title: Regulatory elements of pancreas development license the initiation of pancreatic ductal adenocarcinoma.

city: Copenhagen

first: Luis

last: Arnes

address: Ole Maaløes Vej 5

country: Denmark

institute: Biotech Research & Innovation Centre

summary: Cellular plasticity and transitional cellular states are crucial for tissue regeneration across multiple organs. In the pancreas, oncogenic Kras hijacks this program, acting on tissue-specific enhancers to prevent the resolution of acinar-to-ductal metaplasia (ADM) and lock regeneration into a pro-inflammatory state that progresses to cancer. Enhancer transcription, an early event during cellular state transitions, can generate stable enhancer-associated long noncoding RNAs (lncRNAs) positioned near key transcription factors and chromatin contact boundaries, often enriched for disease-associated variants. While enhancer-associated lncRNAs have been implicated in transcriptional regulation and genome organization, their role in pancreas regeneration and cancer initiation has remained unexplored. In this study, we identified epithelial long noncoding RNAs (lncRNAs) and their target genes in PDAC precursor lesion formation. We demonstrate that LINC00673, expressed from a Sox9-associated super-enhancer during pancreatic development, is reactivated in PDAC. Conditional deletion of LINC00673 in the murine pancreatic epithelium accelerates resolution of ADM and significantly impairs PDAC initiation. Furthermore, we highlight a previously unrecognized role of transcribed super-enhancers in facilitating long-range gene regulation and genome organization during pancreatic cancer initiation. Our study identifies a critical function of LINC00673 in regulating both cell-autonomous and non-cell-autonomous processes during pancreas regeneration and Kras-driven cancer initiation. These findings reveal a novel regulatory layer linking developmental enhancer activity to pancreatic disease progression and highlight new therapeutic opportunities targeting regenerative programs at the earliest stages of neoplastic transformation.

overall_design: RNA sequencing was performed on pancreas of E15.5 embryos of WT (mLINC00673fl/fl) and conditional deletion (Pdx1Cre, mLINC00673fl/fl) of the mouse ortholog of LINC00673 (2610035D17Rik). Each replicate represents an independent animal.

first: Marta

last: Ballester

first: Anita

last: Kurilla

first: Yifan

last: Dai

first: Leire

last: Bergara-Muguruza

first: Katarzyna

last: Radke

first: Carlo

last: Maurer

first: Elisa

last: Espinet

first: Kristina

last: Høj

first: Aida

last: Marisch Delgado

first: Philip

last: Seymour

first: Saynab

last: Omar

first: Charlotte

last: Vestrup Rift

first: Jane

last: Hasselby

first: Pia

last: Klausen

first: Peter

last: Vilmann

first: Ainara

last: Castellanos-Rubio

first: Izortze

last: Santin

first: Albin

last: Sandelin


title: Effect of Serendipita indica on gene expression in Arabidopsis thaliana seedlings under control and salt stress conditions

status: Public on Jan 17 2026

city: Pozuelo de Alarcón

first: Begoña

last: Benito-Casado

state: Madrid

address: Campus de Montegancedo, Autovía M-40 (km 38)

department: Centro de Biotecnolgía y Genómica de Plantas (UPM-INIA/CSIC)

country: Spain

institute: Universidad Politécnica de Madrid

type: Expression profiling by high throughput sequencing

summary: Serendipita indica, a widely studied beneficial root fungal endophyte, promotes plant growth under saline conditions by reducing Na⁺ accumulation in host plants, including Arabidopsis thaliana. This reduction in Na⁺ levels likely contribute to salt detoxification, though the underlying mechanisms remain unclear. Previous studies have demonstrated that SOS1, a key Na+ transporter and major determinant of salt tolerance in plants, is not involved in this reduction. To explore whether other plant transporters might participate in Na+ reduction, we first characterized the full Arabidopsis transportome, with putative substrates and subcellular localizations, and performed a comprehensive transcriptomic analysis of the full set of transporter proteins. In this study, we investigated and ruled out the possible contribution of HKT1, another relevant Na+ transporter implicated in salt adaptation in Arabidopsis. By examining differentially expressed transporters under salt stress, we identified a subset of candidate genes potentially involved in Na⁺ transport. Among these, we evaluated the role of CNGC10 and CNGC13 using mutant lines under both S. indica- and non-colonized conditions. Interestingly, both transporters appeared to be involved in the endophyte-induced decrease in Na⁺ accumulation although, other, yet-unidentified transporters may also contribute to this phenomenon, warranting further functional investigation of the candidate genes highlighted in our analysis.

overall_design: RNA-seq profiling of wild-type Columbia-0 Arabidopsis thaliana seedlings inoculated or non-inoculated with Serendipita indica in salt stress (50 mM NaCl) or control conditions (0 mM NaCl).

first: Adrián

last: González Ortega-Villaizán

first: Lorena

last: Blázquez-Conchillo

first: Carmen

last: Guerrero-Galán

first: Stephan

last: Pollmann

first: Rosario

last: Haro-Hidalgo


title: Single-Cell Profiling and Cell-Cell Communication Analysis of Splenic CD11c⁺ Cells in Wild-Type Mice

status: Public on Jan 18 2026

city: Mainz

first: Xinyuan

last: Liu

address: Langenbeckstraße 1

department: Institute for Molecular Medicine

country: Germany

institute: University Medical Center, Johannes Gutenberg University Mainz

summary: Single-Cell  RNA-sequencing and Cell-Cell Communication analysis of Splenic CD11c⁺ Cells from Wild-Type Mice

overall_design: We conducted single-cell analysis of splenic CD11c⁺ cells from wild-type mice to characterize immune cell heterogeneity and intercellular communication. CD11c⁺ cells were enriched using MACS beads and labeled with a multiplexing kit before capture on the BD Rhapsody Single-Cell Analysis System. Mouse macrophages (MMMs) and Langerin⁺ cDC1s were identified and subsetted using Seurat, and cell-cell communication networks were inferred using the CellChat R package. This approach enables detailed mapping of immune interactions within the splenic microenvironment.

first: Ari

last: Waisman


title: Single-Cell Transcriptomics Reveals FXR1 as an Actionable Target for siRNA Therapy in Ovarian Cancer

city: Milwaukee

first: Masaki

last: Lin

state: Wisconsin

address: 8701 W Watertown Plank Rd

country: USA

institute: Medical College of Wisconsin

summary: Ovarian cancer is one of the leading causes of cancer-related mortality among women and remains exceptionally difficult to manage and treat effectively in the clinic. Fragile X-related protein 1 (FXR1) is significantly amplified and overexpressed in ovarian and various other cancers. We have shown that FXR1 acts as a key regulator of the stability and translation of multiple oncogenic mRNAs, establishing it as an excellent therapeutic target for ovarian cancer. Our Single-cell RNA sequencing (scRNA-seq) analysis demonstrates a complex involvement of FXR1 in cancer progression mainly due to its dual role attributed through its autonomous actions in tumor cells and the modulation of tumor microenvironment (TME). Recent advances in RNA interference (RNAi) therapies have enabled targeting previously undruggable genes. In this study, we developed a locked nucleic acid (LNA)-based small interfering RNA (siRNA) to target FXR1 for ovarian cancer therapy. Compared to native siRNA, siFXR1-LNA demonstrates resistance to RNase degradation, improved tumor tissue uptake, and robust inhibition of its target FXR1. siFXR1-LNA inhibited proteins essential for tumor growth and survival while increasing the levels of pro-apoptotic proteins. Importantly, the polyethylenimine-mediated delivery of siFXR1-LNA effectively reduced tumor growth and peritoneal metastasis in ovarian cancer models, without causing toxicity in both immunocompromised and immunocompetent mice. scRNA-seq further revealed that siFXR1-LNA treatment not only suppressed FXR1 in cancer cells but also disrupted translation mechanisms linked to oncogenesis. In TME, siFXR1-LNA diminished tumor cell proliferation, reduced tumor-promoting M2-like macrophages, increased tumor inhibitory T and NK cells and increased dendritic cells with anti-tumor characteristics. Given the autonomous role of FXR1 in tumor cells and TME for oncogenesis, targeting FXR1 with siFXR1-LNA presents a unique opportunity for treating ovarian cancer and other cancers express high levels of FXR1.

overall_design: For scRNA-seq, mouse ascites from siCont(n=2) and siFXR1-LNA (n=2) was harvested and processed for scRNA-seq was performed using the Chromium Next GEM Single Cell 3ʹ Reagent Kits v3.1 (Dual Index).

first: Jasmine

last: George

first: Xiaolong

last: Ma

first: Ishaque

last: Pulikkal Kadamberi

first: Ajay

last: Nair

first: Sonam

last: Mittal

first: Elaheh

last: Hashemi

first: Sudhir

last: Kumar

first: Mona

last: Singh


title: The Landscape of regulatory element evolution in Panicum hallii

status: Public on Jan 16 2026

city: Austin

first: TASLIMA

middle: E.

last: HAQUE

state: TX

address: J.T. Patterson Laboratories Bldg, 2415 Speedway

department: Department of Integrative Biology

institute: University of Texas at Austin

type: Genome binding/occupancy profiling by high throughput sequencing

summary: In this study, we use comparative genomics and chromatin accessibility profiling to study the molecular evolution of putative functional noncoding regulatory regions in Panicoid grasses.

sample_organism:
Panicum hallii var. filipes
Panicum hallii var. hallii

overall_design: Each experiment (RNASeq or ATACSeq) has three replicates of coastal and inland ecotype of Panicum hallii

first: Taslima

last: Haque

first: Bhaskara

last: Govinal Badiger

first: Robert J.

last: Schmitz

first: Thomas E.

last: Juenger


title: H3K27me3Alpha-Ketoglutarate Drives an Osteogenic and Extracellular Matrix Gene Program in Periodontal Ligament Fibroblasts via Selective Reduction of H3K27me3 [ATAC-Seq]

city: Okayama

first: Shigeki

last: Suzuki

state: Okayama

address: 2-5-1 Shikata-cho, Kita-ku

department: Department of Operative Dentistry

country: Japan

institute: Okayama University

summary: Periodontal disease is a chronic inflammatory condition that destroys tooth-supporting tissues, particularly alveolar bone and the periodontal ligament, and effective regenerative therapies remain limited. While the role of metabolic-epigenomic crosstalk in determining cell fate is well established, the specific mechanism by which a tricarboxylic acid (TCA) cycle metabolite can modulate chromatin regulation to promote periodontal regeneration remains to be elucidated. The impact of one TCA-cycle metabolite, alpha-ketoglutarate (α-KG), was examined in human periodontal ligament fibroblasts cultured under osteogenic induction and profiled by ALP assays, RT-qPCR, analyses of multiple histone modifications, ATAC-seq, and RNA-seq. α-KG increased ALP activity and up-regulated genes associated with osteogenesis and the extracellular matrix (ECM). ATAC-seq revealed minimal genome-wide accessibility changes, whereas histone analyses showed reduced H3K27me3, consistent with an epigenetic mechanism that does not require extensive chromatin opening. The RNA-seq identified α-KG-induced 14 genes upregulated, including multiple components of the OGN-OMD-PLAP1/ASPN-ECM2 locus, supporting an osteogenic/ECM transcriptional program. In a mouse periodontal regeneration model, oral administration of α-KG enhanced alveolar bone regeneration and reduced H3K27me3 signals and collagen-rich tissue organization within the periodontal ligament space. These findings identify α-KG as a metabolite-driven epigenetic modulator that alleviates H3K27me3-mediated repression and supports periodontal regeneration.

overall_design: Examination of the effects of aKG  on chromatin accessiblity in PDLF cells.

first: Ryu

last: Hasegawa


title: A bacterial YopJ-family acetyltransferasesuppresseshost immune response by Nε-acetylation of JAK1

city: Xiamen

first: Guosheng

last: Hu

state: Fujian

address: Xiang'an South Road, Xiang'an District

department: School of Pharmaceutical Sciences

country: China

institute: xiamen University

summary: A common host response to pathogen infection involves the production of robust interferons or proinflammatory cytokines to activate the JAK-STAT pathway, thereby limiting pathogen replication. The bacterial pathogen Legionella pneumophila creates an intracellular niche and evades host immunity utilizing a cohort of effectors by diverse biochemical activities, thereby permissive for its intracellular replication. However, roles of the JAK-STAT pathway during bacterial infection remain elusive. Here, we identify for the first time that L.pneumophila acetyltransferase effector Lem17 acts as a negative regulator of the JAK-STAT signaling. Lem17 directly interacts with JAK1 through a JAK1-binding Box1-like motif, preventing its recruitment by cytokine receptors. As a YopJ-family acetyltransferase, Lem17 catalyzes Nε-lysine acetylation of JAK1 and impairs its kinase activity, thereby disrupting JAK1-mediated signaling transduction. Our findings provide new insights into the mechanism by which L. pneumophila subverts host immunity through acetylation and underscore the role of the JAK-STAT pathway against bacterial infection.

overall_design: RNA-sequencing (RNA-seq) analysis on IFN-β-primed HeLa cells ectopically expressing Lem17 or an empty vector.

first: Tao-Tao

last: Chen

first: Si-Ru

last: Zheng


title: Chromosomal instability shapes the tumor microenvironment of esophageal adenocarcinoma via a cGAS–chemokine–myeloid axis [RNA-seq]

city: Oxford

first: Eileen

last: Parkes

address: Off Roosevelt Drive

department: Department of Oncology

country: United Kingdom

institute: University of Oxford

summary: Chromosomal instability (CIN), a pervasive feature of esophageal adenocarcinoma (EAC), drives tumor aggressiveness and metastasis. CIN stimulates the cGAS–STING pathway, typically linked to anti-tumor immunity. However, despite the high CIN burden in EAC, the cGAS–STING pathway remains largely intact. To address this paradox, we interrogated multiple esophageal cancer models, discovering myeloid-attracting chemokines – with CXCL8 as a prominent hit – as conserved CIN-driven targets in EAC. Using multiplexed immunofluorescence microscopy, we quantified ongoing CIN in human EAC tumors by measuring cGAS-positive micronuclei, validated by whole-genome sequencing. Coupling in situ CIN detection with single-nucleus RNA sequencing and multiplex immunophenotyping of human EAC, we link CIN to tumor-intrinsic innate immune activation, CXCL8 expression, and myeloid cell-mediated immunosuppression. In EAC patients, CIN-high, myeloid-dominated tumors correlate with poor outcomes and aberrant cGAS–STING signaling. These insights explain the counterintuitive maintenance of cGAS–STING and highlight disruption of the CIN–cGAS–inflammation axis as a potential therapeutic strategy in EAC.

overall_design: RNA-seq of cGAS-proficient (Cas9 expressing) and cGAS-deficient (CRISPR-Cas9-mediated cGAS KO) esophageal adenocarcinoma cell line clones (OE33 and SK-GT-4). Cells were treated with the MPS1 inhibitor reversine (pharmacological induction of chromosomal instability) or diluent (DMSO; control) for 48h.

first: Bruno

last: Beernaert

middle: E


title: Chromosomal instability shapes the tumor microenvironment of esophageal adenocarcinoma via a cGAS–chemokine–myeloid axis [snRNA-Seq]

overall_design: Single-nucleus RNA sequencing (snRNA-seq) of 16,127 nuclei derived from 9 fresh-frozen esophageal adenocarcinoma (EAC) samples.


title: Chromosomal instability shapes the tumor microenvironment of esophageal adenocarcinoma via a cGAS–chemokine–myeloid axis

overall_design: RNA-seq was performed on isogenic CP-A cell lines exhibiting distinct inherent levels of chromosomal instability (CIN). CIN was progressively induced through sequential CRISPR–Cas9-mediated depletion of TP53 (p53) and CDKN2A (p16), followed by overexpression of a dominant-negative form of the mitotic kinesin MCAK (dnMCAK). Serial genetic alterations were introduced independently across three clonal lineages. A Cas9-expressing parental CP-A clone was included as a control to account for potential confounding effects of Cas9 overexpression.


title: H3K27me3Alpha-Ketoglutarate Drives an Osteogenic and Extracellular Matrix Gene Program in Periodontal Ligament Fibroblasts via Selective Reduction of H3K27me3 [RNA-Seq]

overall_design: Examination of the effects of aKG on gene expression in human periodontal ligament cells


title: Targeting HMGB2 acts as dual immunomodulator by bolstering CD8+ T cell function and inhibiting tumor growth in hepatocellular carcinoma [ATAC-seq]

city: SHANGHAI

first: WEIFENG

last: QU

address: No.180 Fenglin Road

institute: Zhongshan Hospital, Fudan university

summary: T cell exhaustion is a critical obstacle for durable treatment response in hepatocellular carcinoma (HCC). Developing drugs that control tumor growth and simultaneously bolster immune function is of great significance. The transcriptional regulator high mobility group box 2 (HMGB2) has emerged as a risk factor in prognosis of HCC. However, the role of HMGB2 in HCC tumor microenvironment (TME) is poorly understood. Here, we discovered HMGB2+ CD8+ T cells as being associated with T cell exhaustion and resistance to anti-PD-1 treatment through single-cell RNA sequencing of human and murine HCC tissues. Mechanistically, HMGB2 impaired the mitochondrial oxidative phosphorylation in CD8+ T cells by increasing the ubiquitination of NRF2, thus reduced the antitumor effector function. In tumor cells, HMGB2 inactivated the interferon-γ (IFN-γ) response through TRIM24/STAT1 pathway, inhibiting susceptibility and recruitment to effector T cells. Tannic acid, a specific inhibitor of HMGB2, synergized with PD-1 antibody to attenuate tumor growth and reverse T cell exhaustion. Collectively, this study revealed that HMGB2, a T cell exhaustion associated molecule, contributed to tumor immune escape by dual action on CD8+ T cells and tumor cells. These data also provided translational insight into synergistic treatment strategies.

overall_design: ATAC-seq of NC versus HMGB2-knockout CD8+ T cells in C57BL/6J mice.

first: Weifeng

last: Qu

first: Guiqi

last: Zhu

first: Yinghong

last: Shi


title: LncRNA P4HA2-AS1 Drives Renal Interstitial Fibrosis via TRIM32-Mediated K63 Ubiquitination of ULK1 and Autophagic Dysregulation

city: Wuhan

first: Kang

last: yang

address: No. 238 Jie-Fang Avenue, Wuhan, Hubei, P.R. China

institute: Renmin Hospital of Wuhan University

summary: Renal interstitial fibrosis (RIF), the central pathological driver of chronic kidney disease (CKD) progression, remains mechanistically incompletely defined. While long non-coding RNAs (lncRNAs) are emerging as critical regulators of CKD, their roles in RIF pathogenesis are poorly understood. Here, we identify the fibrosis-associated lncRNA P4HA2-AS1 as a key modulator of RIF through integrated analyses of unilateral ureteral obstruction (UUO) mice and TGF-β-stimulated human renal tubular epithelial cells (HK-2), combined with RNA sequencing, RNA pull-down, ubiquitination profiling, and autophagic flux assays. P4HA2-AS1 was markedly upregulated in fibrotic kidneys, and its suppression attenuated fibrotic phenotypes in vivo and in vitro while restoring autophagic flux. Mechanistically, P4HA2-AS1 directly binds the E3 ubiquitin ligase TRIM32, impeding its proteasomal degradation. This stabilization enhances TRIM32-mediated K63-linked ubiquitination of ULK1, a master autophagy initiator, leading to aberrant autophagic activation and fibrotic progression. Our study uncovers a previously unrecognized P4HA2-AS1/TRIM32/ULK1 axis that couples dysregulated autophagy to RIF, proposing lncRNA-protein interaction targeting as a therapeutic strategy against renal fibrosis.

overall_design: RNA-seq profiling of  TGF-β (10ng/ml for 24h) treated or untreated HK-2 cells and  their knockdown derivative (shP4HA2-AS1).

first: Zhou

last: Pan

first: Fei

last: Xiao

first: Wei

first: Ting

last: Liu

first: Wenjing

last: Shu

first: Yan

last: Leng

first: Qingqing

last: Yi

last: Zeng

first: Fan

last: Cheng

first: Hengcheng

last: Yang


title: Genome-wide binding sites of transcription factor RGSV P3 by DAP-Seq

city: Fuzhou

first: Baogang

last: Zhang

state: Fujian Province

address: No. 15 Shangxiadian Road, Cangshan District

institute: Fujian Agriculture and Forestry University

summary: This study maps the cistrome of RGSV P3 in Oryza sativa using DAP-Seq. Includes 2 libraries: treatment and input control.

overall_design: DAP-Seq was performed with RGSV P3 protein; Input as control. Peaks were called using MACS2  with default parameters against the input control.


title: Distinct miR319a identified from Persicaria chinensis mediates cross-kingdom suppression of cervical cancer by targeting ITGA3

city: Beijing

first: Yueyue

last: Yan

state: Beijing

address: No. 1 ShuaiFuyuan Road, Dongcheng District

institute: Chinese Academy of Medical Sciences & Peking Union Medical College

type: Non-coding RNA profiling by high throughput sequencing

summary: Persicaria chinensis, a well-known traditional Chinese medicinal herb that is both edible and medicinal, has been widely acknowledged for its therapeutic effects, such as anti-inflammatory, antioxidant, and antitumor activities. However, the role of miRNAs from this plant in the cross-kingdom regulation of human diseases has not been investigated. In this study, we analyze the miRNA expression profile of P. chinensis using high-throughput sequencing and identify a total of 673 miRNAs, including 422 novel miRNAs that are unique to this plant and 251 conserved miRNAs. Among the conserved miRNAs, pch-miR319a is found to be the most abundant. Moreover, food-oriented pch-miR319a accumulates in the uterus and tumors and exhibits a rich repertoire of target genes within cancer-related pathways, demonstrating significant cross-kingdom regulatory potential. Utilizing the dual-luciferase reporter gene assay, we demonstrate that pch-miR319a from P. chinensis targets the Itga3 gene, which is associated with cervical cancer progression. Overexpression of pch-miR319a significantly decreases the viability, migration, and induces apoptosis of HeLa cervical cancer cells in vitro. Moreover, in a syngeneic mouse tumor model of cervical cancer, treatment with pch-miR319a effectively inhibits tumor growth and downregulates the expression of ITGA3 and the proliferation marker Ki-67. Our study highlights the potential of pch-miR319a from P. chinensis as a novel therapeutic agent for cervical cancer by targeting ITGA3 and provides new insights into the cross-kingdom regulatory mechanisms of plant miRNAs in human diseases.

sample_organism:
Homo sapiens
Mus musculus
Persicaria chinensis

overall_design: 1. Small RNA-seq of Persicaria chinensis: Persicaria chinensis samples were collected from Guangdong Province, China. Total RNA was first extracted from Persicaria chinensis samples by adding Trizol reagent for lysis, followed by chloroform partitioning, isopropanol precipitation, and ethanol washing. The concentration and purity of the RNA were then assessed using a NanoDrop spectrophotometer (Thermo Fisher Scientific, MA, USA), and RNA integrity was evaluated by electrophoresis. Subsequently, miRNA sequencing libraries were constructed using the QIASeq miRNA Library Kit. A pre-adenylated DNA adapter was ligated to the 3′ end of miRNAs, and unbound adapters were removed. An RNA adapter was then ligated to the 5′ end, followed by reverse transcription using a primer with an integrated unique molecular index to generate cDNA. Impurities were removed by magnetic bead purification, and indexed libraries were created through amplification with sample-specific indices, followed by a final round of magnetic bead purification to obtain the miRNA sequencing libraries. The libraries were typically sequenced on the NextSeq 500 System (Illumina Corp) using a paired-end 150 bp sequencing strategy. After sequencing, bioinformatics analysis was performed on the data. 2. mRNA-seq after pch-miR319a transfection in cervical cancer cells: To further elucidate the regulatory effects of pch-miR319a on its target genes, we conducted a comprehensive RNA-seq analysis to determine the differential expression of target genes in response to pch-miR319a overexpression. Cells were seeded into 24-well plates and transiently transfected of control vector or pch-miR319a plasmid using Lipofectamine 3000 (Invitrogen, CA, USA). After 48 hours of transfection, the transfected cells were selected for RNA-seq analysis.

first: Dan

last: Bai

first: Lei

last: Li

first: Leimei

last: Xu

first: Hua

first: Yuhui

last: Wang

first: Han

last: Feng

first: Lan


title: Multi-tissue DNA methylation analysis to identify an appropriate surrogate tissue for a unique neurological tissue specific to spina bifida

city: Boston

first: Maitreyi

last: Mazumdar

state: MA

address: Department of Neurology

institute: Boston Children's Hospital & Harvard Medical School

type: Methylation profiling by genome tiling array

summary:
Background: Animal models suggest a role of epigenetic mechanisms, including DNA methylation, in neural tube closure; however, studies characterizing DNA methylation profiles in nervous system tissue from humans with spina bifida are limited, In this study, we assessed DNA methylation profiles in dural tissue of infants with spina bifida, collected at the time of surgical closure of the defect, and examined whether whole blood or buccal swab are appropriate surrogate tissues, as they are more practical to collect in large-scale epidemiological studies, DNA methylation was measured in dural tissue, buccal swab, and whole blood samples collected from 27 unique infants using the Illumina Infinium MethylationEPIC BeadChip array,
Results: Correlation analysis for each CpG site comparing DNA methylation from all participants in dural tissue to DNA methylation in whole blood DNA or buccal swab DNA yielded 1,555 statistically significant associations for the whole blood analysis and 920 significant associations for the buccal swab analysis at the Bonferroni threshold of significance, We also performed paired analysis, calculating differences between tissues within each individual and then averaging differences across individuals, After accounting for multiple hypothesis testing using the FDR adjustment, 33% of CpG sites assessed were not significantly differentially methylated between dural tissue and whole blood samples, compared to the 27% of sites not differentially methylated between dural tissue and buccal swab samples,
Conclusions: These results suggest that in the absence of dural tissue, both whole blood and buccal swab samples may be considered as surrogates for dural tissue, The study warrants replication in larger groups to validate findings and may assist researchers restricted to more accessible biospecimens (i,e, blood) to further characterize epigenetic contributors to neural tube defect etiology,

overall_design:
This dataset comprises EPIC v1,0 DNAme data for 27 infants with spina bifida, where each participant provided dural tissue, buccal swab, and whole blood samples for DNAme assessment (81 total DNAme samples), DNA was extracted using the QIAsymphony DSP DNA Midi Kit (Qiagen, Valencia, CA), Dural samples were treated with EtOH to remove the OCT gel, and DNA was extracted from dural tissue samples using the DNeasy Blood and Tissue Kit (Qiagen, Valencia, CA), DNA was bisulfite converted (Zymo D5007 Kit, Zymo Research, Irvine, CA), DNA was then ampligied, fragmented, purified, and processed on Illumina Infinium MethylationEPIC BeadChips (Illumina, San Diego, CA) according to the manufacturer's instructions, Quality control of the DNAme data was perfomed with the ewastools and minfi packages in R, all samples passed the default thresholds of the control probes and had a mean detection p-values > 0,05, Data were normalized with preprocessNoob and preprocessQuantile using the minfi package, Probes were then filtered to exclude sites with detection p-values > 0,01 in at least one sample, sites mapping to the X and Y chromosomes, sites with annotated probe SNPs, and cross-reactive probes identified by Chen et al, (2013) and Pidsley et al, (2016), A total of 680,819 CpGs in 81 samples remained for downstream analysis across the tissues,
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The IDAT files have not been provided for participant confidentiality regarding the 56 rs genotyping probes present on the EPIC v1.0 array. These probes have been excluded from the submitted dataset and the raw data have thus been provided as methylated and unmethylated signal intensities with corresponding detection p-values, rather than in IDAT form.  IDAT files will be made available upon reasonable request to MM for research use.
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first: Gwen

last: Tindula

first: Sudipta Kumer

last: Mukherjee

first: Sheikh Muhammad

last: Ekramullah

first: D

middle: M

last: Arman

first: Joynul

last: Islam

first: Subrata Kumar

last: Biswas

first: Md Nafaur

last: Rahman

first: Md

last: Ziauddin

first: Ansar Uddin

last: Ahmed

first: Hafiza Sultana

last: Suchanda

first: Benjamin

middle: C

last: Warf

first: David

last: Christiani

first: Bernardo

last: Lemos

first: Liming

last: Liang

first: Andres

last: Cardenas


title: Dynamic Transcriptomic Remodeling in Grafted Human Neural Progenitor Cells Uncovers Mechanisms for Vision Preservation in Retinitis Pigmentosa

city: Los Angeles

first: Shaughn

last: Bell

state: CA

address: 8700 Beverly Blvd

department: Regenerative Medicine Institute

institute: Cedars-Sinai Medical Center

summary: Human neural progenitor cells (hNPCs) show promise in slowing retinal degeneration and are currently being tested in clinical trials for retinitis pigmentosa (RP). However, the long-term fate of grafted hNPCs and their interaction with host retinal cells remains unclear. Here, we used single-cell transcriptomics to investigate temporal gene expression changes in grafted hNPCs and host retinal cells following subretinal injection into a rodent model of RP, revealing dynamic transcriptomic changes in the degenerative retinal environment. Grafted hNPCs primarily differentiate into an astroglial phenotype and mature over time, contributing to photoreceptor protection through trophic factor secretion, metabolic modulation, suppression of apoptosis, oxidative stress, and inflammation, alongside extracellular matrix remodeling. CellChat analysis revealed a decline in intercellular signaling and communication strength over time, correlating with weakened hNPC-host interactions. These findings suggest that enhancing trophic factor support, particularly MANF, and improving the host retinal environment are critical for sustaining long-term vision preservation.

sample_organism:
Homo sapiens
Rattus norvegicus

platform_organism:
Homo sapiens
Rattus norvegicus

overall_design:
Following hNPC treatment, rats were sacrificed and retinas were dissected at postnatal days 60 (P60) and 90 (P90). Grafted hNPCs and host retinal cells were isolated by FACS and analyzed using single-cell RNA sequencing. Pre-grafted hNPCs were also sequenced as a control for the grafted hNPCs. Single-cell RNA sequencing data (samples GSM6403183 & GSM640318) from rat retinas from another study (Series GSE209872) were used as a non-disease controls.

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The table below lists GEO accessions reused/reanalyzed for this study.
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first: Saba

last: Shahin

first: Bin

last: Lu

first: Somanshu

last: Banerjee

first: Vivek

last: Swarup

first: Hui

last: Xu

first: Jason

last: Chetsawang

first: Stephany

last: Ramirez

first: Jorge

middle: S

last: Alfaro

first: Alexander

last: Laperle

first: Soshana

last: Svendsen

first: Clive

middle: N

first: Shaomei

last: Wang


title: Dnmt3a-dependent de novo DNA methylation enforces lineage commitment and preserves functionality of memory Th1 and Tfh cells [WGEM-seq]

city: Salt Lake City

first: Jeffrey

middle: Scott

last: Hale

state: Utah

address: 15 North Medical Drive

department: Pathology

institute: University of Utah

type: Methylation profiling by high throughput sequencing

summary: Following acute viral infection, naïve CD4+ T cells differentiate into T follicular helper (Tfh) and T helper 1 (Th1) cells that generate long-lived memory cells. However, it is unclear how memory Tfh and Th1 cells maintain their lineage commitment. We demonstrate that Tfh and Th1 lineages acquire distinct Dnmt3a-dependent de novo DNA methylation programs that are preserved into memory.  Dnmt3a deletion impairs lineage commitment and functionality of memory Th1 and Tfh cells, resulting in aberrant Runx1 upregulation that represses germinal center Tfh cell differentiation. In contrast, transient pharmacological DNA methyltransferase inhibition during priming impairs repression of Tfh-associated genes while properly silencing Runx1, and results in enhanced Tfh cell functionality in primary and secondary responses to viral infections. Together, these findings demonstrate that Dnmt3a-mediated epigenetic programing is required to enforce T helper lineage commitment and preserve Tfh and Th1-specific functions during the recall response to infection, and reveal novel strategies to improve long-lived adaptive immunity against infectious diseases.

overall_design: Mouse antigen specific CD4+ T cells (SMARTA TCR Transgenic) were sorted from spleens of non-infected mice (CD4+ T cell naïve samples) and LCMV Armstrong infected mice at 7 days post infection (effector Th1 and effector Tfh samples) for Whole Genome Enzymatic Methyl sequencing

first: Scott

first: Bryant

last: Perkins


title: Dnmt3a-dependent de novo DNA methylation enforces lineage commitment and preserves functionality of memory Th1 and Tfh cells [RNA-seq]

overall_design: Mouse antigen specific WT and Dnmt3a KO CD4+ T cells (SMARTA TCR Transgenic) were sorted from spleens of  LCMV Armstrong infected mice at 7 days post infection (effector Th1 and effector Tfh samples) for RNA sequencing


title: The RNA-binding protein NOVA-1 regulates circRNA expression, alternative splicing, and aging in C. elegans

status: Public on Jan 15 2026

city: Reno

first: Emmanuel

last: Adeyemi

state: NV

address: 1664 N. Virginia Street,

department: Biology

institute: University of Nevada Reno

summary: Circular RNA (circRNA) biogenesis is regulated by RNA-binding proteins (RBPs) that alter back-splicing of exons in protein coding genes. However, few in vivo roles for RBPs in the regulation of circRNA biogenesis have been characterized. In this study, we performed total RNA-seq on wildtype and RBP mutant, nova-1. Our findings indicate that the RBP, nova-1, regulates circRNA expression,  alternative splicing, and aging in C. elegans

overall_design: In this project, total RNA-Sequencing was performed to profile circular RNA expression and linear mRNA splicing differences between C. elegans wild-type and NOVA-1 mutant animals. Total RNA was extracted from Day-3 adult worms using the Purelink RNA mini-kit, followed by a DNase I treatment following the manufacturer's protocol. RNA integrity number ranged from 9.6 to 10.0. Samples were stored at -80C prior to RNA-sequencing.

first: Hussam

last: Alshareef

first: Jaffar

last: Bhat

first: Pedro

last: Miura

last: van der Linden


title: scRNA-sequence of NeuroD1-astrocyte therapy post-TBI mouse

city: 广州

first: shuo

last: zhang

address: 黄埔大道西601号

institute: 暨南大学

summary: Astrocytes, the most abundant glial cells in the central nervous system (CNS), play a critical role in brain injury responses. While NeuroD1 overexpression in astrocytes has been shown to reverse glial scar formation and promote tissue repair in mouse models of traumatic brain injury (TBI), the underlying molecular mechanisms remain incompletely understood.

overall_design: To address this, we performed single-cell transcriptomic analysis on a controlled cortical impact (CCI) mouse model using recombinant adeno-associated virus (rAAV)-mediated astrocyte-specific NeuroD1 overexpression.Our findings demonstrate that NeuroD1 overexpression suppresses microglial activation and mitigates brain damage post-TBI. Single-cell RNA sequencing revealed significant shifts in astrocyte subtypes, with upregulated neuroinflammatory pathways and downregulated oxygen metabolism in TBI mice. Conversely, NeuroD1 overexpression reshaped astrocyte subpopulation dynamics, enhanced oxygen metabolism-related gene expression, and attenuated neuroinflammatory signaling. This study provides a comprehensive transcriptomic dataset detailing cellular and astrocyte subtype-specific changes following NeuroD1-mediated brain repair. These insights advance our understanding of cell fate modulation in TBI and support the development of NeuroD1-based gene therapies, offering a valuable resource for future TBI research and therapeutic strategies.

first: Shuo

last: Zhang


title: Transcriptomics Analysis of bulk RNA from liver tissues of male mice treated with high-fat diet and formoterol

city: Charleston

first: Jessica

middle: H

last: Hartman

state: South Carolina

address: 70 President St., Drug Discovery Bldg/Rm DD220

department: Biochemistry and Molecular Biology

institute: Medical University of South Carolina

summary: To establish the consequences of formoterol treatment on high fat diet-induced liver steatosis and inflammation, we isolated RNA from bulk liver tissue of male C57BL/6J mice that were treated with a high-fat diet for 20 weeks, with treatment with vehicle (DMSO) or formoterol (1 mg/kg) daily for the last 4 weeks of the diet. Mice were euthanized using CO2 and cervical dislocation prior to liver dissection.

overall_design: Samples include male mice treated with vehicle (n=4) or formoterol (n=5)

first: Brennan

last: Winkler

first: Kristina

last: Stayer

first: Abhinav

middle: K

last: Rao

first: Ehtesham

last: Arif

first: Tsultrim

middle: T

last: Mendenhall

first: Kristy

middle: L

last: Thomas

first: Kylie

middle: R

last: Driggers

first: Xiaofeng

last: Zuo

first: Wayne

last: Fitzgibbon

first: Peifeng

last: Deng

first: Yanhui

last: Su

first: Yujing

last: Dang

first: Marie

last: Gerges

first: Daniel

last: Kagan

first: Vishwajeeth

last: Pasham

first: Bethany

last: Wolf

first: Don

last: Rockey

first: Joshua

last: Lipschutz


title: Disruption of basal cell identity by Rank signaling drives mammary tumorigenesis

city: Madrid

first: Jaime

last: Redondo-Pedraza

address: Melchor Fernandez Almagro 3, CNIO

department: Molecular Oncology

institute: CNIO

summary: Rank signaling regulates mammary gland development and epithelial cell differentiation. Rank receptor is expressed by mammary basal and luminal populations, but, unlike luminal Rank, the contribution of basal Rank signaling to MG homeostasis remains poorly studied. We have combined timely regulated basal specific Rank expression with lineage tracing models and unveiled that basal Rank signaling controls basal cell identity in postnatal mammary glands. Ectopic basal Rank disrupts basal but also luminal cell identity, resulting in aberrant luminal-like differentiation of basal cells and impaired lactogenesis. Mechanistically, overactivation of basal Rank signaling leads to basal cell lineage infidelity, illustrated by the appearance of premalignant lesions composed by a basal-derived hybrid population with alveolar features which ultimately generates basal and luminal breast adenocarcinomas. Proteomic, transcriptomic and chromatin analyses support that the loss of tumor suppressive epigenetic regulators driven by basal Rank contributes to epithelial cell dedifferentiation and tumorigenesis. The basal Rank signature generated associates to poor prognosis particularly in human adenocarcinomas of the luminal subtype stressing the clinical relevance of our findings. Interestingly, our results reinforce the idea that luminal breast tumors might originate from basal cells that have suffered a luminal-like aberrant dedifferentiation triggered by Rank signaling

overall_design: Assay for Transposase-Accessible Chromatin DNA sequencing (ATAC-seq) for mammary gland luminal and basal epithelial cells from K14-Ctrl and K14-Rank females; and a basal-luminal hybrid population found in K14-Rank mammary glands  Mice treatment pior ATAC-seq: 4 week old female mice were treated  with 1 mg/ml doxycycline + 20mg/ml sucrose, ad libitum in the drinking water for 4 weeks and treated with 50mg/ml MPA pellet   (Innovative Research of America #NP-161) from week 6 of age for 21 days.

first: Jose

last: Terrón-Bautista

first: Patricia

middle: G

last: Santamaria

first: Felipe

last: Costés-Ledesma

first: Eva

last: González-Suárez


title: Transcriptomics Analysis of bulk RNA from HepaRG cells exposed to free fatty acids (oleic and palmitic acid), formoterol, or both

first: Jessica

last: Hartman

summary: To establish the consequences of formoterol treatment, fatty acid overload, and the combination in HepaRG cells, we isolated RNA from cell lysates after three days of treatment. Cells were differentiated for four weeks before treatment: for two weeks they were allowed to reach confluence in normal growth media and then they were further differentiated for the following two weeks by adding 1% DMSO to the media for one media change, and then 2% DMSO for two weeks. Cells were subsequently treated with 30 nM formoterol and/or 0.25 mM palmitic + 0.5 mM oleic acids for three days with fresh treatment each day.

overall_design: Samples include control cells treated with 1% BSA as a vehicle and cells treated with formoterol alone, free fatty acids alone, or a combination of the two. N=4 independent replicates are included for each group.

first: Brennan

last: Winkler

first: Kristina

last: Stayer

first: Abhinav

last: Rao

first: Ehtesham

last: Arif

first: Tsultrim

last: Mendenhall

first: Kristy

last: Thomas

first: Kylie

last: Driggers


title: Efficient transgene-free multiplexed genome editing via viral delivery of an engineered TnpB

city: Berkeley

first: Marena

middle: Isabelle

last: Trinidad

address: 2151 Berkeley Way

institute: Innovative Genomics Institute

summary: Virus-induced genome editing (VIGE) using compact RNA-guided endonucleases is a transformational new approach in plant biotechnology, enabling tissue-culture-independent and transgene-free genome editing. We recently established a transgene-free VIGE approach for heritable editing at single loci in Arabidopsis by delivering ISYmu1 TnpB (Ymu1) and its guide RNA (gRNA) via Tobacco Rattle Virus (TRV). Here, we greatly improved this system by devising a multiple gRNA expression system and by utilizing an engineered high-activity Ymu1 variant (Ymu1-WFR) to develop an efficient multiplexed genome editing approach.

overall_design: Bulk bacterial RNA sequencing was performed to characterize heterologous RNA expression from a defined plasmid construct in Escherichia coli. Cells were grown under identical conditions and induced with arabinose prior to RNA extraction. Each sample represents total RNA isolated from an induced bacterial culture processed through rRNA depletion and small-RNA-seq library preparation. Sequencing reads were aligned to the Ymu1 locus to assess RNA expression profiles.

first: Honglue

last: Shi

first: Kamakshi

last: Vohra

middle: I


title: 5′ UTR length shapes alternative N-terminal protein isoforms across cancers and in rare disease

city: Cambridge

first: Jimmy

last: Ly

state: Massachusetts

address: 455 main street

institute: Whitehead Institute

summary: The 5′ untranslated region (5′ UTR) of an mRNA is classically viewed as a regulatory region that controls the amount of protein production, but not the resulting protein sequence. Here, we demonstrate that 5′ UTR length also plays a direct role in alternative N-terminal protein isoform production by controlling start codon selection. We find that very short 5′ UTRs enhance leaky scanning, thereby promoting the production of truncated alternative N-terminal protein isoforms. Changes in 5′ UTR length due to alternative transcription initiation can tune the relative abundance of alternative N-terminal isoforms from the same gene. In addition, we identify mutations in rare genetic diseases that alter 5′ UTR length, including a deletion in the VHL 5′ UTR in von Hippel–Lindau disease that shifts translation toward the shorter VHLp19 isoform. Together, our results implicate 5′ UTR length as a determinant of alternative N-terminal isoform production and reveal an underappreciated mechanism by which noncoding mutations can reshape the proteome.

overall_design: Whole cell RNA was extracted from asynchronously growing HeLa cells and CAGE-Seq was performed on the resulting mRNA.

first: Iain

last: Cheeseman


title: A scaffold attachment factor PHM-2 regulates synaptic transmission through SLO-2 potassium channel in C. elegans

city: Denton

first: Bojun

last: Chen

address: 1511 W Sycamore St

department: Biological Sciences

institute: University of North Texas

summary: Scaffold attachment factor B (SAFB) proteins are evolutionarily conserved DNA/RNA binding proteins that are involved in multiple processes of gene expression. These proteins are broadly expressed with particular high expression observed in the nervous system. However, their physiological roles in neurons are largely unclear. Here we show that PHM-2, the sole SAFB ortholog in C. elegans, regulates synaptic transmission at the neuromuscular junctions through an effect on SLO-2 potassium channel. We found that phm-2 knockout suppresses a sluggish phenotype of worms expressing a hyperactive SLO-2 channel, greatly reduces SLO-2-mediated neuronal whole-cell currents, and enhances neuromuscular synaptic transmission. In addition, we found that PHM-2 genetically interacts with another DNA/RNA binding protein, HRPU-2/hnRNP U, to control SLO-2 expression through a posttranscriptional mechanism. These results reveal a novel function of a SAFB protein in regulating neuronal activity, and may help understand the physiological roles of SAFB proteins in the nervous system of other species.

overall_design: Examination of gene expression in wild type and phm-2 mutant worms in three biological replicates.

first: Niu

last: Longgang

first: Murugasen

last: Karthika

first: Hanggodo

last: Shannon

first: Ferdousy

last: Sakia

first: Zhu

last: Lishuang

first: Chen

last: Bojun


title: Dnmt3a-dependent de novo DNA methylation enforces lineage commitment and preserves functionality of memory Th1 and Tfh cells

first: Jeffrey

last: Hale

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

overall_design: Refer to individual Series


title: Single-cell RNA-sequencing of CD45+ immune cells from a kidney transplant biopsy and matched peripheral blood

city: Houston

first: Dawei

last: Zou

address: 6670 Bertner Ave

department: Surgery

institute: Houston Methodist Research Institute

summary: T cells are central mediators of transplant rejection, yet the differentiation trajectories that sustain this process remain incompletely defined. To delineate the differentiation trajectory of CD8+ T cells, we performed single-cell transcriptomic profiling of matched allograft and peripheral blood mononuclear cell (PBMC) samples obtained from the same patient.

overall_design: A renal allograft biopsy was obtained percutaneously under ultrasound guidance using a 14-gauge core biopsy needle. The biopsy tissue was immediately placed on ice and rapidly processed for downstream analysis. Peripheral blood mononuclear cells (PBMCs) were collected from the same subject to enable matched sequencing. CD45+ immune cells from the biopsy and PBMC sample were isolated and profiled by single-cell RNA sequencing.

first: Stephanie

last: Yi

first: Yulin

last: Dai

first: Wenhao


title: A Polyamine-mediated Posttranslational Modification Required for Macrophage Tissue Residency [scRNA-seq 2]

city: Baltimore

first: Immunometabolism

last: Department

state: Maryland

address: 1650 Orleans Street

department: Immunometabolism

institute: Johns Hopkins University

summary: Tissue-resident macrophages (RTMs) form during embryogenesis, self-renew locally, and regulate tissue homeostasis by clearing dead cells and debris. During tissue damage, however, bone marrow-derived monocytes enter tissue sites and differentiate into RTM, repairing the tissue and replenishing macrophages in the niche. Universal cell-intrinsic mechanisms that control the monocyte to RTM transition remain elusive. We investigated mice with myeloid cell deletions in deoxyhypusine synthase (DHPS), an enzyme that mediates the polyamine-dependent hypusine modification of the translation factor eIF5A, and found that DHPS is required for cell adhesion and signaling programs critical for RTMs. Without DHPS expression, immature tissue macrophages form, but RTM and associated homeostatic functions are lost. Thus, the polyamine-hypusine pathway is a global, tissue-agnostic program driving the differentiation trajectory of monocyte-derived macrophages into RTM.

overall_design: Single cells were isolated from the lung of indicated animals with 3 biological replicates per genotype (KO and DHPS) and prepared for single cell RNA sequencing using the GEM-X 3' Gene Expression kit (v4) from 10X Genomics.

first: Erika

last: Pearce

first: David

last: Sanin

first: Gustavo

last: Carrizo


title: High efficiency CRISPR knock-in demonstrates that TCF1 is insufficient to reverse T cell exhaustion

city: Melbourne

first: Ian

last: Parish

state: VIC

address: 305 Grattan Street

country: Australia

institute: Peter MacCallum Cancer Centre

summary: In this study we investigated the role of TCF1 in reversing T cell exhaustion by CRISPR-HDR technology.

overall_design: C57BL/6 mice received CRISPR-edited CD45.1+ P14 cells and were infected with LCMV Clone 13. 20 days later, the CD45.1 P14 cells were isolated from the spleens of the recipient mice, sorted and analysed.

first: Maria

last: Nogueira de Menezes

first: Nicole

last: Saw


title: A Polyamine-mediated Posttranslational Modification Required for Macrophage Tissue Residency


title: A Cellular and Transcriptomic Atlas of the Aged Mouse Hematopoietic System

city: Tarrytown

first: Kun

last: Xiong

state: NY

address: 777 Old Saw Mill River Road

department: Molecular Profiling and Data Science

institute: Regeneron Pharmaceuticals

summary: Aging is a dominant risk factor for chronic diseases characterized by the functional decline of tissues and organs. During aging, the hematopoietic system declines in regenerative capacity – seemingly attributable to increases in DNA damage, replicative stress, and autophagic flux – resulting in skewing towards a myeloid lineage and away from a lymphoid lineage. Here, we characterized the transcriptomic and cellular landscape of the aged C57Bl6/J mouse hematopoietic system using a combination of bulk RNAseq and single cell RNAseq (scRNAseq). We show that aging leads to global transcriptional alterations in bulk peripheral blood mononuclear cells (PBMCs), lineage marker-depleted bone marrow cells (lin- BM), and in hematopoietic stem cells (HSCs) marked by lineage- (lin-) Sca1+cKit+ (LSK+). These changes indicate widespread activation of inflammatory processes, namely in PBMCs and lin-BM cells. Interestingly, there is also a downregulation of cell cycle genes in HSCs during aging. scRNAseq across 39 hematopoietic cell types revealed age-related skewing in cell composition. Aged PBMCs showed significant decreases in CD4 and CD8 naïve cells concomitant with increases in CD4/8 memory and CD8 exhausted T cell populations. Lin- BM cells showed significant myeloid skewing in common myeloid progenitor (CMP) cells as well as in the HSC population. We also identified a unique HSC population marked by increased Vwf, Wwtr1, and Clca3a1 expression that does not exist in young HSCs, thus likely marking true aged HSCs. Collectively, this works encompasses a significant resource for uses in therapeutically targeting the aged hematopoietic system.

overall_design: Bulk RNAseq and scRNA seq of PBMC and lineage negative bone marrow from young and old mice. Bulk RNAseq of HSC from young and old mice

first: Ryan

last: White

first: Matthew

last: Wakai

first: Allison

last: Surian

first: Christina

last: Adler

last: Negron

first: Min

last: Ni

first: Tea

last: Shavlakadze

first: Yu

last: Bai

middle: J

last: Glass


title: Dynamics of phage-host interactions in Bacteroides fragilis resolved by single-cell transcriptomics [scRNA-Seq data]

city: Seattle

first: Dmitry

last: Sutormin

state: WA

address: 401 Terry Ave N

institute: Institute for Systems Biology

summary: The interactions between lytic phages and their hosts are typically studied in bulk culture, which obscures cell-cell differences in infection susceptibility or expression of protective factors. Here, we use bacterial single-cell RNA sequencing to profile the transcriptomes of ~50,000 cells from cultures of a human pathobiont, Bacteroides fragilis, infected with a lytic bacteriophage. From a single sampling, we quantified the asynchronous progression of phage infection in individual bacterial cells and reconstructed the infection timeline, characterizing both host and phage transcriptomic changes as infection unfolded. Further, we discovered phenotypic subpopulations of bacteria that remained uninfected. Each cell's vulnerability to phage infection was influenced by expression of multiple genetic loci, most prominently phase-variable capsular polysaccharide (CPS) biosynthesis pathways and an operon predicted to encode fimbrial genes. These findings uncovered genome-wide phase variation and stochasticity that enable bacterial survival and re-growth without acquiring additional mutations. Overall, we establish bacterial single-cell RNA sequencing as a powerful platform for investigating the dynamics of host-phage interactions and revealing the roles of phase variation and stochasticity in bacterial defenses.

overall_design: Exponentialy growing Bacteroides fragilis NCTC 9343 culture was a) cultivated in chopped meat carbohydrate (CMC) media; b) infected with Bf12P1 phage in CMC media; c) cultivated in CMC media supplemented with 100µM bile acid DCA; d) infected with Bf12P1 phage in CMC media supplemented with 100µM bile acid DCA. Cells were fixed in 4% formaldehyde and processed via microSPLiT protocol.

first: Anika

last: Gupta

first: Norma

last: Morella

first: Anna

last: Kuchina


title: The Ess1 prolyl isomerase represses TERRA transcription and promotes telomere replication in Saccharomyces cerevisiae

city: Shanghai

first: JUXIU

last: CHEN

state: Shanghai

address: 115 Jinzun Road, Pudong New Distract

department: Shanghai Institute of Precision Medicine

institute: Ninth People’s Hospital of Shanghai Jiao Tong University School of Medicine

summary: The conserved Ess1 prolyl isomerase (PIN1 in human) binds the carboxy-terminal domain (CTD) of RNA Pol II, and plays multiple roles in transcription regulation. Consistent with an essential role of the human PIN1 in telomere maintenance, previous screenings have identified the yeast Ess1 as a telomere length maintenance gene. Here, we provide evidence that Ess1 is involved in regulating both telomere transcription and replication. We find that depletion of Ess1 leads to a failure in transcription termination, explaining the essential role of Ess1 in maintaining a low level of telomere repeat containing RNA (TERRA). Furthermore, we show that Ess1 depletion promotes telomere shortening and accelerates senescence in telomerase-deficient cells. Notably, the depletion of Ess1 causes synthetic growth defects and telomere shortening in mre11Δ cells, and compromises rif2Δ-induced telomere elongation. Additionally, Ess1 depletion also accelerates senescence and eliminates type II telomere recombination in rad50Δ tlc1Δ cells. Lastly, Ess1 depletion decreases the accumulation of single-stranded DNA at telomere ends. These results support the model that Ess1 positively regulates both telomerase- and recombination-dependent telomere replication by promoting telomere-end resection. Taken together, this study reveals the yeast Ess1 as a new regulator of telomere transcription and replication via a distinct mechanism from the human PIN1.

overall_design: RNA-seq profiling of ESS1-AID cells treated with either DMSO(control) or 2 mM IAA(experimental) for 3 hours. Each group includes two biological replicates.

first: Juxiu

last: Chen

first: Lin

last: Yang

first: Xiaohan

last: Zhu

first: Jian

last: Wu

first: Zhenfang

first: Ming

last: Lei


title: Single-cell RNA Sequencing of Wildtype and/or Dazl Mutant Mouse Ovarian Cells Across Embryonic Developmental Stages (E10.5 (Wild type), E11.5 (Wild type and Dazl-/-), E12.5 (Dazl-/-), E15.5 (Wild type)

first: Allan

last: Spradling

address: 3520 San Martin Dr

institute: Howard Hughes Medical Institute Research Laboratories, Department of Embryology, Carnegie Institution for Science

summary: We have identified a Golgi- and microtubule-rich vesicular structure, "fusome" which resembles the Drosophila fusome and accumulates asymmetrically during germ cell cyst divisions starting at E11.5. Genes associated with fusome become enriched in presumptive oocytes during cyst divisions and early meiosis, suggesting a role in oocyte rejuvenation. To investigate this further, we performed single-cell RNA sequencing (scRNA-seq) of mouse fetal germ cells at E10.5, E11.5, and E15.5, including developmental stages not previously covered in earlier datasets (GSE136441), thereby generating a composite dataset of E10.5-P5 germ cells. Additionally, we analyzed Dazl homozygous and heterozygous mutant ovarian germ cells at E11.5 and E12.5 to study the impact of Dazl loss on cyst formation and fusome-associated gene expression dynamics. This dataset provides a comprehensive resource to explore transcriptional changes across key stages of fetal ovarian development and in the context of Dazl function.

overall_design: Embryonic ovaries were dissected, and fetal sex was identified using Quinacrine and DAPI staining of tail samples to exclude males in E10.5/E11.5 gonad samples. Female gonads were pooled and dissociated into single cells using 0.25% Trypsin at 37°C for 5–7 minutes with gentle trituration. Trypsin was neutralized with 10% FBS, and cells were filtered through a 30 μm strainer. After centrifugation and resuspension in 0.04% BSA, cell viability was assessed with trypan blue, and high-quality samples (>90% viability) were loaded (~10,000 cells) onto the 10X  (Genomics Chromium platform (v3/v4 chemistry) per manufacturer’s instructions. For mutant samples, Dazl+/- males and females were mated, and embryos collected at E11.5 and E12.5. Tail DNA was extracted using the KAPA Express Extract Kit and genotyped using standard JAX protocols (strain 035880). Identified homozygous and heterozygous fetal gonads were dissociated as above and subjected to scRNA-seq on the same 10X chromium platform.

first: Madhulika

last: Pathak


title: Irisin improves obesity and glucose intolerance through an IL-33-ST2 pathway

first: CBDM

last: Lab

address: 77 Avenue Louis Pasteur

department: Microbiology and Immunobiology

institute: Harvard Medical School

summary: Irisin is secreted by muscle, increased with exercise, and conveys certain physiological benefits. Earlier studies showed that short-term irisin treatment caused browning of subcutaneous white fat in mice, with improved glucose tolerance; the effects of more chronic irisin treatment and mechanisms at play have not been explored. We demonstrate here that chronic irisin application improves obesity and dramatically reduces glucose intolerance. This treatment increases an IL-33+ mesenchymal stromal cell (mSC) population, while genetic ablation of irisin reduces plasma IL-33 levels and decreases thermogenic gene expression in subcutaneous adipose tissue. Importantly, irisin directly induces IL-33 expression in mSCs and stimulates ST2+regulatory T (Treg) cells, inducing their tissue accumulation. Inhibition of IL-33  blunts these irisin-mediated effects on energy expenditure and glucose homeostasis, largely through IL33-mediated regulation of ST2+ Treg cells. These data indicate that irisin improves obesity and glucose intolerance, with no muscle loss, through a key immunomodulatory pathway in obese mice .

overall_design: To verify whether irisin/HSP90α could change mSC fate from adipocyte precursors to immunomodulatory stromal cells, IL-33 (EGFP)- mSCs from eWAT were treated with PBS or 10nM irisin/HSP90α for 3 days.

first: Gang

last: Wang

first: Diane

last: Mathis


title: Cyclophilin A Stabilizes the Capsid Protein p72 to Facilitate African Swine Fever Virus Replication

city: Harbin

first: Liqin

address: haping road 678

department: Harbin Veterinary Research Institute

institute: Chinese Academy of Agricultural Sciences

summary: African swine fever virus (ASFV) is a large DNA virus that poses a major threat to the global swine industry. Its virion is encapsulated by an icosahedral capsid predominantly composed of the structural protein p72, which constitutes approximately one-third of the total virion mass. Despite its abundance, the mechanisms regulating p72 stability remain poorly understood. Here, we demonstrate that host-mediated stabilization of p72 is essential for efficient ASFV replication. Mass spectrometry of p72 co-precipitates identified host cyclophilin A (CypA, also known as PPIA) as a key binding partner of p72. CypA interacts with p72 both in vitro and in vivo, specifically engaging exposed regions of p72 via its hydrophobic cavity. CypA interaction stabilizes p72 by reducing K63-linked ubiquitination and preventing proteasomal degradation, whereas cyclic CypA inhibitors destabilize p72 by disrupting this interaction and promoting its ubiquitination. Importantly, genetic or pharmacological inhibition of CypA markedly impairs ASFV replication. Mechanistically, CypA inhibition disrupts viral factory formation and virion assembly by decreasing p72 protein accumulation without affecting its transcription. Together, our findings uncover a previously unrecognized host-dependent mechanism regulating capsid protein stability and highlight host CypA as a promising target for antiviral strategies against ASFV.

overall_design: RNA-seq profiling of porcine alveolar macrophages to compare transcriptomic profiles under ASFV infection and NIM811 treatment conditions, including four experimental groups: (1) uninfected with DMSO control, (2) uninfected with NIM811, (3) ASFV-infected with DMSO, and (4) ASFV-infected with NIM811.

first: Hui

last: Kong

first: Xiangpeng

last: Sheng

first: Dongming

last: Zhao


title: A Polyamine-mediated Posttranslational Modification Required for Macrophage Tissue Residency [scRNA-seq]

first: Immunometabolism

last: Department

overall_design: Single cells were isolated from the peritoneal cavity of indicated animals with 3-4 biological replicates per genotype (KO and DHPS) and prepared for single cell RNA sequencing using the GemCode Single Cell Platform with GemCode Gel Beads, Chip and Library Kits (v3) and 10X Genomics Chromium Controller following the manufacturer’s protocol.

first: Erika

last: Pearce

first: David

last: Sanin

first: Gustavo

last: Carrizo


title: A Polyamine-mediated Posttranslational Modification Required for Macrophage Tissue Residency [RNA-Seq]

overall_design: Macrophages from several tissues were obtained from 4 separate WT or DHPS KO mice via FACS.


title: Cell-free genomics reveals fundamental regulatory principles of the Mycobacterium tuberculosis transcription cycle

city: New York

first: Ruby

last: Froom

address: 1230 York Avenue

institute: Rockefeller University

summary: Tiers of gene regulation govern cellular life. The intrinsic activities of RNA polymerase (RNAP) constitute a primary tier, while direct modulation by accessory transcription factors (TFs) constitutes a secondary tier. Cellular signaling cascades and feedback loops generate tertiary and higher-order tiers. Dissecting gene regulation requires distinguishing direct TF targets at genome-scale from indirect network effects. A major obstacle is the lack of tools to interrogate transcription machineries from difficult-to-culture microbes—such as pathogens, commensals, and environmental species—at genome scale. Here, we introduce cell-free genomics (CFG), an empirical approach that identifies the direct targets of RNAP and TFs and systematizes their transcriptional effects. We demonstrate the efficacy of CFG by characterizing global and essential transcription initiation (CRP and holo-WhiB1) and elongation–termination factors (NusA and NusG) from the deadly pathogen, Mycobacterium tuberculosis. CFG expands our understanding of transcription principles and is broadly extensible to other perturbations and diverse species.

overall_design: RNA samples were prepared by incubating a mixture of purified M. tuberculosis (Mtb) RNA polymerase core enzyme, co-purified Mtb sigma factor A (SigA) and Mtb RbpA, purified Mtb CarD, sonicated Mtb genomic DNA, ribonucleotides, RNase inhibitor, and pyrophosphatase for 1 hour - 5 hours at 37ºC, in the presence or absence of transcription factors of interest (Mtb CRP, Mtb WhiB1, Mtb NusG, Mtb NusA). The aim was to identify TSSs or TTSs where these TFs can individually affect transcription. Similarly-derived in vitro RNA from the E. coli genome was spiked into all reactions at equivalent amounts to control for different amounts of total RNA across samples. 5' or 3' ends of the RNA were then enriched and sequenced. Core RNAP only samples were used to filter out non-SigA-dependent (i.e. non-specific) TSSs from the RNAP-SigA holoenzyme TSS samples. Genomic DNA input samples were used to filter out any TTSs that may be enriched due to non-random fragmentation of the genomic DNA input from the RNAP-SigA holoenzyme TTS samples.

first: Michael

last: Wolfe

first: Kelly

last: Eckartt

first: Rachel

last: Mooney

first: Madeleine

last: Delbeau

first: Alexis Jaramillo

last: Cartagena

first: Jeremy

last: Rock

first: Seth

last: Darst

first: Robert

last: Landick

first: Elizabeth

last: Campbell


title: Gene expression profile at single cell level of CD45+ immune cells in both peripheral blood mononuclear cells (PBMCs) and allograft biopsy samples obtained from kidney transplant recipients

first: Yulin

last: Dai

address: 7000 fannin, suite 600

department: School of Biomedical Informatics

institute: University of Texas health science center at Houston

summary: Transplant rejection is mediated by immune cells, especially T cells. In this study, we employed single-cell RNA sequencing (scRNA-seq) to analyze the states of these cells in response to kidney transplantation

overall_design: Subjects were retrospectively selected following prospective recruitment and consent at the time of renal biopsy for clinical indications (protocol biopsy for high immune risk, “for cause” such as allograft dysfunction, and post-rejection treatment). Live CD45+ cells were sorted from PBMC or kidney biopsy samples and analyzed by scRNA-seq

first: Stepanie

last: Yi

first: Dawei

last: Zou

first: Wenhao

last: Chen


title: A Polyamine-mediated Posttranslational Modification Required for Macrophage Tissue Residency [Ribo-seq]

first: Immunometabolism

last: Department

overall_design: Freshly isolated cells from total peritoneal lavage from 3 WT or 3 DHPS KO mice were used for ribosomal analysis.

first: Erika

last: Pearce


title: mRNA transcriptome data of granulosa cells cultured either with BSA (bovine serum albumin) or NEFA (non estrified fatty acid) mix

city: Dummerstorf

first: Vijay simha

last: Baddela

address: Wilhelm-Stahl-Allee 2

department: Reproductive biology

institute: Leibniz institute for farm animal biology

summary: Postpartum negative energy balance could contribute to the reduced fertility rates in females, partly due to elevated levels of non-esterified fatty acids (NEFA) in blood and in ovarian follicular fluid. NEFA has been shown to influence ovarian cell metabolism and function, yet the underlying molecular mechanisms remain incompletely understood. During the present investigation, transcriptome differences induced by a mixture of oleate (200 µM), palmitate (100 µM) and stearate (100 µM) were were  analyzed to understand the specific effects of NEFA in ovarian follicular granulosa cells.

overall_design: RNA from BSA (4n) and NEFA (4n) treated GC were processed for microarray analysis

first: Vijay


title: Monocyte-derived IL-10 drives sex differences in pain duration

status: Public on Jan 14 2026

city: Chapel Hill

first: Sarah

last: Linnstaedt

state: NC

address: 109 Mason Farm Road

institute: University of North Carolina at Chapel Hill

summary: Women frequently experience longer-lasting pain than men, indicating delayed pain resolution. While we understand that pain can be orchestrated by the close interplay between the sensory nervous system and the immune system, it remains unclear whether this interaction contributes to the longer duration of pain in women. Here, we demonstrate that interleukin (IL)-10+ monocytes resolve inflammatory pain by signaling to IL-10R1+ sensory neurons in a mouse model of skin inflammation. A higher number of IL-10+ monocytes in males enables faster resolution of inflammatory pain compared to females. In both sexes, pain resolution was impaired by deleting Il10 from monocytes or Il10ra from sensory neurons. Similarly, in humans, men’s pain resolved faster than women’s after traumatic injury, which was associated with higher levels of circulating monocytes and IL-10 in men. In mice, androgen signaling promotes IL-10 production by monocytes, resulting in sex differences in the number of IL-10+ monocytes. Enhancing IL-10+ monocytes in the inflamed skin through Resolvin D1 treatment accelerated pain resolution in both sexes of mice. Our findings uncover a novel role for peripheral IL-10+ monocytes in driving sex differences in pain resolution. These results reveal a previously underappreciated   contribution of immune cells to resolving pain and preventing the transition to chronic pain.

overall_design:
RNA-seq profiling  of human whole-blood samples collected at enrollment. A supplementary file available at the foot of this record named "GEO_sumission_sample_supplementary_info.xlsx" contains sample metadata and a key to variables.

***************************************************************
Raw files for human/patient samples were not submitted to GEO due to concerns about submitting personally identifiable sequence data for open access.  The raw data files are available under controlled access: DOI:10.15154/e9fp-1e38
***************************************************************

first: Jaewon

last: Sim

last: O’Guin

first: Chiho

last: Sugimoto

first: Sophie

last: Laumet

first: Karli

last: Monahan

first: Matthew

middle: P

last: Bernard

first: Samuel

middle: A

last: McLean

first: Liz

last: Albertorio-Sáez

first: Ying

last: Zhao

first: Hariharan

last: Ramakrishnan

first: Sabrina

last: de Souza

first: Olivia

last: Eller

first: Christine

last: Smoyer

first: Kyle

last: Baumbauer

first: Matthias

last: Mack

first: Joseph

last: Folger

first: Alfred

last: Robison

middle: D

first: Geoffroy


title: RiboBright reveals cell-type specific differences in ribosome organization and movement

city: Nijmegen

first: Wim

last: Velema

address: Heyendaalseweg 135

country: Netherlands

institute: Radboud University

summary: Ribosomes are responsible for protein synthesis in all living systems. Determining their cellular organization, movement and translational activity is crucial for dissecting ribosomes’ complex functions. In this study, we describe the development of a selective fluorescent probe for eukaryotic ribosomes — RiboBright. Using C-H activation, the natural product cycloheximide was aminated at the C13-position and fluorescently modified to afford RiboBright. We employ RiboBright for quantification of ribosome content in 10 cell lines through microscopy and flow cytometry. RiboBright is applicable in live cells for tracking and quantification of ribosome movement and in fixed cells for visualization of sub-micrometer sized spots, at the single cell level. Strikingly, RiboBright reveals lineage-specific ribosome content, organization, and movement upon differentiation into either extraembryonic endoderm or ectoderm-like lineages. Thus, RiboBright provides a versatile and convenient approach for imaging the cellular dynamics of ribosomes.

overall_design: DMS_MAP_seq of ribobright and cycloheximide treated samples

first: Georgia

last: Poulladofonou

first: Carmen

last: Grandi

first: Xinyu

last: Hu

first: Phillip

last: Yesley

first: Willem

first: Maike

last: Hansen


title: Transcriptome profiles of bovine muscle stem cells cultured in serum-containing condition and small molecule–supplemented serum-free media by RNA-seq analysis

city: 江苏省南京市

first: 浩

last: 路

address: 江苏省南京市南京农业大学滨江校区

institute: 南京农业大学郭仁朋课题组

summary: Cultured meat, as an emerging sustainable food production technology, offers multiple advantages. However, its large-scale application still faces critical technical bottlenecks, most notably the strong reliance on fetal bovine serum (FBS). In recent years, serum-free culture systems for bovine muscle stem cells (bMuSCs) have made certain progress, such as the Beefy-9 system and its subsequent optimized versions; nevertheless, existing serum-free formulations remain insufficient to fully replace traditional serum-containing culture conditions in both cost control and functional performance. Meanwhile, the use of small-molecule compounds to precisely regulate cell proliferation and fate determination has gradually emerged as a potentially effective strategy to reduce culture costs, simplify culture systems, and enhance functional stability. In this study, through a functional screening of proliferation activators in bMuSCs, we identified forskolin and a p38 pathway inhibitor SB202190 to robustly promote cell proliferation and maintain myogenic capacity of bMuSCs under serum-free conditions. Based on this, RNA-sequencing analysis was committed to systematically elucidate the molecular differences between serum-free small-molecule regulatory strategies and conventional serum-containing conditions in bMuSCs.

overall_design: BMuSCs with biological replicates were collected simultaneously for RNA extraction and RNA-seq analysis. Specifically, at the fifth passage of proliferation (corresponding to three consecutive passages under different culture conditions), cells cultured in medium containing 15% FBS (the FBS group), in Beefy-9 medium (the Beefy 9 group), and in Beefy-9 medium supplemented with forskolin or/and SB202190 (the Beefy F group, the Beefy S group, and the Beefy FS group) were harvested, with three biological replicates included for RNA-seq analysis.


title: Alteration of global transcription by the Tormentil and its constituents in Acinetobacter baumannii AB5075

city: London

first: Kavita

last: Gadar

address: Kingston Lane

institute: Brunel University

summary: We perform RNA-seq comparing a treatment with 50 μM agrimoniin, 2.3 μM ellagic acid, 0.05 mg/mL of Wicklow tormentil root extract to a mock treatment (DMSO) in A. baumannii AB5075 in order to describe the alterations in global transcription produced by these treatments. As a result, Agrimoniin elicited a response that led to significant differential expression in 414 genes, with 216 showing upregulation and 198 showing downregulation. Ellagic acid exerted an even more pronounced effect, with 636 genes exhibiting significant differential expression; among these, 455 were upregulated and 181 were downregulated. Similarly, Wicklow tormentil root extract impacted gene expression resulting in significant differential expression in 517 genes, wherein 378 were upregulated and 139 were downregulated.  In highlights, the gene functional groups showing the strongest transcriptional alterations were those related to iron acquisition, storage, siderophore biosynthesis and iron transport genes.

overall_design: A. baumannii AB5075 cultures were grown in LB medium in the presence of with 50 μM agrimoniin, 2.3 μM ellagic acid, 0.05 mg/mL of Wicklow tormentil root extract or a DMSO control (3 biological replicates per condition) until reaching mid-exponential phase. At this point, cells were harvested, treated with RNAlater for preservation of total RNA and stored at -80 C. After that, total RNA was extracted from each sample. Three independent replicates of A. baumannii AB5075 were grown to mid-exponential phase in LB medium supplemented with 50 μM agrimoniin, 2.3 μM ellagic acid or 0.05 mg/mL of Wicklow tormentil root extract and compared to three independent replicates grown in the same conditions but receiving a mock treatment (equivalent volume of DMSO).

first: Maria

last: Pigott

first: Cillian

last: Gately

first: Ismael

last: Obaidi

first: Shipra

last: Nagar

first: Helen

last: Sheridan

first: Ronan

last: McCarthy


title: Melittin enhances PD-L1 blockade in prostate cancer by inhibiting M2 macrophage polarization and recruitment

first: Rucheng

last: Yan

address: 1800,yuntai road

institute: Shanghai East Hospital

summary: Objective: The immunosuppressive tumor microenvironment (TME) limits the efficacy of immunotherapy in prostate cancer treatment. This study aims to investigate how melittin remodels the TME in prostate cancer and enhances the response mechanism to anti-PD-L1 therapy. Methods: The anti-tumor efficacy of melittin was evaluated in a C57BL/6J mouse prostate cancer model. An in vitro co-culture model of prostate cancer cells (PC-3, 22RV1) and THP-1-derived macrophages was established. RNA sequencing, flow cytometry, qPCR, Western blot, ELISA, Transwell migration assays, and immunohistochemistry were employed to explore the anti-tumor mechanisms of melittin. The synergistic effect of combining melittin with an anti-PD-L1 antibody was assessed in vivo. Results: Melittin significantly inhibited tumor growth in vivo. It remodeled the TME by increasing CD8⁺ T cell infiltration and reducing macrophage numbers. Furthermore, melittin specifically inhibited M2 macrophage polarization, downregulating the expression of CD206, CD163, and TGF-β, an effect potentially mediated through inhibition of the JAK-STAT pathway. Additionally, melittin reduced macrophage recruitment by downregulating tumor-derived CCL2. Combination therapy using melittin and anti-PD-L1 antibody demonstrated synergistic anti-tumor effects, significantly reducing tumor volume and weight, decreasing intratumoral expression of Ki67 and PD-L1, and enhancing CD8⁺ T cell infiltration. Conclusion: Melittin reverses the immunosuppressive TME in prostate cancer by simultaneously inhibiting JAK-STAT-mediated M2 polarization and CCL2-dependent macrophage recruitment. This reprogramming of the TME, combined with PD-L1 blockade, offers a novel combination immunotherapy strategy for prostate cancer.

overall_design: THP-1 cells were differentiated with 100 ng/ml PMA for 48 h in the lower chamber of a Transwell system. Tumor cells were then seeded in the upper chamber and co-cultured with 3 μg/mL melittin for 48 h before.The induced macrophages were usd to RNA-seq.


title: Downregulation of MGST3 promotes colorectal cancer progression

city: Qingdao

first: yuchun

last: wu

state: Shandong Province

address: Laoshan District, Ningxia Road

institute: Qingdao University

summary: Colorectal cancer (CRC) is a common malignancy worldwide, and its molecular mechanisms of progression remain incompletely understood. In this study, RNA sequencing was performed on colorectal tissues representing normal tissue, adenomas, early-stage tumors and advanced carcinomas to identify differentially expressed genes associated with tumor progression. Paired-end RNA-seq data were generated on an Illumina NovaSeq 6000 platform. Gene expression levels were quantified and summarized as FPKM values. The resulting dataset provides a transcriptomic resource for investigating molecular changes during colorectal tumorigenesis, including the role of MGST3.

overall_design: A retrospective study was conducted on colorectal tissue samples representing normal tissue, adenomas, early-stage tumors and advanced carcinomas. Fresh-frozen tumor tissues and paired adjacent normal tissues were collected. Total RNA was extracted and subjected to bulk RNA sequencing using paired-end 150-bp reads on an Illumina NovaSeq 6000 platform. Sequencing reads were quality-trimmed, aligned to the hg38 reference genome, and gene expression levels were quantified using Cufflinks.

first: Jianxun

last: Wang

first: Yuqu

last: He

first: Yuchun

last: Wu


title: Functional Dynamic Modulation of Colorectal Cancer Initiation and Metastatic Capacity by a Novel MiR-7974 Regulatory Axis

city: Taoyuan

first: Yi-Tung

last: Chen

address: No.259, Wenhua 1st Rd., Guishan Dist.

country: Taiwan

institute: Chang Gung University

summary: To investgate the funcitonal role of miR-7974 overexpression on transcriptomic regulation

overall_design:
We performed gene expression profiling analysis using data obtained from RNA-seq (2 replicate)
Differentiated gene expression profiling analysis of RNA-seq data for Ctrl and miR-7974 HCT116 cells

first: Yu-Hao

last: Liu


title: Assessing mifepristone's effects on endometrial tissue in women with BRCA mutations: A randomised clinical trial

city: Solna

first: Nageswara Rao

last: Boggavarapu

state: stockholm

address: Visionsgatan 4

department: Women and Children health

country: Sweden

institute: Karolinska Institutet

summary:
Background: The endometrium, regulated by steroid hormones, is particularly susceptible to disease under imbalanced hormonal conditions. Progesterone regulates cell growth differently across tissues, acting as a pro-tumorigenic agent in the breast while serving as a tumor suppressor in the endometrium by countering the effects of oestradiol. Progesterone receptor modulators like mifepristone may prevent breast cancer formation but raise concerns about unopposed oestradiol exposure in the endometrium. This study examines mifepristone’s impact on the endometrium, particularly its potential link to endometrial carcinogenesis in BRCA mutation carriers, who have DNA repair and replication vulnerabilities.
Methods: This study was part of a randomised, double-blind, placebo-controlled trial in which pre-menopausal women carrying BRCA1 or BRCA2 mutations were assigned to a three-month treatment with either mifepristone (50 mg) or a non-hormonal comparator (TrioB) every second day. Endometrial biopsies were collected pre- and post- treatment, processed, and analysed for changes in endometrial thickness, cellular composition, methylation patterns, and gene expression profiles. Compliance and safety monitoring were rigorously maintained.
Results: Mifepristone treatment led to amenorrhea in all treated participants, consistent with its inhibition of ovulation. Ultrasound showed a non-significant increase in endometrial thickness post-treatment. Cellular analysis indicated a shift in composition, with a reduction in epithelial cells and an increase in fibroblast levels, suggesting that endometrial thickening may primarily reflect stromal expansion rather than epithelial proliferation. This distinction is clinically important, as epithelial proliferation is more closely associated with carcinogenesis. DNA methylation analysis revealed no significant alterations in the TCGA-EC methylation index, and gene expression profiling showed no significant elevation in carcinogenesis-related genes.
Conclusions: Mifepristone treatment in BRCA mutation carriers does not significantly impact methylation or gene expression profiles associated with endometrial carcinogenesis. The findings support from the safety of short-term mifepristone use in this population, although long-time safety of mifepristone use in BRCA mutation carriers will be needed.

overall_design: Molecular analysis involved RNA and DNA extraction from 15 paired biopsies, RNA sequencing using the Smart-seq2 protocol, and methylation profiling with Illumina Human Methylation EPIC arrays. RNA-seq data were processed using Partek Flow, identifying genes of interest, while DNA methylation data supported the development of an endometrial cancer index. This index, trained on TCGA UCEC data, demonstrated robust accuracy and was applied to the study dataset to explore its diagnostic utility.


title: Protein C-Terminal Variations Impact Proteostasis

city: Taipei

first: Hsueh-Chi

last: Yen

address: No. 128, Sec. 2, Academia Rd.

department: Institute of Molecular Biology

institute: Academia Sinica

summary: Protein C-termini can vary due to errors or programmed regulation, contributing to proteome diversity, yet their impact on the proteome remains poorly understood. Although aberrant C-termini are often liked to protein degradation, it is unclear if this holds true universally. In this study, we examine how C-terminal variations--arising from disease-associated nonstop mutations, alternative splicing, and translational readthrough--affect protein half-lives. Our findings indicate that, contrary to previous studies, erroneous C-termini can either stabilize or destabilize proteins. We have identified multiple oncoproteins and tumor suppressors whose protein stability is altered by disease-relevant nonstop mutations. Notably, we have found that C-terminal variations commonly influence the stability of canonical proteins, extending beyond their role in protein quality control. Furthermore, we have uncovered C-terminal features that distinguish erroneous from wild-type proteins and reveal that hydrophobic C-termini are targeted by a complex ubiquitin ligase network. Overall, our work broadens the understanding of C-terminal-dependent protein degradation and supports that C-terminal variation is a widespread strategy for generating protein forms with distinct half-lives to exert diverse biological functions.

overall_design: For the GPS peptidomic screen, amplicon sequencing was performed on GPS reporter library cells sorted into eight bins by fluorescence-activated cell sorting (FACS). Only reads that perfectly matched the designed sequences were retained. Two biological replicates were performed. For the CRISPR/Cas9 screen targeting proteostasis pathways, sgRNA sequences were amplified from reporter cells representing the top 5% of GFP/BFP ratios, while the total population was used as a control. The CRISPR screening results were analyzed using casTLE algorithm.

first: Ching-Yu

last: Chu

first: Shu-Yu

last: Hsu


title: Cutaneous adipose tissue has a strong inflammatory signature in psoriasis patients, and it is partly IL-17 dependent.

first: James

last: Krueger

department: Center for Clinical and Translational Science

institute: The Rockefeller University

summary: Background: Psoriasis is an inflammatory skin disease associated with systemic inflammation and comorbidities such as diabetes and cardiovascular disease. Although the association between psoriasis and obesity has been studied extensively, the role of cutaneous adipose tissue (CAT) in pathogenesis of psoriasis remains unclear. Objectives This study aimed to provide a comprehensive evaluation of the CAT transcriptome in psoriasis patients and investigate the effects of IL-17 pathway blockade on adipose tissue inflammation. Methods: In this randomized, double-blind, placebo-controlled phase 4 study (ObePso study), CAT biopsies were obtained from lesional (LS-CAT) and non-lesional skin (NL-CAT) of 82 psoriasis patients and 15 healthy controls. Patients were randomized to receive either secukinumab or placebo for 12 weeks. RNA sequencing and subsequent analyses were performed to identify differentially expressed genes and pathways. Results: Psoriatic CAT showed significant gene expression differences compared to controls, with 2132 differentially expressed transcripts identified. Both LS-CAT and NL-CAT exhibited activation of IL-17-induced, antimicrobial peptides-related, and neutrophil degranulation-related pathways. Obesity expanded differential gene expression in psoriasis by more than 100%, suggesting an additive or synergistic interaction between psoriasis and adiposity. Obese psoriasis patients showed activation of pathways related to collagen metabolism, cytokine storm signaling, and IL-17A signaling. Secukinumab treatment significantly improved inflammation in psoriatic CAT, with obese patients showing greater improvement than non-obese patients. Conclusions: This study provides the first comprehensive evaluation of the adipose tissue transcriptome in psoriasis patients. The findings reveal a strong inflammatory signature in psoriatic CAT, which is partly IL-17 dependent. The study also demonstrates that obesity amplifies the inflammatory response in psoriatic adipose tissue. IL-17 blockade with secukinumab significantly improved CAT inflammation, with enhanced benefits observed in obese individuals. These results highlight the potential role of adipose tissue in psoriasis pathogenesis and suggest that targeting adipose tissue inflammation may be a valuable therapeutic approach, particularly in obese psoriasis patients.

overall_design: Cutaneous adipose tissue biopsies were taken from lesional and non-lesional skin of 82 psoriasis patients. Samples were also collected from 15 healthy subjects using the same procedure. RNA was isolated from adipose tissue samples using the RNeasy Lipid Tissue Mini Kit (Qiagen)

first: Naomi

last: Shishido-Takahashi

first: Sandra

last: Garcet


title: Synaptic effects of interleukin-6 on human iPSC-derived dopaminergic neurons

city: Atlanta

first: Zhexing

last: Wen

state: GA

address: 615 Michael Street

institute: Emory University

summary: Increased inﬂammation has been linked to behavioral pathogenesis in depression. Previous studies have shown that administration of inﬂammatory stimuli induces motivational deﬁcits associated with reduced activation of the ventral striatum in association with reduced dopamine (DA) availability and release. However, the underlying mechanisms of inﬂammation-induced DA dysfunction remain largely unknown. Here, we investigated the in vitro effects of the inﬂammatory cytokine interleukin (IL)-6 on female and male human induced pluripotent stem cell (iPSC)-derived DAergic neurons from healthy volunteers. We identiﬁed inhibitory effects of IL-6 on female DA neurons, including reduced DA release, neuronal ﬁring, velocity of synaptic vesicle (SV) transport, and density of docked SV, which was further supported by transcriptomic analyses. In contrast, male DA neurons exhibited an IL-6-induced compensatory phenotype, including increased velocity and density of SV and increased presynaptic terminal density. The long noncoding RNA (lncRNA) MIAT mediated these differences in male DA neurons, potentially via interaction with genes involved in the IL-6 signaling pathway and DA regulation. Moreover, by knocking out MIAT expression in male DA neurons, IL-6-induced deﬁcits emerged, including reduced DA release, neuronal ﬁring, and SV docking. Lastly, we found that the Janus kinase (JAK) inhibitor baricitinib reversed the inhibitory effects of IL-6 on female DA neurons. This work extends our understanding of the impact of inﬂammation on DA neurons, while identifying important sex differences and pharmacologic targets, ultimately laying the foundation for anti-inﬂammatory treatments of depressed patients with increased inﬂammation.

overall_design: RNA-seq profiling of eight-week-old human iPSC-derived dopaminergic neurons treated with vehicle or 5 ng/mL interleukin-6 for 24hrs

first: Yiqi

last: Huang


title: Chemotherapy-induced extracellular matrix remodelling in HGSOC

first: Eleni

last: Maniati

address: John Vane Science Centre, Charterhouse Square

department: Barts Cancer Institute

institute: Queen Mary University of London

summary: In this study we used two murine orthtotopic, transplantable synegeneic models, one that displays excellent response (60577) to carboplatin/paclitaxel and one that is highly chemoresistant (HGS2) and displays a weak response. We analysed the transcriptomes of these murine HGSOC tumours from both models across time in a therapeutic scheme that resembles the human condition.

overall_design: RNA sequencing on whole tumours from two murine orthtotopic, transplantable synegeneic HGSOC models (HGS2 timepoint-1 control, n = 3; HGS2 timepoint-1 treated, n = 3; HGS2 timepoint-2 control, n = 4; HGS2 timepoint-2 treated, n = 3; HGS2 timepoint-3 treated, n = 4; 60577 timepoint-1 control, n = 3; 60577 timepoint-1 treated, n = 3; 60577 timepoint-2 control, n = 3; 60577 timepoint-2 treated, n = 4; 60577 timepoint-3 treated, n = 4) . RNAseq was also performed on the 60577 and HGS2 cell lines grown in-vitro as monocultures (n = 2 perc cell line).

first: Panoraia

last: Kotantaki

first: Florian

last: Laforets

first: Frances

last: Balkwill


title: Macrophage Immune-Competent Colon Assembloids for Functional Interrogation of Neuroinflammation-Induced Colonic Dysmotility

status: Public on Jan 13 2026

city: College Station

first: Shreya

last: Raghavan

state: Texas

address: Texas A&M University, Emerging Technologies Building 3120, 101 Bizzell St

department: Department of Biomedical Engineering

institute: Texas A&M University

summary: Functional gastrointestinal disorders (FGIDs) affect ∼40% of the global population and are frequently characterized by colonic dysmotility. Symptomatic manifestations of colonic dysmotility significantly reduce quality of life in inflammatory bowel disease (IBD), diabetes, and Gulf War Illness (GWI). Current in vitro models lack the integration of functional physiology with immune and neuronal complexity required to establish causal links between neuroinflammation and dysmotility. Here, an immune-competent bioengineered colon assembloid is introduced that integrates multiple cell types of the external colonic wall, along with functional readouts of motility. Within bioengineered colon assembloids, various inflammatory insults resulted in enteric neuroinflammation, cascading to changes in colonic motility. Key mechanisms of dysmotility following inflammatory insult within the bioengineered colon assembloids included impaired neuronal regeneration, and aberrant smooth muscle remodeling. The bioengineered colon assembloid model mimicked diverse aspects of enteric neuroinflammation. Ultimately, the platform offers a physiologically relevant avenue to interrogate neuroimmune crosstalk and dissect mechanisms of colonic dysmotility, paving the way to new therapeutic strategies to improve colonic motility.

overall_design: RNA-Seq profiling of Bioengineered Colon Assembloids exposed to inflammatory insult using Pyridostigmine Bromide (PB) and Tumor Necrosis Factor- alpha (TNF-α) under Acute (Day 4) and Chronic (Day 7) conditions.

first: Claudia

last: Collier

first: Karla

last: Ortega Sandoval

first: Aelita

last: Salikhova

first: Shrinarayanee

last: Rengarajan

first: Anvitha

last: Tharakesh

first: Alana

last: Aristimuno Millan

first: Shanthi

last: Srinivasan


title: Expression data from mice spleens

city: SEOUL

first: SOYOUN

last: WOO

address: 25, Magokdong-ro 2-gil, Gangseo-gu

country: South Korea

institute: Ewha Womans University, College of Medicine

summary:
Female C57BL/6J mice, 8 weeks old, were DNCB-induced dermatitis on skin. For the effect of tonsil-derived mesenchymal stem cells (T-MSCs)treatment, cells were added to dermatitis model.
After 10 days, spleen cells were isolated for RNA expression analysis.

overall_design:
Vehicle control, Vehicle + T-MSCs, DNCB (138630; Sigma-Aldrich), and DNCB + T-MSCs
contributor: Macrogen

first: Hyun

last: Kim

first: Kyung-Ah

last: Cho

first: So-Youn

last: Woo


title: Improvement of Enfumafungin Production by Hormonema carpetanum via Mutagenesis and Process Optimization: Mutant Generation and Preliminary Transcriptomic Analysis

first: Haodong

last: Chen

address: Gebaini Road 285#

institute: China State Institute of Pharmaceutical Industry

summary: Enfumafungin, a triterpenoid antifungal compound, serves as the key starting material for the synthesis of ibrexafungerp and SCY-247. However, its low fermentation yield and high production cost constrain its supply, limiting drug accessibility and the ability to meet clinical demand. Consequently, enhancing enfumafungin biosynthesis is crucial for achieving large-scale production. In this study, physical and chemical mutagenesis treatments were adopted for Hormonema carpetanum ATCC 74360, and a genetically stable high-producing mutant, H. carpetanum ENF-5-29, was generated. This mutant produced 817 mg/L enfumafungin in flasks, a 30-fold increase over that of wild-type ATCC 74360. Comparative transcriptome analysis revealed that the proposed biosynthetic pathway from glucose to enfumafungin presented the most significant upregulation in the mutant. The fermentation medium and conditions were subsequently optimized to further enhance enfumafungin production. Transcriptome analysis revealed improved yields under low-temperature culture, likely due to the upregulated expression of key genes in the mevalonate pathway and the enfumafungin biosynthetic gene cluster (BGC). Together, these transcriptome findings provide molecular insight into enhanced enfumafungin production. Furthermore, batch fermentation of ENF-5-29 in a 5 L bioreactor achieved a yield of 1,621 mg/L, the highest yield reported to date. Our results demonstrate the efficacy of mutagenesis for H. carpetanum improvement and pinpoint key targets for future genetic engineering aimed at enhancing enfumafungin biosynthesis.

overall_design: RNA-seq profiling of wildtype ATCC 74360 and mutant ENF-5-29 at stationary phase of fermentation.

first: Junyi

last: Wang

first: Haolong

last: Huang

first: Jiali

last: Gui

first: Songbai

last: Yang

first: Wen

last: Tang

first: Jiawei

first: Shaoxin