TFs) of the predicted autism-relevant gne regulatory networks (GRNs).

overall_design: We introduce premature stop codons in TCF4, MEF2C, and RORB via cytosine base editing system with reporter editing enrichment, causing a permanent gene knockout (KO) in iPSCs. The iPSC-derived glutmatergic and GABAergic neurons were co-cultured with primary rat astrocytes and treated with KCl to model neuronal activity. Transcriptional effects of each TF KO were assayed by scRNA-seq.

first: Duan

last: Jubao

first: He

last: Xin

first: Liang

last: Lifan

first: Zhang

last: Hanwen


title: H3K18 lactylation-mediated ΔNp63α expression promotes self-renewal in limbal stem cells

status: Public on Jan 14 2026

city: Tsingdao

first: Longfei

last: Li

address: yushan road no.5

institute: Ocean university of China

summary: In the present study, we established MYC-overexpressing limbal epithelial stem cell line (oeMYC-LESC) that exhibits a biomarker expression profile resembling that of limbal progenitor cells (LPCs). The self-renewal capacity of oeMYC-LESCs was markedly enhanced compared to high-passage cells, primarily through lactylation-dependent mechanisms. Specifically, H3K18la upregulates ΔNp63α, a key transcriptional regulator essential for epithelial stem cell function and the maintenance of stratified epithelial integrity [a]. In vivo studies further demonstrated that the H3K18la‑ΔNp63α axis promotes corneal epithelial regeneration.

overall_design: CUT&Tag-seq of H3K18la modification in rLESCs. This expertimental aims at explore how H3K18la affect LESCs proliferation and self-renewal.


title: Bidirectional regulation of social memory by two distinct types of GABAergic neurons in the lateral septum

status: Public on Jan 13 2026

city: ChongQing

first: Mingrui

last: Xu

address: Xinqiao

institute: Second Affiliated Hospital of Army Medical University

summary: Humans and animals memorize and recognize familiar conspecifics during social interactions, known associal memory. While the hippocampus is crucial for social memory, the dynamic regulation social memory, particularly the negative regulation, remains unclear. Here, we identified two molecularly distinct subpopulations of GABAergic neurons in the mouse lateral septum(LS) expressing somatostatin(SST) and calbindin1(CB), respectively, with complementary distribution patterns. Activation of SST+ neurons enhances social memory acquisition, whereas activation of CB+ neurons inhibits it. Optogenetic manipulation of SST+ neurons regulates theta rhythm oscillations, correlating with their impact on social memory. SST+-dLS neurons and CB+-vLS neurons preferentially receive stronger excitatory inputs from the dorsal (vCA1d) and ventral(vCA1v) parts of vCA1, respectively. The vCA1d→SST+-dLS→lateral hypothalamic area (LHA) circuit positively regulates social memory acquisition, whereas thevCA1v→CB+-vLS→anterior hypothalamic nucleus (AHN) pathway negatively regulates it. This study uncovers two parallel subcortical neural circuits underpinning the dynamic regulation of social memory.

overall_design: The lateral septum tissue of male C57BL/6 mice at 2-month old were taken for single cell RNA-seq

first: Li

last: Zhang

first: Mengbing

last: Huang

first: Chao-Liang

last: Ye

first: Zhiwei

last: Tang

first: Yuan

first: Ting

first: Shu

last: Luo

first: Rui

last: Ji

first: Chang

last: Yu

first: Hongyan

first: Peng

last: Cao

first: Qing-Feng

last: Wu

first: Man

last: Jiang


title: Humanized and Charge-Optimized CSPG4-Specific CAR-T Cells Show Enhanced Efficacy Against Head and Neck Squamous Cell Carcinoma

status: Public on Jan 06 2026

city: shanghai

first: wang

last: zhitong

state: shanghai

address: No. 138, Fenyang Road, Xuhui District

department: Otorhinolaryngology

institute: Eye & ENT Hospital

summary: Chimeric antigen receptor (CAR) T cell therapy for head and neck squamous cell carcinoma (HNSCC) is hampered by the lack of a robust tumor antigen and a suitable CAR design.CSPG4 is highly expressed in HNSCC clinical samples and cell lines, correlating with poor prognosis. Its knockout markedly reduced tumor cell proliferation in vitro and in vivo, validating CSPG4 as an attractive CAR target. First‑generation CSPG4.CAR‑T cells bearing the murine scFv 763.74 showed potent in vitro cytotoxicity but failed to control tumor growth in vivo due to excessive tonic signaling and early exhaustion. By humanizing the scFv framework to reduce positive_x001E_charge residues and immunogenicity, we generated CAR_x001E_T cells with low tonic signaling, diminished exhaustion and differentiation, enhanced tumor_x001E_specific killing, and prolonged in vivo persistence, resulting in superior antitumor activity in both xenograft and PDX models.

overall_design: We confirmed CSPG4’s expression and oncogenic role via qPCR and immunohistochemistry on primary HNSCC specimens, and by CRISPR‑mediated knockout in cell lines and xenografts. To optimize CAR design, we grafted the murine scFv 763.74 CDRs onto a human antibody framework engineered to minimize surface positive‑charge patches and immunogenic epitopes. Humanized CSPG4.CAR‑T cells were then evaluated for tonic signaling, exhaustion marker expression, proliferation, and cytotoxicity in vitro, as well as for antitumor efficacy and persistence in cell‑line xenograft and patient‑derived xenograft (PDX) models.

first: Jian

last: Chen

first: Xiang

first: Shizhen

last: Qiu

first: Zhitong

last: Wang

first: Haopeng


title: Small nucleolar RNA Snora61 drives self-renewal of small intestinal stem cells via initiation of Lgr5 transcription

city: Beijing

first: Jiacheng

last: He

state: Beijing

address: No.15 DaTun Road

institute: IBP

summary: Intestinal epithelium relies on intestinal stem cells (ISCs) for rapid and precise tissue replenishment to maintain gut normal function. The self-renewal maintenance of ISCs is finely regulated by multiple stemness factors and signaling pathways. However, the transcription mechanisms of some key stemness factors remain poorly understood. Here we identified that small nucleolar RNA Snora61 is highly expressed in ISCs. Snora61 is mainly distributed in the nucleoplasm. Snora61 knockout impairs ISC self-renewal and intestinal regeneration. Mechanistically, Snora61 binds to the promoter region of Lgr5 gene and engages with RNA-binding protein RBMX to recruit HMGB2 onto Lgr5 promoter, leading to Lgr5 transcription and expression. Snora61 promotes the self-renewal of small intestinal stem cells, which in turn enhances the proliferation of downstream differentiated cells, thereby contributing to the maintenance of intestinal homeostasis. Conversely, Snora61 knockout causes reduced LGR5 expression. Deletion of Lgr5 with Snora61 displays more severely impaired ISC self-renewal and intestinal regeneration. Our findings reveal a novel regulatory mechanism of Lgr5 transcription underlying ISC self-renewal maintenance.

overall_design: ChIRP-seq of Snora61 in ISCs


title: Gene regulatory network determinants of rapid recall in human memory T cells [WGS]

status: Public on Jan 05 2026

city: Cincinnati

first: Artem

last: Barski

address: 3333 Burnet Av

department: Allergy

institute: Cincinnati Children's Hospital

summary: We applied sc-multiome-seq technology (tandem transcriptome and chromatin accessibility) to a TCR activation time course of naive and memory human CD4+ T cells, to elucidate the molecular drivers of rapid recall at genome scale. WGS data were used to deconvolute donors within the same scMultiome library.

overall_design: Whole genome sequencing and variant calling: DNA was isolated using a PureLink Genomic DNA Kit (Thermo Fisher). Whole-genome sequencing was performed at Novogene.

first: Alex

last: Katko

first: Svetlana

last: Korinfskaya

first: Michael

last: Kotliar

first: Leah

last: Kottyan

first: Emily

last: Miraldi

first: Sarah

last: Potter


title: A rise in prepubertal DHEA in the spiny mouse reveals the effect of adrenarche on the reproductive axis

status: Public on May 14 2026

city: Ness ziona

first: Maya

last: Sudman

address: sahlav

country: Israel

institute: Technion

summary: Adrenarche, characterized by rising adrenal dehydroepiandrosterone (DHEA) levels, precedes puberty and has been implicated in reproductive maturation, and disorders like polycystic ovary syndrome (PCOS). However, the mechanisms by which DHEA influences the hypothalamic-pituitary-gonadal (HPG) axis remain poorly understood, largely due to the absence of an appropriate animal model. The spiny mouse (genus Acomys), which has a prolonged juvenile phase and endogenous prepubertal DHEA production, provides a valuable system to investigate the effects of early-life exposure to DHEA. We confirmed the spiny mouse prepubertal rise in circulating DHEA levels, which occurs independently of HPG axis activation. Transcriptomic analysis revealed increased ovarian expression of steroidogenic and estrogen-responsive genes, suggesting possible effects of DHEA. We show in vitro that DHEA induces Prlr and Prl expression seemingly via the estrogen receptor. Adrenalectomy (Adx) followed by DHEA “rescue” (AdxDHEA) revealed that DHEA can be synthesized and metabolized outside the adrenal glands. Ovarian transcriptomes from AdxDHEA mice exhibited extensive changes, including upregulation of immune response-related genes, and downregulation of cholesterol-metabolism and estrogen-synthesis genes, most notably Cyp19a1. The reduced Cyp19a1 expression is likely due to elevated Amhr2, and was accompanied by a high androgen-to-estrogen ratio, indicating a DHEA-induced, PCOS-like phenotype. The rise in DHEA during an extended juvenile phase establishes the spiny mouse as a suitable model for studying the consequences of elevated DHEA in childhood. Our findings reveal that prepubertal exposure to DHEA alters ovarian gene expression and steroidogenesis, providing mechanistic insight into how early androgen excess may predispose to reproductive dysfunction.

overall_design: RNA-seq of spiny mice ovaries. The experimental groups are (1) Sham, (2) adrenalectomised and (3) adrenalectomised mice receiving DHEA food supplement. All animals were euthenised one week after the operation.

first: Hadas

last: Gruber

first: Ben

last: Bar-Sadeh

first: Tal

last: Refael

first: Gil

last: Golan

first: Lilach

last: Pnueli

first: Noga

last: Kronfeld-Schor

first: Philippa

last: Melamed


title: Glucocorticoid resistance during chronic social stress in mice: RNA-seq of prefrontal cortex

status: Public on May 13 2026

city: Novosibirsk

first: Natalya

last: Bondar

address: 10, Ac. Lavrentieva ave.

country: Russia

institute: Institute of Cytology and Genetics SB RAS

summary: Chronic stress often leads to the development of various psychopathologies and is usually associated with a change in the function of the HPA axis. An elevated level of glucocorticoid (GC) hormones in the blood initially causes an acute reaction of the body, which subsequently fades, even with continued stimulation with glucocorticoids. It is known that the degree of resistance to elevated hormone levels can affect the effectiveness of therapy in the treatment of stress-induced psychopathologies. In order to identify the molecular basis for the formation of GC resistance, we analyzed the effect of chronic social stress on the transcriptome of the prefrontal cortex in an experimental model of depression. We assessed the level of gene expression in the prefrontal cortex of the control C57BL/6 mice and mice with stress experience for 30 days, both in the basal state and with additional stimulation with dexamethasone. The introduction of dexamethasone made it possible to simulate the situation of an increase in the level of glucocorticoids and activation of the glucocorticoid receptor.

overall_design: RNA-seq of the prefrontal cortex was performed in control C57BL/6 male mice and mice subjected to chronic social stress for 30 days. Using behavioral profiling in the agonistic confrontation test followed by clustering of responses during non-aggressive contact, we identified two subgroups of stressed mice that differed in coping strategy: dep1 (passive coping strategy) and dep2 (active coping strategy). Transcriptomic responses were analyzed in basal conditions (saline injection) and 6h following dexamethasone stimulation (2 mg/kg).

first: Polina

last: Ritter


title: Gene regulatory network determinants of rapid recall in human memory T cells

first: Artem

last: Barski

summary: Rapid recall is the hallmark of memory T cells. While naïve T cells require days to mount an effector response to a new threat, antigen-experienced memory T cells can produce cytokines within hours of the repeatencounter. The establishment of memory and control of rapid recall across lifespan is poorly understood, yet the mechanisms are fundamental to pathogen defense and immunological diseases. Epigenetic poising is a likely mechanism. Indeed, compared to naïve, memory cells exhibit enhanced chromatin accessibility proximal to rapid recall genes, but the transcription factors (TFs) that establish, maintain and utilize these putative regulatory elements are unknown. Here, we leverage single-nuclei (sn)multiome-seq (simultaneous snRNA-seq and snATAC-seq) to (1) characterize the dynamic activation responses of naïve and memory CD4+ T cell subsets and (2) reconstruct the underlying gene regulatory networks, at genome scale.  Our analysis uncovered thousands of genes and putative regulatory elements with rapid-recall dynamics, shared and unique across the several memory populations. A core of memory-associated TFs (MAF, PRDM1, RUNX2, SMAD3 and KLF6) was predicted to orchestrate rapid recall and maintain accessible chromatin at rapid-recall gene enhancers in resting memory cells.  KLF6 binding to its predicted target genes was confirmed by ChIP-seq, while the memory-associated activities of all five factors replicated in independent scRNA-seq studies. Using GWAS to link our T cell populations and their dynamic chromatin landscapes to human phenotypes, we nominate CD4+ T cell populations, rapid recall responses and gene regulatory mechanisms that might mediate genetic risk to autoimmune and inflammatory diseases.

overall_design:
We applied sc-multiome-seq technology (tandem transcriptome and chromatin accessibility) to a TCR activation time course of naïve and memory human CD4+ T cells, to elucidate the molecular drivers of rapid recall at genome scale. WGS was used to deconvolute donors. ChIP-sequencing of a CD4T cells stimulated for 5 hours was performed with two separate KLF6 antibodies to confirm the GRN-predicted role of KLF6.
Suspensions of primary hCD4 T cells from healthy donors were partially depleted of CD27+ cells (TCM and naive populations) to improve resolution of TEM populations. TCR stimulation time course includes four time points: resting, 2.5h (early activation), 5h (peak activation for memory cells), and 15h (late activation), for a total of 16 scMultiome-Seq experiments (4 time points x 4 donors; each sample includes fifth spike-in resting control donor cells).

first: Sarah J


title: Effect of aging on gene expression in the skeletal muscle

status: Public on Jan 01 2026

city: Saint louis

first: Kentaro

last: Mori

state: Missouri

address: 660 S. Euclid Avenue

institute: Washington University School of Medicine

summary: To identify the anti-aging myokine, we looked for genes whose expressions are lower in aged skeletal muscle compared with young skeletal muscle

overall_design: Comparative gene expression profiling analysis of RNA-seq data for skeletal muscle from young and aged mice

first: Shin-ichiro

last: Imai


title: S100A4-lineage Cells Contribute Modesty to Angiotensin II-mediated Thoracic Aortic Aneurysms Through Angiotensin II Type 1a Receptor in Mice

city: Lexington

first: Hisashi

last: Sawada

state: KY

address: 741 South Limestone BBSRB B251

institute: University of Kentucky

summary: Background: Angiotensin II (AngII) exerts a critical role in thoracic aortic aneurysm (TAA) formation via AngII type 1a receptor (AT1aR). However, the principal cell type mediating this process remains unclear. Our previous study demonstrated that S100A4-lineage cells are present in the aortic wall and involved in AngII-induced vascular remodeling. In the present study, we investigated whether S100A4-lineage cells contribute to AngII-mediated TAA formation through AT1aR. Methods: Proteomic, bulk RNA sequencing, and single-cell RNA sequencing data were analyzed to assess changes in S100A4 abundance in response to AngII infusion. Lineage tracing was performed to track S100A4-lineage cells during AngII-mediated TAA formation. Either saline or AngII was infused in mice with genetic deletion of AT1aR in S100A4-lineage cells and their wild-type littermates. Results: AngII infusion increased S100A4 protein and mRNA abundance significantly in the ascending aorta, particularly within smooth muscle cells and fibroblasts. Under basal conditions, S100A4-positive cells were localized to the media and adventitia. Following AngII infusion, these cells expanded markedly and populated the entire aortic wall. Deletion of AT1aR in S100A4-lineage cells modestly reduced AngII-induced TAA formation. Conclusions: S100A4-lineage cells modestly contribute to AngII-mediated TAA development through AT1aR in mice.

overall_design: Comparative gene expression analysis of RNA-seq data for ascending, descending, suprarenal abdominal, and infrarenal abdominal aortas of C57BL/6J male and femal mice with either saline or AngII infusion for 3 days.


title: Single-nucleus Multiome Profiling of Infant and Adult Human Spleen

city: New York

first: Siddhi

last: Nargund

state: NY

address: 3960 Broadway, Lasker 203A

department: Department of Systems Biology

institute: Columbia University

summary: We performed joint single-cell RNA and ATAC-seq on T cells from spleen of infant and adult donors.

overall_design: Multiome-seq: Single nuclei extracted form spleens of Infants and Adults. Joint snRNA and snATAC-seq libraries were prepared using the 10x Genomics platform

first: Peter A

last: Szabo

first: Donna L

last: Farber

last: Sims


title: RNA sequencing of dystrophin- and utrophin-deficient HeLa cells reveals overlapping transcriptomic alterations

city: Poznań

first: Paulina

last: Kościelniak-Wawro

address: Uniwersytetu Poznańskiego 6

institute: Adam Mickiewicz University

summary: CRISPR/Cas9 and iRNA approaches were used to knock-out and knock-down expression of the dystrophin (DMD) and utrophin (UTRN) genes. RNA-sequencing analyses revealed overlapping transcriptomic alterations in HeLa cell lines relating to the observed phenotypic abnormalities, including increased membrane permeability and intracellular calcium levels, aggregation of mitochondria, elevated reactive oxygen species, increased cyto- and genotoxicity, and apoptosis.

overall_design: RNA-seq profiling of wild-type HeLa cells after control siRNA (siCtrl) delivery, DMD knock-out HeLa cells after siUTRN delivery.

first: Patryk

last: Konieczny

first: Sylwia

last: Szwec

first: Alicja

last: Durska


title: GDF15 Expression in Thermogenic Adipocytes Regulates Energy Homeostasis in a Sex-dependent Manner

status: Public on Dec 31 2025

city: Iowa City

first: Renata

middle: O

last: Pereira

state: Iowa

address: 169 Newton Rd

department: Internal Medicine

institute: University of Iowa

summary: Diet-induced obesity (DIO) induces growth differentiation factor 15 (GDF15) in various tissues, leading to increased GDF15 serum levels. The liver is the primary source of circulating GDF15 during DIO, but other tissues are also required. We investigated whether brown adipose tissue (BAT) contributes to GDF15 circulating levels and whether Gdf15 induction in BAT regulates systemic metabolism during DIO. We generated mice with selective Gdf15 deletion in thermogenic adipocytes (KO) and subjected them to 12 weeks of high-fat diet (HFD) feeding. Although in ad-libitum fed conditions GDF15 serum levels were unchanged between genotypes regardless of sex, female KO mice demonstrated reduced food intake, increased mitochondrial fatty acid oxidation in BAT, and were resistant to DIO, which was prevented by ovariectomy. Conversely, male KO mice demonstrated increased food intake, reduced mitochondrial respiratory capacity, and increased fibro-inflammation in BAT, resulting in increased body weight and fat mass accrual. Together, our data show that Gdf15 expression in BAT is required to regulate energy metabolism in mice in a sex-dependent manner.

overall_design: RNA-seq profiling of brown adipose tissue from male or female mice fed a high fat diet for 12-weeks. Mice either had an intact GDF15 gene or it was knocked out specifically in the brown adipose tissue.

first: Jayashree

last: Jena

first: Eric

middle: T

last: Weatherford


title: Core protein synthesis adaptations drive biological novelty in octopus

city: Cambridge

first: Rishav

last: Mitra

state: Massachusetts

address: 16 Divinity Avenue

institute: Harvard University

summary: Much of biology focuses on how differences in the genetic code give rise to new functions, but far less attention is given to adaptations in other components of the central dogma. Octopuses exhibit complex nervous systems and sophisticated behaviors that rival vertebrates, but via an entirely distinct evolutionary history. How did octopuses distinctly evolve such novel traits? Here, we serendipitously discover that octopus ribosomes contain a structural adaptation in the catalytic ribosomal RNA (rRNA) domain, a conserved center for protein synthesis across all life1. This rRNA modification is unique among all animals and mediates enhanced accuracy of protein synthesis, decreases protein misfolding and aggregation, and supports translation during adaptive RNA editing when occupying new environments. Thus, the octopus uses modifications in the core protein synthesis machinery to drive biological novelty, a strategy which could support the evolution of unique organismal traits across life.

sample_organism:
Octopus bimaculoides
Euprymna berryi

platform_organism:
Octopus bimaculoides
Euprymna berryi

overall_design: To characterise gene expression differences in cephalopods, we performed RNA-Seq on arm and brain tissues derived from Octopus bimaculoides and Euprymna berryi. Additionally, to quantify RNA editing, we performed RNA seq from octopus and squid tissues that were subjected to a cold acclimation protocol (6 degrees C decline in ambient temperature over 2 weeks).

first: Amy

last: Lee

first: Nicholas

last: Bellono


title: RNA-seq analysis further corroborated the reversal effect of asp on AOA-enhanced ISG expression in L929 cells [2]

city: Shanghai

first: YH

last: Liao

address: Dongan road 131

institute: Fudan university

summary: To assess the functional significance of asp in the cGAS-STING pathway, these two metabolites were individually added along with AOA to the culture medium, followed by HT-DNA stimulation for 6 hours. Interestingly, asp fully reversed the amplification effect of A on STING-mediated immune response

overall_design: L929 cells were treated with 0.5 mM A for 1h followed by HT-DNA stimulation for 6h in the absence or presence of 20 mM asp, and then cells were harvested for qPCR analysis of IFN response gene expression

first: Yuheng

first: Hao

last: Lin


title: Mapping the total transcriptome at near cellular resolution

first: Joao

last: Xavier

address: 430 E 67th St

institute: Sloan Kettering Institute

summary: Spatial transcriptomics provides context to gene expression information, however most methods are only sensitive to a subset of the RNA species. Many noncoding and microbial RNA molecules lack the poly(A) tail which is used to capture RNAs in sequencing-based methods. These transcripts represent valuable analytes for studying gene regulation and host-microbe interactions, respectively. We and others recently showed that in situ polyadenylation combined with poly(dT) capture enables broad analysis of coding, noncoding, and non-host RNAs. However, current implementations neither attain single-cell resolution or retain spatial information. Recent commercialization of spatial transcriptomics tools have enabled broad adoption of these technologies. Several new tools have been developed which can attain near cellular resolution, including SlideSeq (Seeker, Takara/Curio Bioscience) and StereoSeq (STOmics, BGI). Here we adapt in situ polyadenylation to two commerical spatial transcriptomics platforms with near cellular resolution and show the spatial heterogeneity of the total transcriptome in the infected murine heart and testis.

overall_design: Frozen testis from DBA/2J mice and frozen reovirus-induced myocarditic hearts collected at 7 days post infection (dpi) following oral gavage with Reovirus type 1 Lang (T1L) were processed for Spatial Total RNA Sequencing using a modified Stereoseq (STOmics) workflow. Tissues were cryosectioned at 10 µm thickness and mounted onto a 1 cm × 1 cm STOmics Stereoseq chip. Sections were fixed in ice-cold methanol for 30 min at −20°C, followed by staining and imaging according to the manufacturer’s Stereoseq/STOmics protocol. In situ polyadenylation was then performed using yeast poly(A) polymerase (yPAP; Thermo Scientific): capture areas were equilibrated with 1× wash buffer, incubated with yPAP enzyme mix at 37°C, and the enzyme was removed by washing. A 15-min enzymatic permeabilization step was subsequently performed prior to continuing with the standard STOmics library preparation workflow to generate cDNA and sequencing libraries.

first: Ioannis

last: Ntekas

first: David

last: McKellar

first: Lena

last: Takayasu

first: Iwijn

last: De Vlaminck


title: Identification of the Role of Vitamin D and VDR in Human Endometrial Stromal Cells

city: RTP

first: Franco

last: Demayo

state: NC

address: 111 TW Alexander Drive

institute: NIEHS

summary: In women undergoing in vitro fertilization, higher vitamin D status has been associated with improved live birth rates. Among women with polycystic ovarian syndrome (PCOS), vitamin D has been associated with improvements in spontaneous ovulation. Vitamin D receptor (VDR) is a nuclear receptor activated by 1,25 dihydroxyvitamin D which is the most active metabolite of vitamin D. Mice that lack the vitamin D receptor exhibit arrested follicular development, uterine hypoplasia, prolonged estrous cycles, and subfertility. Also, one study of mice reported that the vitamin D receptor is expressed in gonadotropin-releasing hormone (GnRH) neurons, which might suggest a role for vitamin D in hypothalamic signaling. Since the vitamin D receptor knockout mouse is sub fertile with uterine hyperplasia, the most likely cause of vitamin D deficiency may be due to estrogen production by the ovary or estrogen responsiveness of the uterus. So, in this study, we want to identify the effect of vitamin D on human endometrial stromal cells associated with female reproduction.

overall_design: Experimental Design: There are 4 groups, and 12 samples in total. All RNAs will be extracted from the human endometrium stromal cell line (T-HESC). 1) Non-targeting siRNA transfection (control) - treated with vehicle (n=3), treated with 1,25-dihydroxyvitamin D3 (n=3) 2) VDR siRNA transfection (VDR knockdown) -  treated with vehicle (n=3), treated with 1,25-dihydroxyvitamin D3 (n=3)  Data Analysis Strategy: Dr. Tianyuan Wang from the informatics group will help us with the analysis.  1) Remove adaptor 2) Require unique mapping and allow 1 mismatch 3) Remove duplicated reads 4) Down-sampling to the appropriate sequencing depth for each 5) Compare between different groups (siNT vs siVDR, Vehicle vs ligand (1,25-dihydroxyvitamin D3))

first: MyeongJin

last: Yi

first: Tianyuan

last: Wang

first: Francesco

last: DeMayo


title: Diversity and immune dynamics of choroid plexus macrophages are shaped by distinct developmental origins [CD45_TotalSeq_ICV_injection]

status: Public on Dec 22 2025

city: Saint Louis

first: Alina

last: Ulezko Antonova

state: MO

address: 660 S. Euclid Ave

department: Path/Immuno

institute: WUSM

summary: The choroid plexus (ChP) forms a critical interface between the central nervous system and systemic circulation. Despite its importance, the identity and dynamics of resident macrophages remain incompletely understood. Using single-cell RNA sequencing, flow cytometry, lineage tracing, and imaging, we identified three biologically distinct macrophage populations in the homeostatic ChP, defined by expression of CD163, MHCII, or CD9. These subsets arise from different combinations of primitive and definitive hematopoietic waves, occupy distinct anatomical niches, and differentially rely on CSF1 and IL34 for survival. TGFβ signaling is required to maintain their phenotype, and deletion of Tgfbr2 in these cells induces phenotypic reprogramming and disrupts the ChP epithelial barrier. During neuroinflammation, ChP macrophages initiate IFN-I responses and secrete chemokines for CD8 T cell recruitment, while microglia mainly express chemokines for B cells. Finally, we identify phenotypically conserved macrophage subsets in the human ChP, suggesting evolutionary preservation of their phenotypic and functional features.

overall_design: 10x Genomics single-cell RNA sequencing of CD45+ cells sorted from the choroid plexus C57BL6 mice after ICV injection of CD45-Hashtag

first: Khai

last: Nguyen

first: Simone

last: Brioschi

first: Marco

last: Colonna


title: Diversity and immune dynamics of choroid plexus macrophages are shaped by distinct developmental origins [scRNA-seq Tgfbr2_cKO]

overall_design: 10x Genomics single-cell RNA sequencing of CD45+ cells sorted from the choroid plexus of Tgfbr2-flox and Tgfbr2-flox : Lyz2-Cre mice


title: High Resolution Spatial Mapping of Microbiome-Host Interactions via in situ Polyadenylation and Spatial RNA Sequencing [Spatial transcriptomics]

summary: Inter-microbial and host-microbial interactions are critical for the functioning of the gut microbiome, but few tools are available to measure these interactions in situ. Here, we report a method for broad spatial sampling of microbiome-host interactions in the gut at high resolution (1 µm). This method combines enzymatic in situ polyadenylation of both bacterial and host RNA with spatial RNA-sequencing to increase bacterial RNA recovery and enable transcriptomic analysis of low-abundance and spatially restricted microbial taxa. We benchmark the method against existing spatial transcriptomic workflows, demonstrating improved sensitivity and resolution. Application of this method in a mouse model of intestinal neoplasia revealed the biogeography of the mouse gut microbiome as function of location in the intestine, frequent strong inter-microbial interactions at short length scales, and tumor-associated changes in the architecture of the host-microbiome interface. This method is compatible with widely available commercial platforms for spatial RNA-sequencing and can therefore be readily adopted to study the role of short-range, bidirectional host-microbe interactions in microbiome health and disease.

overall_design:
Spatial transcriptomics
Cryosections were obtained from the ileum of  two 13 weeks old mice (male and female). For spatial total RNA sequencing, tissue sections (10 µm thick) were processed with a modified Stereoseq (STOmics) protocol.


title: Hybrid capture RNA-seq defines temporal gene expression in Rickettsia

first: Allison

last: Scott

state: MA

address: 31 Ames St

department: Biology

institute: Massachusetts Institute of Technology

summary: Pathogenic Rickettsia species are obligate intracellular bacteria that must reside in a mammalian host or arthropod vector cell to survive. Although these bacteria transition between different intracellular environments during infection, they encode few putative transcription factors, and their gene regulatory networks are largely unknown. Because of their inextricable relationship with eukaryotic cells, transcriptional profiling of the pathogen is complicated by the abundance of contaminating host RNA, especially in infection conditions or stages where the bacterial burden is inherently low. Here, we employ a hybrid capture technique (PatH-Cap) to improve library preparation by enriching bacterial transcripts while depleting host and rRNA molecules. Using PatH-Cap, we explored transcriptional changes throughout the first 24 hours of infection, including infection initiation – an infection stage which has been difficult to profile with standard library preparation methods. We then clustered genes based on their temporal trends, revealing cohorts of genes whose expression is up- or downregulated at different stages of infection. We also highlighted the diverse temporal expression trends of genes with known roles in growth and pathogenesis, including translation and cell division genes, secreted effectors, and secretion system components. Lastly, we identified 310 antisense RNA molecules, many of which also showed strong temporal trends. This work demonstrates that sensitive transcriptional profiling approaches like PatH-Cap hold great promise for dissecting gene expression networks driving infection in intracellular pathogens that have historically posed significant technical challenges.

overall_design: Hybrid capture (PatH-Cap) proof of concept with the intracellular bacterium, R. parkeri, at 0, 24, and 48 hours post infection (Samples 1-32). Time course PatH-Cap RNA-seq of R. parkeri during the first 24 hours of infection (Samples 33-86)

first: Vincent

last: Butty

first: Stuart

last: Levine

first: Rebecca

last: Lamason


title: Diversity and immune dynamics of choroid plexus macrophages are shaped by distinct developmental origins

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Diversity and immune dynamics of choroid plexus macrophages are shaped by distinct developmental origins [scRNA-seq steady state]

summary: The choroid plexus, responsible for cerebrospinal fluid production, is vital for brain functions. This organ serves as a crucial interface between the central nervous system and systemic circulation and thus faces constant immunological challenges. While resident macrophages within the choroid plexus provide immunosurveillance, their biological characteristics and immune dynamics remain poorly understood. In this study, we extensively examined the phenotype of choroid plexus macrophages using high-throughput single-cell RNA sequencing, flow cytometry, and imaging techniques. Our data unveiled three distinct macrophage populations within the homeostatic choroid plexus expressing either CD163, MHCII, or CD9. These macrophage subsets exhibited differential input from primitive and definitive hematopoietic waves, different spatial location and relied on distinct factors for survival. Upon neuroinflammation, these cells orchestrated IFN responses producing chemokines for effector CD8 T cells, while microglia predominantly expressed chemokines for B cells. Finally, we present evidence of phenotypically conserved macrophage subsets in the human choroid plexus.

overall_design: scRNA-seq of FACS sorted choroid plexus CD45+ cells.

first: Siling

last: Du


title: Diversity and immune dynamics of choroid plexus macrophages are shaped by distinct developmental origins [bulk RNA-seq]

overall_design: Bulk RNA-seq of the total RNA extracted from the choroid plexus, dissected from lateral and fourth ventricles of the mouse brain, to assess cytokine expression.


title: CRISPR/Cas9-mediated validation of candidate Master Regulators Proteins in DMG/GBM Cell Lines

first: Lorenzo

last: Tomassoni

address: 1130 St Nicholas Avenue

summary: Three GBM and three DMG cell lines were selected to be used in a function validation CRISPR screening to elucidate essentiality of canidate Master Regulator proteins

overall_design: A pooled CRISPR/Cas9-mediated KO screen was performed in three human DMG cell lines (SF8628, DIPG4 and DIPG17) and three human GBM cell lines (GBM22, KNS42 and GBM43)—using guide RNAs (sgRNAs) targeting 1,433 genes

first: Ester

last: Fernandez

first: Xu

last: Zhang

first: Junqiang

first: Aleksandar

last: Obradovic

first: Pasquale

last: Laise

first: Aaron

last: Griffin

first: Lukas

last: Vlahos

first: Hanna

last: Minns

first: Diana

middle: V

last: Morales

first: Christian

last: Simmons

first: Matthew

last: Gallitto

first: Hong-Jian

last: Wei

first: Timothy

last: Martins

first: Pamela

last: Becker

first: John

last: Crawford

first: Theophilos

last: Tzaridis

first: Robert

last: Wechsler-Reya

first: James

last: Garvin

first: Robyn

middle: D

last: Gartrell

first: Luca

last: Szalontay

first: Stergios

last: Zacharoulis

first: Cheng-Chia

last: Wu

first: Zhiguo

first: Andrea

last: Califano

first: Jovana

last: Pavisic