title: Developmental conversion of the nucleolus into an RNA Polymerase II transcriptional platform in Drosophila spermatocytes

status: Public on May 20 2026

city: Cambridge

first: Yukiko

last: Yamashita

address: 455 main ST

institute: Whitehead Institute for Biomedical Research

summary: The nucleolus is widely regarded as a specialized compartment for RNA polymerase I (Pol I)-driven ribosomal RNA transcription and ribosome biogenesis. Yet the presence of “atypical nucleoli”, or nucleolus-like bodies (NLBs), which lack rRNA transcription despite containing canonical nucleolar components, has long been recognized, most notably during mammalian oogenesis and spermatogenesis. NLBs have been shown to have an essential function independent of rRNA transcription, but the nature of that function remained unclear. Here, we demonstrate that the nucleolus becomes an NLB during spermatocyte development in Drosophila melanogaster and, surprisingly, that this NLB serves as a platform for RNA polymerase II (Pol II)-mediated transcription. We find that the Y chromosome-linked fertility genes, which are heterochromatic in most cell types but highly expressed in spermatocytes, are transcribed at the spermatocyte NLB. We further show that the recruitment of active Pol II to the NLB requires known spermatocyte-specific transcriptional regulators. In their absence, the Y-linked fertility genes embedded within heterochromatin are not properly transcribed. Our findings reveal an active role for an NLB as a Pol II platform, and we propose that other NLBs may have similar functionality.

overall_design:
Total RNA-seq from control (GSE268126: GSM8286089, GSM8286092, GSM8286095), aly RNAi, and sa RNAi Drosophila testes, with three biological replicates and two technical replicates per genotype. The samples were processed and sequenced together, but the control was used in a previous study (GSE268126). Data (including the control, which we re-processed for this study) were trimmed and aligned to dm6.38 and the count matrix was generated from the BAM files and used in downstream analyses.

***************************************************************
The table below lists GEO accessions reused/reanalyzed for this study.
***************************************************************

first: Jaclyn

last: Fingerhut

first: Jun

first: Rebecca

middle: Y

last: Li

first: Romain

last: Lannes

last: Ashok


title: PRO-cap from T-47D and transverse colon

status: Public on May 19 2026

city: Ithaca

first: Haiyuan

last: Yu

state: NY

address: 10 East Ave.

country: USA

institute: Cornell University

summary:
A run-on assay, PRO-cap, that precisely maps the transcription start sites genome-wide with high sensitivity and specificity in the T-47D cells.
A run-on assay, PRO-cap, that precisely maps the transcription start sites genome-wide with high sensitivity and specificity in transverse colon.

overall_design:
Two biological replicates of T-47D cells
One PRO-cap experiment of transverse colon sample.

first: Sagar R.

last: Shah

first: Alden King-Yung

last: Leung

first: Li

last: Yao


title: BDNF engages pituitary stem cells

status: Public on May 18 2026

city: London

first: Probir

last: Chakravarty

address: 1Midland Road

country: United Kingdom

institute: Francis Crick

type: Expression profiling by high throughput sequencing

summary: The development of complex organs relies on the balanced expansion of cells of different lineages in order to establish a functional tissue. In the pituitary gland, maintenance of the adult corticotrope lineage relies heavily on replication of differentiated cells. In contrast in pathological conditions, such as adrenalectomy,  that deplete circulating glucocorticoids (Gc), pituitary stem cells are activated to increase the number of corticotropes. In the present work, we used the POMC knockout mouse model (POMC-/-) of Gc deficiency to identify and characterize pre-corticotrope precursors that are normally rare and short lived but accumulate in this model. Differentiation of PSCs into pre-corticotropes is repressed by Gc and requires the lineage-specific transcription factor Tpit. Pre-corticotrope maintenance is dependent on a BDNF autocrine loop that is sensitive to Gc. In addition, BDNF is a critical signal for engagement of pituitary stem cells into proliferation and differentiation during the postnatal expansion of the gland.

overall_design: Single cell analysis from whole male pituitaries after Adrenalectomy or Sham surgery

first: Kevin

last: Sochodolsky

first: Konstantin

last: Khetchoumian

first: Aurelio

last: Balsalobre

first: Ryan

last: Freeley

first: Margaret

middle: E

last: Rice

first: Robin

last: Lovell-Badge

first: Karine

last: Rizzoti

first: Jacques

last: Drouin


title: Defective Autophagy in GNE Myopathy is Reversed by Inhibition of Supplementary mTOR Activation

city: Seoul

first: Eun-Ji

last: Kwon

address: 1, Gwanak-ro

country: South Korea

institute: Seoul National University

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

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: Refer to individual Series


title: Endothelin-1 overexpression in mice increases vascular Vegfa164 and Vegfa188 alternative splice isoforms via enhanced Khdrbs3 expression

status: Public on May 15 2026

city: Montreal

first: Pierre

last: Paradis

state: QC

address: 3755 ch. de la Côte-Sainte-Catherine

country: Canada

institute: Lady Davis Institute for medical research, Jewish General Hospital, McGill University

type: Non-coding RNA profiling by high throughput sequencing


title: In Vivo Massively Parallel Reporter Assay Reveals Sequence Determinants of mRNA Localization in Astrocytes

status: Public on May 17 2026

city: St. Louis

first: Joseph

middle: D

last: Dougherty

state: MO

address: 4370 Duncan Ave

department: Genetics

institute: Washington University in St. Louis

summary: Subcellular mRNA localization and local translation are essential mechanisms for fine-tuning the spatiotemporal regulation of gene expression in the nervous system. While these processes have been extensively characterized in neurons, the cis-regulatory sequences mediating them in astrocytes remains poorly understood. Here, we developed an in vivo Massively Parallel Reporter Assay (MPRA), termed SN-MPRA, to systematically interrogate the sequence determinants of mRNA localization and local translation in astrocytes. To our knowledge, this represents the first application of an in vivo MPRA to study these processes. Using the SN-MPRA, we comprehensively tiled the 3′ untranslated regions (UTRs) of two locally translated mRNAs in astrocytes, Glt1 and Sparc. This approach enabled us to evaluate multiple models of RNA localization, including increased transcript abundance, “zip-code” elements, and RNA secondary structure. Given that astrocytes do not exhibit the high, unidirectional polarity of neurons, one potential mechanism of driving mRNA localization is that increased transcript abundance leads to increased likelihood of delivery or diffusion to peripheral astrocyte processes (PAPs). Although transcript abundance showed a moderate association with localization, it was insufficient to fully explain differences in localization patterns, suggesting additional sequence-dependent mechanisms. Global 3’ UTR features such as GC content and secondary structure did not correlate with localization. Instead, we identified groups of overlapping tiles with consistent localization, suggesting the presence of cis-regulatory sequence motifs. We validated the sufficiency and necessity of one of these groups[JD1.1] to drive increased local translation and found that this region had similar expression to the full 3’ UTR throughout the entire cell, whereas deletion of this region decreased expression. To further resolve the sequence motifs causing these effects, we designed a single-nucleotide mutagenesis SN-MPRA library targeting 8 element groups with shared localization. This analysis uncovered discrete regions in which nucleotide mutations disrupt localization and local translation. While a subset of these regions overlapped with known RNA-binding protein motifs, including KHDRBS1, many did not correspond to previously annotated binding sites, suggesting that multiple and potentially distinct mechanisms, such as RNA:protein interactions, RNA stability, and other cis-regulatory features, may contribute to mRNA localization in astrocytes. Together, these findings establish a high-throughput in vivo framework for identifying cis-regulatory sequences driving RNA localization and local translation and reveal that astrocytes likely employ diverse mechanisms to regulate subcellular gene expression. More broadly, the SN-MPRA provides a platform for studying RNA localization in vivo, where cellular context and intercellular interactions are preserved.

sample_organism:
Escherichia coli
Homo sapiens
Mus musculus

first: Sarah

middle: K

last: Koester

first: Kristina

last: Sakers

first: Gareth

middle: M

last: Rurak

first: Stephen

middle: P

last: Plassmeyer

first: Kelli

last: McFarland White

first: Sebastian

last: Alves Ferreira Dias

first: Peter

last: Baird

first: Dina

middle: J

last: Kornbluth


summary: Transgenic mice with tamoxifen-inducible endothelium-restricted human endothelin-1 overexpression (ieET-1) exhibited blood pressure (BP) elevation after 3 weeks and 3 months induction. Vascular injury was observed only after a 3-month exposure to human ET-1 overexpression. It is unknown whether 3-week or 3-month exposure to ET-1 overexpression results in gene dysregulation. We aimed to identify differentially expressed (DE) microRNAs and total RNA in mesenteric arteries of ieET-1 mice after 3-week and 3-month induction of human ET-1 overexpression.

overall_design: Ten to 12-week-old male ieET-1 mice and control ieCre mice expressing a tamoxifen-inducible Cre recombinase under the control of endothelium-specific Tie2 promoter were treated with tamoxifen (1 mg/kg/day, s.c.) for 5 days and sacrificed 16 days or 3 months later. RNA was extracted from mesenteric arteries for small and total RNA-sequencing using Illumina HiSeq-2500 and further studied using a systems biology approach.

first: Olga

last: Berillo

first: Suellen

middle: C

last: Coelho

first: Nathanne

last: Dos Santos Ferreira

first: Chantal

last: Richer

first: Daniel

last: Sinnett

first: Ernesto

middle: L

last: Schiffrin


title: Effect of MINK1 deficiency on gene expression in CD8+ T cells activation

status: Public on May 14 2026

city: Hangzhou

first: Kaixiang

last: Zhu

address: 866  Yuhangtang Road

department: school of medicine

country: China

institute: Zhejiang university

summary: The accumulation of ROS in the tumor microenvironment is a major driving factor for immunosuppression. While its detrimental effects on T cell activation are recognized, the precise molecular mechanisms remain unclear. In this study, we identify MINK1 as a ROS-responsive kinase in regulating CD8+ T cell-mediated anti-tumor immunity. We found that MINK1 ablation enhances the effector function of intratumoral CD8⁺ T cells by facilitate CD8+ effector T-cell differentiation, thereby enabling sustained tumor control. Mechanistically, MINK1 interacts with LATS1 and activates the Hippo pathway, thereby suppressing cytotoxic gene expression and inhibiting CD8+ T cell differentiation into effector subtypes. Finally, we proved that targeting MINK1 in both CAR-T and TCR-T cells could improve anti-tumor CD8+ T cell response in solid tumor models. Pharmacological inhibition of MINK1 also enhances anti-tumor immune responses in mice. Thus, this work uncovered MINK1 as a pivotal driver for CD8+ T cell dysfunction in tumors and highlights its potential as a therapeutic target for enhancing cancer immunotherapy.

overall_design: To reveal the phenotypic changes of CD8+ TILs in Mink1 knockout mice, we isolated WT and KO CD8+ T cells from tumor. Then we performed gene expression profiling analysis using data obtained from scRNA-seq of WT and MINK1 KO CD8+ T cells.

first: Lize

last: Wu

first: Fan

last: Zhao

first: Linrong

last: Lu


title: Inflammatory immune modulators of AML lung infiltration and respiratory failure

status: Public on May 22 2026

city: New York

first: Ziyan

last: Lin

department: Applied Bioinformatics Laboratories

institute: NYU Grossman School of Medicine

summary: Acute myeloid leukemia (AML) is a blood cancer with poor survival outcomes. In the acute setting, respiratory failure occurs frequently due to leukemia infiltration of the lungs. Underlying mechanisms remain unexplored and therapeutic interventions are only empiric. Here, we map the landscape of the AML lung microenvironment at both spatial and single-cell resolution. We show that inflammatory responses are triggered, as a part of an extensive remodeling of the lung stroma and immune microenvironment. Tumor cell infiltration impairs lung integrity and function; however, steroid treatment significantly slows down inflammation and lung infiltration and rapidly improves oxygenation and pulmonary function in AML patients with respiratory compromise attributed to leukemic infiltrates in the absence of infection. As a mechanistic correlate, we show that expression of the S-type lectin Lgals9 is triggered by inflammation and mediates cell-cell interactions within the infiltrated lungs. Also, we show that the cytokine IL-33 and its receptor are involved in cell-cell interactions within the leukemic lung microenvironment. Targeting of either the Lgals9 or IL33 axis significantly decreases levels of lung infiltration, by reshaping the immune landscape and AML cells. Our study is the first to characterize extra-medullary AML tumor microenvironments and to map pulmonary infiltration phenotypes in acute leukemia, opening the way for the design of novel treatment strategies.

overall_design: Spatial Transcriptomics Xenium (5k plex planel) on paraffin sections from Normal and AML-infiltrated anonymized human lung biopsies.

first: Varvara

last: Paraskevopoulou

first: Casado-Pelaez

last: Marta

first: Manel

last: Esteller

first: Iannis

last: Aifantis


title: Investigation of the impact of transcription factor SP1,MITF and CREB3L1 in HeLa cells

status: Public on May 13 2026

city: Pozzuoli

first: Rossella

last: De Cegli

address: Via Campi Flegrei 34

country: Italy

institute: Tigem

summary: Our previous studies on golgi biogenesis identified candidate Transcription Factors(TFs) that can support this process. Further bioinformatical ad in-vitro analysis revealed that MITF,SP1 and CREB3L1 emerged as the mayor TFs associated with Golgi biogenesis. In this study, we investigated the impact of the overexpression of these TFs in HeLa cells to determine whether the TFs can influence the transcriptome (and in particular golgi genes)

overall_design: HeLa cells were cultured and transfected with control plasmid, MITF-A EGFP, SP1-HA, full lenght CREB3L1 (CREB3L1FL) and costitutively active CREB3L1 (CACREB3L1). 48H after transfection, RNA was collected for digital mRNA-seq

first: De Cegli

last: Rossella

first: Abete

last: Domenico


title: Understanding the transcriptome changes in HeLa cells after inactivation of endosomes/lysosomes

summary: In this study, we optimized an experimental approach to inactivate endo/lysosomal compartment, inducing the formation of new endosomes. Endo/lysosomes inactivation was executed through DAB- mediated depletion of endosomes/lysosomes in HeLa cells, which previously internalized Horseradish peroxidase (HRP). These cells, 18 hours after inactivation, can regenerate new endosomes capable of HRP uptake. We further observed the transcriptional response in HeLa cells driven by endo/lysosomes inactivation,  discovering that, unlike the control condition, in which HRP was internalized but DAB solution was not added to the cells, a substantial number of endosomes/lysosomes related genes are activated

overall_design: HeLa cells were first incubated for 90 min at 37°C in DHB solution (DMEM + 20 mM HEPES + 0,1% BSA). Then, 2mg/mL HRP in DHB was given for 30 min at 37°C, whereupon cells were washed 4 times with cold PBS to eliminate the Extracellular HRP. DAB-treated cells were incubated in DAB solution (0,1 M Tris HCL pH 7,4 + 0,25 mg/mL DAB + 0,02% H2O2) for 2 minutes at room temperature; Control cells, instead, were incubated with control solution(Tris HCL pH 7,4 + 0,02% H2O2) for 2 minutes at room temperature. DAB-treated cells and control cells are collected immediately (0H), 6, and 18 hours after incubation with the DAB or control solution.


summary: Acute myeloid leukemia (AML) is a blood cancer with poor survival outcomes. Limited studies have reported lethal complications in patients due to leukemia infiltration into solid tissues such as the lung, but the related mechanisms remain understudied. Here, we map the transcriptional landscape of the mouse lung microenvironment at single-cell resolution in the AML-infiltrated lungs. Our analysis demonstrated a considerable remodeling of the lung microenvironment under leukemia conditions, as indicated by expansion of stromal myofibroblasts and reduction of endothelial capillary aerocytes. Those changes were accompanied by changes in immune resident cells of the lung microenvironment, as supported by reduction of B- and T- cell proportions, and increased frequencies of activated neutrophils and monocyte populations. We show an induction of inflammatory response within the microenvironment of the leukemic lung. We dissect the spatial interplay between AML and the lung microenvironment, and we identify previously unappreciated interactions driven by inflammatory mediators within the leukemic milieu. Of note, we show that Lgals9 (encoding for Galectin-9) mediates most of cell-cell interactions within the microenvironment of the AML-infiltrated lungs. LGALS9 is highly expressed in AML patients and its role in AML remains elusive. Targeting Galectin-9 reduces the AML burden in the lungs and reverses the infiltration phenotype. Combining single-cell, spatial transcriptomics approaches and functional experiments in vivo, our study is the first to characterize the pulmonary infiltration phenotype in AML, opening the route for novel treatment strategies in acute leukemia.

overall_design: Spatial Transcriptome of 5000 genes detected by in situ imaging using Xenium Instrument of paraffin sections from Normal and AML-infiltrated lungs.

first: Paraskevopoulou

last: Varvara

first: Lin

last: Ziyan

first: Marta

last: Casado-Pelaez

first: Esteller

last: Manel

first: Aifantis

last: Iannis


title: Transposable Element-Driven Expansion of Enhancer RNA Repertoires Underlies Regulatory Innovation and Polyploid Adaptation in Cereal Crops [ChIP-seq]

status: Public on Jun 22 2026

city: shanghai

first: yijing

last: zhang

address: 2005 Songhu Road

department: Biochemistry

institute: Fudan University

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Cereal genomes have undergone repeated polyploidization and transposable element (TE) proliferation, collectively generating complex regulatory landscapes. The evolutionary trajectories and functional implications of these landscapes, however, remain largely unexplored. By employing chromatin-bound RNA sequencing across seven cereal species, we systematically mapped 45,952 regulatory element transcripts (RETs), including 32,867 distal RETs corresponding to enhancer RNAs (eRNAs). Our analysis reveals that 56% of lineage-specific eRNAs originate from TE expansions, suggesting TEs as significant reservoirs of species-specific regulatory innovation in cereals. Notably, we uncovered a remarkable similarity in defense-related function, root-specific expression, and TE-derived origin of eRNAs across ancient and recent evolutionary layers of Triticeae, suggesting recurrent recruitment of TE-derived root-associated regulatory elements during Triticeae evolution. Furthermore, we found that young eRNA pairs in hexaploid wheat with high sequence similarity, many originating from RLG_famc8.3 and DTC_famc4.3, exhibit pronounced root specificity and coordinated expression, suggesting a targeted amplification and refinement of the successful ancestral regulatory strategy established after Triticeae divergence. To facilitate community access, we developed Cereal-eRNAdb (http://bioinfo.cemps.ac.cn/Cereal-eRNAdb/), a comprehensive database integrating 69,426 eRNAs with functional annotations across 296 samples. Our work indicates that TE-mediated innovation of root-specific eRNAs as a candidate mechanism that may contribute to Triticeae adaptation and provides a foundational resource for exploiting regulatory variation in cereal crop breeding.

sample_organism:
Secale cereale
Triticum aestivum
Aegilops tauschii

overall_design: Seedlings (above-ground) of common wheat (Triticum aestivum cultivars ‘Chinesespring’‘AK58’ and ‘Fielder’), barley (Hordeum vulgare cultivar ‘Morex’), rye (Secale cereale cultivar ‘Weining’), maize (Zea mays cultivar ‘B73’) and rice (Oryza sativa cultivars ‘ZH11’ and ‘Jap’) were harvested after 9-day growth. The roots, leaf and embryos of three wheat species (Triticum aestivum cultivar ‘Chinese Spring’, Triticum urartu cultivar ‘G1812’ and Aegilops tauschii cultivar ‘AL8-78’) were collected as follows: roots in the Hoagland solution were harvested after 9-day growth; the fresh immature embryos were isolated 14 days post anthesis; leaf were were harvested after 9-day growth. All the above materials were flash frozen in liquid nitrogen followed by nuclei isolation. Nuclei were isolated from 1 mL tissue powder solubilized in 20 mL ice-cold Honda buffer (0.44 M sucrose, 1.25% Ficoll, 2.5% Dextron T40, 20 mM HEPES, pH7.4, 10 mM MgCl2, 0.75% Triton X-100, 0.5 mM EDTA, 1 mM DTT, 8 mM β-mercaptoethanol, 2 µg/mL pepstatin A, 2 µg/mL aprotinin, 2 mM PMSF). The mixture was incubated on ice for 5 min, then filtered through 110 µm nylon mesh and a 40 µm cell strainer. The crude nuclei were spun down at 3,500 g for 5 min at 4°C, followed by washes with 150 µL of resuspension buffer (50% Glycerol, 0.5 mM EDTA, 25 mM Tris-HCl, pH 7.5, 100 mM NaCl, 1 mM DTT, 8 mM β-mercaptoethanol, 2 µg/mL pepstatin A, 2 µg/mL aprotinin, 2 mM PMSF, 0.4 U/µL RNase inhibitor) and 300 µL of wash buffer (25 mM Tris-HCl, pH 7.5, 300 mM NaCl, 1 M urea, 0.5 mM EDTA, 1% Tween 20, 1 mM DTT, 8 mM β-mercaptoethanol, 2 µg/mL pepstatin A, 2 µg/mL aprotinin, 2 mM PMSF, 0.4 U/µL RNase inhibitor). Again, the obtained nuclei were washed with another 150 µL of resuspension buffer and 150 µL of wash buffer. CB RNA was extracted from washed nuclei using TRIzol reagent and subjected to genomic DNA removal by TURBOTM DNase (Life Technologies). After purification with RNA Clean & ConcentratorTM-5 kit (Zymo Research, R1013), ~1 µg CB RNA was subjected to rRNA depletion by a riboPOOL kit (siTOOLs Biotech, PanPlant-10 nmol) and polyA RNA removal by oligo (dT) beads (NEB, S1419). PolyA RNA was enriched from total RNA by oligo(dT) beads. Purified CB RNA and PolyA RNA were transformed into cDNA libraries using the NEBNext Ultra II Directional RNA Library Prep Kit for Illumina (NEB #E7765) and sequenced on an Illumina NovaSeq platform.

first: Yijing

last: Zhang


title: RIP-seq analysis in primary neuroblastoma tumor cells.

status: Public on May 31 2026

city: Wuhan

first: Yingzhe

last: Fang

address: Donghu Road

institute: Wuhan University

summary: Cells were subjected to immunoprecipitation using an antibody against IGF2BP1and co-precipitated RNAs were extracted for high-throughput sequencing.Input was included as controls. The study aims to characterize the RNA-binding profile of IGF2BP1.

overall_design: For RIP-seq, ten million NLF or IMR32 cells were lysed in RIP lysis buffer (20 mM Tris-HCl pH 7.6, 150 mM NaCl, 1% NP-40, 1 mM EDTA, 0.1% SDS), supplemented with 100 U/mL RNasin Ribonuclease Inhibitors (Promega, #N2611) for 30 min on ice. After centrifugation, the supernatant was co-incubated with the IGF2BP1 antibody (Cell Signaling Technology, #8482; 5 μg) and rabbit anti-IgG (ABclonal, #AC005; 5 μg) at 4 °C overnight. Subsequently, the protein-G magnetic beads (Invitrogen, #10004D), which had been washed thrice with RIP buffer, were added and incubated for an additional 2 hours to enrich the protein-RNA complex.


title: The extreme diversity of retinal amacrine cells has deep evolutionary roots [mouse lemur]

city: Berkeley

first: Dario

last: Tommasini

address: 242 Stanley Hall

institute: UC Berkeley

summary: Amacrine cells (ACs) comprise a heterogeneous class of inhibitory neurons in the vertebrate retina, exhibiting morphological and functional complexity rivaling that of cortical interneurons. Here, we integrate single-cell and single-nucleus transcriptomic atlases from 24 vertebrate species to reconstruct the evolutionary origins of this extreme diversity. We identify 42 orthologous AC types (oACs), most of which exhibit a one-to-one correspondence across amniotes and, in many cases, across vertebrates. While core molecular identities are conserved, AC types vary in abundance and gene expression across species, likely reflecting adaptations to distinct visual ecologies. AC diversity scales with that of retinal ganglion cells (RGCs), indicative of co-evolution. Finally, we suggest that ACs arose from an AC-RGC hybrid precursor, with glycinergic ACs diverging early in vertebrate evolution, followed by a bifurcation between RGCs and GABAergic ACs. Together, these findings establish a unified evolutionary framework for understanding the diversity, development, and function of a class of inhibitory neurons across vertebrates.

overall_design: We enriched RGCs and BCs by using fluorescence-activated nuclei sorting for the nuclear antigens NEUN/RBFOX3 and CHX10/VSX2 respectively. Frozen retinal tissue was dissociated with a Dounce homogenizer in NP-40–based lysis buffer containing Tris, CaCl₂, MgCl₂, NaCl, RNase inhibitor, and DNase I. The suspension was filtered (40 µm), nuclei were pelleted (500 rcf, 5 min), and resuspended in staining buffer. Nuclei were incubated with NEUN antibodies for 12 min at 4 °C, washed, and resuspended in sorting buffer followed by DAPI staining. NEUN⁺ and CHX10⁺ nuclei were isolated by FANS (BD FACSDiva v8.02) and washed again before being placed in 0.04% BSA/PBS at ~1,000 nuclei/µl. Nuclear quality was confirmed microscopically prior to loading ~8,000 nuclei per channel onto a 10x Chromium Single Cell Chip. Since AC types express RBFOX3 non-uniformly, the cell type proportions in the raw atlases are not reflective of their natural abundance.

first: Aboozar

last: Monavarfeshani

first: Vishruth

last: Dinesh

first: Josh

last: Hahn

first: Jared

last: Tangeman

first: Olivier

last: Marre

first: Seth

last: Blackshaw

first: Teresa

last: Puthussery

last: R. Sanes

first: Karthik

last: Shekhar


title: NSD1 governs H3K36me2-mediated DNA methylation and drives differentiation of human iPSCs by regulating lncRNA expression [ChIP-seq]

city: Aachen

first: Deepika

last: Puri

address: Pauwelsstraße 20

country: Germany

institute: Helmholtz Institute For Biomedical Engineering, Uniklinik Aachen

summary: Epigenetic regulatory mechanisms, which include histone modifications and DNA methylation, play a central role in development and aging. Dimethylation of H3K36, deposited mainly by the histone methyltransferase NSD1, occurs predominantly in intergenic regions and recruits the DNA methyltransferase DNMT3A to facilitate DNA methylation. Haploinsufficiency of NSD1 results in the overgrowth disorder Sotos syndrome in vivo, which is associated with aberrant DNA methylation signatures and an enhanced epigenetic age. To understand the mechanism by which NSD1 may regulate development, differentiation and diseases, we generated human iPSC lines deficient in functional NSD1 (NSD1-KO). NSD1-KO cells exhibit a substrate-specific decrease in proliferation, reduced H3K36me2 levels and extensive DNA hypomethylation. Notably, loss of functional NSD1 altered the differentiation potential of iPSCs, with aberrant endodermal and mesodermal lineage commitment. Further analysis revealed that NSD1 might drive endodermal differentiation by regulating the expression of an endodermal lncRNA ‘HIDEN’ by mechanisms independent of the regulation of DNA methylation. Our NSD1-KO iPSC lines partially recapitulate the DNA methylation defects associated with NSD1-related disorders. Additionally, we uncovered a novel mechanism by which NSD1 may regulate endodermal differentiation of human iPSCs.

overall_design: NSD1-KO hIPSC lines were generated by CRISPR Cas9 mediated knockout in WT hIPSC lines. Wild type cells and generated knockout cells were expanded and fixed, after cell lysis and quenching, chromatin was fragmented by sonivcation and ChIP protocol was perfomed according to the manufacturer’s recommendations (Active motif #53042). ChIP-Seq libraries and sequencing was carried out by Cologne Genomics Centre.

first: Anna

last: Hansknecht

first: Martina

last: Mankarious

first: Monica

last: Varona Baranda

first: Esra

last: Dursun Torlak

first: Wolfgang

last: Wagner

first: Kira

last: Zeevaert


title: Mechanically regulated transcriptional and DNA methylation programs in skeletal muscle stem cells

city: Grand Forks

first: Susan

last: Eliazer

state: ND

address: 1301 N Columbia Rd.

department: Biomedical Sciences

institute: University of North Dakota School of Medicine and Health Sciences

type: Methylation profiling by high throughput sequencing

summary: RhoA-mediated mechanical signaling is an important regulator of muscle stem cell (MuSC) quiescence and activation. To define how RhoA influences gene regulation in MuSCs, we performed RNA sequencing (RNA-seq) and enzymatic methyl sequencing (EM-seq) on freshly isolated MuSCs from control and SC-RhoAfl/+ mice. RNA-seq analysis revealed widespread transcriptional changes associated with RhoA depletion, including genes involved in cytoskeletal organization, cell adhesion, and stem cell activation. In addition, we identified extensive alternative splicing events, indicating that RhoA signaling influences transcript isoform diversity. EM-seq profiling uncovered global changes in DNA methylation, with differentially methylated regions enriched in gene bodies. Comparative analysis suggests links between DNA methylation, transcriptional output, and splicing regulation at loci associated with cell-matrix interactions and stem cell state transitions. Together, these datasets provide a resource to understand how mechanical signaling through RhoA coordinates transcriptional, epigenetic, and splicing programs in MuSCs.

overall_design: Enzymatic Methyl sequencing was performed on freshly isolated FACS-purified MuSCs from control and SC-RhoAfl/+ mice to identify genome-wide DNA methylation changes following reduced RhoA activity.

first: Pukana

last: Jayaraman

first: Damien

last: Parrello


title: NSD1 governs H3K36me2-mediated DNA methylation and drives differentiation of human iPSCs by regulating lncRNA expression [RNA-seq]

overall_design: NSD1-KO hIPSC lines were generated by CRISPR Cas9 mediated knockout in WT hIPSC lines. The DNAisolated from 3 replicates of WT and 2 clones of NSD1-KO were analysed by Illumina Beachip Epic Array


title: NSD1 governs H3K36me2-mediated DNA methylation and drives differentiation of human iPSCs by regulating lncRNA expression [methylation array]

type: Methylation profiling by genome tiling array

middle: V

last: Baranda

last: Torlak


title: De novo  Golgi biogenesis requires orchestrated transactivation of Golgi genes

first: Rossella

last: De Cegli

summary: Golgi biogenesis is a crucial cellular process, yet its study has been hindered by the lack of easy methods to induce massive production of new Golgi units. In this study, we optimized an enzyme inactivation approach to stimulate the formation of fully functional Golgi stacks. Massive Golgi biogenesis was achieved through DAB-mediated inactivation of preexisting Golgi structures in cells stably expressing the chimeric Golgi enzyme Mannosidase II fused with horse radish peroxidase (HRP). Within 10 to 18 hours post-Golgi inactivation, substantial number of cells regenerated new Golgi stacks capable of transporting various cargo proteins to their appropriate destinations. This functional and structural recovery of the Golgi in ManII-HRP cells offers an efficient system to study Golgi biogenesis and associated cellular responses. We further explored transcriptomic changes in ManII-HRP cells, discovering that the extensive biogenesis of Golgi membranes induces the transcriptional activation of numerous Golgi-associated genes. These genes encode proteins involved in diverse functions such as glycosylation, membrane tethering, and ion/sugar transport. The timing of this gene transactivation correlates with the restoration of Golgi cisternae architecture and trafficking capabilities, suggesting that this transcriptional response plays an integral role in the biogenesis of new Golgi units.

overall_design: HeLA cells expresing ManII-HRP were subjected to inactivation of the Golgi complex via HRP mediated deposition of DAB inside the lumen of organelle. The cells were collected for scRNA-seq immediately after inactivation (control, time point 0h) or 2, 6, 10, 14, 18 and 24h after incubation with fresh medium that allows cells to generate new Golgi units.

first: Roman

last: Polishchuk

first: Xabier

last: Bujanda Cundin


title: Kidney Hematopoietic Stem and Progenitor Cells Contribute to Myeloid Development and Pathology in Lupus Nephritis

city: Daejeon

first: Seyoung

last: Jung

address: 291, Daehak-ro, Yuseong-gu

department: Graduate School of Medical Science and Engineering

institute: Korea Advanced Institute of Science and Technology

summary: Objectives The hematopoietic system maintains homeostasis by balancing myeloid and lymphoid cell production in the bone marrow (BM). In response to increased hematopoietic demand, extramedullary hematopoiesis (EMH) may occur in non-lymphoid organs. We investigated the role of EMH and kidney-resident hematopoietic stem and progenitor cells (HSPCs) in lupus nephritis (LN) pathogenesis. Methods Two murine LN models (MRL/lpr and TLR7 agonist-induced) were used to identify and characterize lineage-negative (Lin⁻) CD45⁺Sca1⁺ progenitor cells in the kidney. The association with disease severity was assessed using clinical parameters and histology. Single-cell RNA sequencing, including BM-to-kidney trajectory analysis and adoptive transfer experiments, evaluated lineage potential and pathogenicity. Stromal cell-derived hyaluronan (HA) was visualized by immunostaining. Urine samples from patients with LN were analyzed for hematopoietic progenitors and HA levels. Results Kidney Lin⁻CD45⁺Sca1⁺ cells were enriched in LN mice and correlated with increased proteinuria, elevated blood urea nitrogen, and kidney histological severity. These cells demonstrated a myeloid differentiation potential and shared transcriptional features with BM progenitors. Trajectory analysis indicated that BM-derived progenitors migrate to the kidneys and undergo local maturation. Adoptive transfer of LN-derived BM HSPCs induced kidney damage and myeloid infiltration, particularly under TLR7 stimulation. Kidney Sca1⁺ cells expressed CD44 and localized near HA-producing stromal cells in the renal pelvis. In human LN, urinary progenitor cells correlated with kidney dysfunction and HA levels. Conclusions EMH occurs in the kidneys during LN and contributes to disease progression through local myeloid cell expansion. Targeting kidney progenitors may offer novel therapeutic strategies to control local inflammation in LN.

overall_design: Two murine LN models (MRL/lpr and TLR7 agonist-induced) were used to identify and characterize lineage-negative (Lin⁻) CD45⁺Sca1⁺ progenitor cells in the kidney. Single-cell RNA sequencing, including BM-to-kidney trajectory analysis and adoptive transfer experiments, evaluated lineage potential and pathogenicity.

first: Hansol

last: Yi

first: Jeong Ho

last: Joo

first: Young-Eun

last: Kim

first: Heounjeong

last: Go

first: Yong-Gil

first: Chang-Keun

last: Lee

first: Bin

last: Yoo

first: Jeong Seok

first: Seokchan

last: Hong


title: Convergence of cytokine dysregulation and antibody deficiency in common variable immunodeficiency with inflammatory complications

status: Public on May 12 2026

city: Boston

first: Feng

last: Feng

state: United States

address: 650 Albany Street X248

institute: Boston University

summary:
Background: Noninfectious complications are the greatest cause of morbidity and mortality in common variable immunodeficiency (CVID), but their pathogenesis remains poorly defined.
Objective: Using high-throughput approaches, we aimed to identify, correlate, and determine the significance of immunologic features of CVID with noninfectious complications (CVIDc).
Methods: We simultaneously applied proteomics, RNA sequencing, and mass cytometry to a large cohort with primary antibody deficiency.
Results: CVIDc is differentiated from uncomplicated CVID, other forms of primary antibody deficiency, and healthy controls by a distinct plasma proteomic profile. In addition to confirming previously reported elevations of 4-1BB, IL-6, IL-18, and IFN-γ, we found elevations of colony-stimulating factor 1, IL-12p40, IL-18R, oncostatin M, TNF, and vascular endothelial growth factor A to differentiate CVIDc. This cytokine dysregulation correlated with deficiency of LPS-specific antibodies and increased soluble CD14, suggesting microbial translocation. Indicating potential significance of reduced LPS-specific antibodies and resultant microbial-induced inflammation, CVIDc had altered LPS-induced gene expression matching plasma proteomics and corresponding with increased CD14+CD16- monocytes, memory T cells, and tissue inflammation ameliorated by T-cell-targeted therapy. Unsupervised machine learning accurately differentiated subjects with CVIDc and supported cytokine dysregulation, antibody deficit, and T-cell activation as defining and convergent features.
Conclusions: Our data expand understanding of CVIDc proteomics, establish its link with deficiency of IgA and LPS-specific antibodies, and implicate altered LPS-induced gene expression and elevated monocytes and T cells in this cytokine dysregulation. This work indicates that CVIDc results when insufficient antibody neutralization of pathogen-associated molecular patterns, like LPS, occurs in those with a heightened response to these inflammatory mediators, suggesting a 2-hit model of pathogenesis requiring further exploration.

overall_design: RNA-seq profiling of peripheral blood mononuclear cells from common variable immunodeficiency patients and healthy donors with and without 18 hours of culture with lipopolysaccharide.

first: Miranda

last: Abyazi

first: Kayla

middle: A

last: Bell

first: Gavin

last: Gyimesi

first: Turner

last: Baker

first: Minji

last: Byun

first: Huaibin

last: M Ko

first: Charlotte

last: Cunningham-Rundles

first: Paul

last: Maglione


title: jasmonic acid treated betelvine plants under pathogenic stress

city: TIKAMGARH

first: Sandeep

middle: Kumar

last: Chaurasia

state: Madhya Pradesh

address: Govt. P. G. College Tikamgarh, Taigore bhawan, new building, kundeshwar road

department: Department of Botany

country: India

institute: GOVT PG COLLEGE TIKAMGARH

summary: Plants' tolerance to pathogenic stress is significantly influenced by jasmonic acid (JA), which promotes induced systemic resistance (ISR) in synergism with ethylene signaling. This study examines the role of exogenous JA priming inducing resistance in Piper betel L. under biotic stress from pathogens such as Colletotrichum, Phytopthora, Xanthomonas, Fusarium. The experimental setup included three groups: control plants that were neither infected nor treated with JA (N), infected plants without JA treatment (P), and JA-priming along with pathogenic infection (T3).

overall_design: The prepared library was loaded onto the NGS platform (Illumina). Using sequencing by synthesis (SBS) method to determine the nucleotide sequence of each DNA fragment. Illumina platforms use fluorescently labelled nucleotides were added, and the sequence was determined by the color of the fluorescence. Sequencing was paired end (reads from both ends)

first: Chinmayee

last: Acharya

first: Jitendra

last: Pandey


title: Human and mouse adrenal glands are characterized by species-specific steroidogenic states and tissue turnover [VisiumHD]

city: Moscow

first: Denis

last: Maksimov

address: Leninskie Gory

country: Russia

institute: MSU

summary: The adrenal gland is a fundamental endocrine organ exhibiting constant renewal. Despite extensive work in rodents, human-specific aspects of hormone-producing cell populations, stem cells, and self-renewal mechanisms are not fully understood. To fill this knowledge gap and address species-specific features, we generated high density single-cell and spatial transcriptomics atlases of adult human and mouse adrenal glands using Visium, VisiumHD and Stereo-seq, covering a spectrum of sexes and ages. Our comparisons between human and murine adrenal gland revealed significant evolutionary divergence despite homology in function of specific regions, which questiones the applicability of mouse models in studies of human adrenal disorders. Self-renewal mechanisms in adrenocortical populations that were previously discovered in mice also revealed human-specific features or were confronted by human-specific transitions not evident in rodents. The latter included specific perivascular mesenchymal progenitors, and dispersed SF1+/EZH2+ progenitor cells, which implies that human adrenocortical cells may be renewed in a localized manner in addition to the centripetal model. We also engaged in cross-comparison of our adult human adrenals with fetal stages to reveal developmental strategies still operating as a part of self-renewal in adults. Unexpectedly, human SF1+/EZH2+ progenitors turned out to be operating during adrenocortical development and later during adult stages, albeit in different degrees. At last, we revealed sex-specific differences in human cholesterol metabolism and other features reflecting human and mouse sexual dimorphism in adrenal glands. Overall, our new comparative mouse-human atlases shall provide an additional resource for further molecular interrogations of adrenal gland biology and pathology.

overall_design: We isolated biopsies from dissected adrenal glands from mouse adults and subjected them to spatial transcriptomics sequencing using 10x Genomics Visium HD approach.

first: Maria

last: Kastriti

first: Julian

last: Petersen

first: Julia

last: Krupinova

first: Marina

last: Utkina

first: Dmitry

last: Beltsevich

first: Anna

last: Roslyakova

first: Olga

last: Glazova

first: Samira

last: Kaziakhmedova

first: Alina

last: Ryabova

last: Kuznezova

first: Anastasia

last: Shcherbakova

first: Ekaterina

last: Bondarenko

first: Zoia

last: Antysheva

first: Eugene

last: Albert

first: Lilia

last: Urusova

last: Lapshina

first: Anastassia

last: Chevais

last: Avsievich

first: Valentin

last: Trofimov

first: Galina

last: Melnichenko

first: Natalya

last: Mokrysheva

first: Ivan

last: Dedov

first: Oleg

last: Gusev

first: Andreas

last: Heinzel

first: Rainer

last: Oberbauer

first: Lukas

last: Englmaier

first: Pavel

last: Volchkov

first: Peter

last: Kharchenko

first: Igor

last: Adameyko


title: Mass spectrometry-based proteomic profiling of human postmortem brain tissues in tauopathies, including corticobasal degeneration, progressive supranuclear palsy, and Alzheimer’s disease

status: Public on May 11 2026

city: Niigata

first: Norikazu

last: Hara

address: 1-757 Asahimachi, Chuo-ku

department: Department of Molecular Genetics, Brain Research Institute

country: Japan

institute: Niigata University

summary:
Background: The molecular mechanisms of tauopathies, characterized by intracellular accumulation of abnormal tau encoded by MAPT, remain poorly understood.
Objectives: To identify proteins associated with the primary tauopathies corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP), as well as the secondary tauopathy Alzheimer’s disease (AD), using mass spectrometry.
Methods: Total homogenates were prepared from human postmortem brains of AD (n = 4), CBD (n = 4), PSP (n = 4), and their respective controls (n = 4), and analyzed by mass spectrometry. Protein levels were compared across the four groups, and proteins showing statistically significant differences were subsequently examined using functional enrichment and protein–protein interaction (PPI) analyses. For a subset of the proteins that showed significant differences, immunohistochemistry was performed to determine their distribution in the brain. Furthermore, single-nucleus RNA sequencing data were analyzed to evaluate the corresponding gene expression across the four groups in a cell-type–specific manner at the RNA level.
Results: In the four-group comparison, 859, 114, 6, and 1 proteins showed P values < 0.05, < 0.01, < 0.005, and < 0.001, respectively. We subsequently focused on the six proteins with P values < 0.005 (AK3, ATP5PD, COX7C, PPA1, PREP, and UQCRC1) and performed functional enrichment and PPI analyses. These analyses revealed that the identified tauopathy-related proteins were shown to be mainly involved in mitochondrial function.
Discussion: Age-related mitochondrial dysfunction could influence the onset and progression of tauopathies.

overall_design:
A total of 16 post‑mortem human frontal cortex specimens were analyzed using 10x Genomics single‑nucleus RNA‑seq, with four donors per diagnostic group (Control, AD, CBD, PSP).

***************************************************************
Raw files for human/patient samples were not submitted to GEO due to concerns about submitting personally identifiable sequence data for open access.
***************************************************************

first: Alfi

middle: R

last: Jannah

first: Mai

last: Hasegawa

first: Jonathan

last: Ham

first: Tamao

last: Tsukie

first: Ai

last: Obinata

first: Masataka

last: Kikuchi

first: Kensaku

last: Kasuga

first: Haruyasu

last: Yamaguchi

first: Hideomi

last: Hamasaki

first: Mari

last: Tada

first: Akiyoshi

last: Kakita

first: Masaki

last: Matsumoto

first: Akinori

last: Miyashita

first: Takeshi

last: Ikeuchi


title: Inositol Pyrophosphates Mediate Chloroplast Lipid Remodeling and Nuclear Gene Repression during High-Light Acclimation in Chlamydomonas reinhardtii

city: Sevilla

first: Rodrigo

last: Bedera-García

state: Sevilla

address: Américo Vespucio 49

country: Spain

institute: Spanish National Research Council

summary: Microalgae are photosynthetic organisms capable of autotrophic growth. Their applicability in multiple industrial fields has been largely studied, thanks to their ability to fixate CO2 into high added value organic products like fatty acids and carotenoids. However, our understanding of the cellular signaling networks that control carbon flux and acclimation to environmental stress remains incomplete. In this study, we used the Chlamydomonas reinhardtii mutant strain vip1-1, which carries a loss-of-function mutation in the hexakisphosphate kinase responsible for the synthesis of inositol pyrophosphates InsP7 and InsP8 (PP-InsPs), to investigate the role of these molecules during high-light acclimation. We show that PP-InsPs participate in chloroplast-specific lipid remodeling by modifying membrane composition and fluidity through fatty acid desaturations and glycerolipid composition. In addition, our findings suggest that PP-InsPs are involved in chloroplast-nucleus communication, where they act as transcriptional repressors of photosynthesis associated nuclear genes (PhANGs), fatty acid desaturases and lipid synthases, contributing to cellular acclimation to high light. We also found that PP-InsPs modulating effect extended to protein synthesis and accumulation of Calvin-Benson-Bassham cycle intermediates. Therefore, we propose that PP-InsPs function as integratory molecules that balance carbon allocation between storage and structural pools, in response to envirnomental cues such as high light. This uncovers a novel function of PP-InsPs in high light acclimation and potentially in chloroplast-nucleus communication, providing new insights that may help engineer more resilient and efficient strains.

overall_design: To investigate the signaling role of the inositol pyrophosphates in the response to high light stress in Chlamydomonas reinhardtii, we performed a gene expression comparative analysis of wild-type and  an inositol pyrophosphates-deficient strain (vip1-1) cells in standard light irradiance (control) and high light stress (high light) conditions. We generated RNA-seq data from 3 biological replicates for each condition.

first: Luis

middle: G

last: Heredia-Martínez

first: María Elena

last: García-Gómez

first: Borja

last: Prieto-Muñiz

first: José

last: Ortega

first: Inmaculada

last: Couso


title: Human and mouse adrenal glands are characterized by species-specific steroidogenic states and tissue turnover [Stereo-seq]

first: Denis

last: Maksimov

overall_design:
We isolated biopsies from dissected adrenal glands from human adults and subjected them to spatial transcriptomics sequencing using STOmics Stereo-seq approach. Human adrenals (one gland per donor) were excised simultaneously with explantation of kidneys from deceased organ donors.

Human raw data fastq files are available through EGA controlled access https://ega-archive.org/dacs/EGAC00001003383

first: Maria

last: Kastriti

first: Julian

last: Petersen

first: Julia

last: Krupinova

first: Marina

last: Utkina

first: Dmitry

last: Beltsevich

first: Anna

last: Roslyakova

first: Olga

last: Glazova

first: Samira

last: Kaziakhmedova

first: Alina

last: Ryabova

last: Kuznezova

first: Anastasia

last: Shcherbakova

first: Ekaterina

last: Bondarenko

first: Zoia

last: Antysheva

first: Eugene

last: Albert

first: Lilia

last: Urusova

last: Lapshina

first: Anastassia

last: Chevais

last: Avsievich

first: Valentin

last: Trofimov

first: Galina

last: Melnichenko

first: Natalya

last: Mokrysheva

first: Ivan

last: Dedov

first: Oleg

last: Gusev

first: Andreas

last: Heinzel

first: Rainer

last: Oberbauer

first: Lukas

last: Englmaier

first: Pavel

last: Volchkov

first: Peter

last: Kharchenko

first: Igor

last: Adameyko


title: Human and mouse adrenal glands are characterized by species-specific steroidogenic states and tissue turnover [Spatial Transcriptomics]

first: Denis

last: Maksimov

overall_design:
We isolated biopsies from dissected adrenal glands from human adults and subjected them to spatial transcriptomics sequencing using 10x Visium approach. Human adrenals (one gland per donor) were excised simultaneously with explantation of kidneys from deceased organ donors.
Human raw data fastq files are available through EGA controlled access https://ega-archive.org/dacs/EGAC00001003383

first: Maria

last: Kastriti

first: Julian

last: Petersen

first: Julia

last: Krupinova

first: Marina

last: Utkina

first: Dmitry

last: Beltsevich

first: Anna

last: Roslyakova

first: Olga

last: Glazova

first: Samira

last: Kaziakhmedova

first: Alina

last: Ryabova

last: Kuznezova

first: Anastasia

last: Shcherbakova

last: Bondarenko

last: Antysheva


title: Human and mouse adrenal glands are characterized by species-specific steroidogenic states and tissue turnover [scRNA-seq]

overall_design:
We isolated individual cells from dissected adrenal glands from human and  mouse adults and subjected them to single cell transcriptomics sequencing using 10x Chromium approach. Human adrenals (one gland per donor) were excised simultaneously with explantation of kidneys from deceased organ donors.
Human raw data fastq files are available through EGA controlled access https://ega-archive.org/dacs/EGAC00001003383

first: Ekaterina

first: Zoia

first: Eugene

last: Albert

first: Lilia

last: Urusova

last: Lapshina

first: Anastassia

last: Chevais

last: Avsievich

first: Valentin

last: Trofimov

first: Galina

last: Melnichenko

first: Natalya

last: Mokrysheva

first: Ivan

last: Dedov

first: Oleg

last: Gusev

first: Andreas

last: Heinzel

last: Oberbauer

last: Englmaier

last: Volchkov


title: The FGF4–integrin β1 axis restores directed collective migration to accelerate diabetic wound regeneration [ChIP-Seq].

status: Public on May 01 2026

city: Wenzhou

first: Zhiming

last: Zhang

address: Chashan Campus of Wenzhou Medical University

institute: Department of Cardiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

summary: This dataset was generated to investigate the mechanism by which Fibroblast Growth Factor 4 (FGF4) regulates the binding of C-FOS to the ITGB1 promoter. ChIP sequencing was performed on high glucose-induced HacaT cells, which were divided into low glucose, high glucose, and high glucose plus FGF4 treatment groups.

overall_design: To investigate the effects of high glucose and FGF4 treatment, this study employed ChIP-seq to analyze the binding of C-FOS to the ITGB1 promoter in HacaT cells under low glucose, high glucose, and high glucose combined with FGF4 treatment conditions.

first: Jian

last: Sun

first: Zhifeng

last: Huang

first: Jie

last: Zhou

first: Shuodan

last: Ding


title: Aberrant brain-type neuronal programs in large-cell pancreatic neuroendocrine carcinoma

status: Public on May 05 2026

city: Berlin

first: Michael

last: Sigal

address: Augustenburger Platz 1

department: Dept. Hepatology and Gastroenterology

institute: Charité Universitätsmedizin

summary: High-grade pancreatic neuroendocrine carcinoma (panNEC) is a rare, aggressive cancer with limited tissue availability. Single-nucleus transcriptomics of five large-cell panNECs revealed two interesting neuroendocrine cell states: one highly proliferative with an aberrant brain-specific neuronal differentiation program and another stress-responsive state enriched for heat stress, hypoxia, and glycolysis. Our findings suggest potential therapeutic vulnerabilities, highlighting the need to evaluate the efficacy of combination therapies.

overall_design:
Fresh-frozen tumors from human high-grade neuroendocrine tumors were selected and subjected to snRNA-seq

***************************************************************
Raw files for human/patient samples has been made available in EGA (https://www.ebi.ac.uk/ega/, study accession EGAS00001008449) for controlled access to the personally identifiable sequence data.
***************************************************************

first: Olivia

last: Debnath

first: Hilmar

last: Berger

first: Katharina

last: Detjen

first: Phillip

last: Kirchner

first: Ilaria

last: Mariononi

first: Thomas

last: Conrad

first: Bertram

last: Wiedenmann

first: Aurel

last: Perren

first: Naveed

last: Ishaque

first: Ines

last: Eichhorn

first: Felix

last: Bolduan


title: The cell states of sea urchin during metamorphosis revealed by single-cell RNA sequencing

status: Public on May 06 2026

city: Xiamen City

first: Yaqi

last: Zhang

address: No. 43, Yindou Road, Jimei District, Xiamen City, Fujian Province

institute: Jimei University

summary: Metamorphosis is a key process in the life history of most sea urchins. However, the understanding of its molecular mechanisms is still lacking, especially the basic cell biology pre-metamorphosis and post-metamorphosis. Therefore, we used single-cell RNA sequencing to obtain the cell states of larvae and juveniles of Heliocidaris crassispina.


title: Early sex-related transcriptional differences in CD8+ T cells responding to chronic viral infection reveal a sex bias in exhaustion development

city: Winnipeg

last: Wilkins

state: Manitoba

address: 66 Chancellors Cir

department: Biological Sciences

institute: University of Manitoba

summary: CD8+ T cell diversity is essential to control infections and chronic antigen stimulation. In acute-resolving infection, effector cells mediate acute responses and memory cells provide long-lived protection against future exposures. In chronic infection and cancer, an altered state called exhaustion occurs. Exhausted CD8+ T cells are molecularly and functionally distinct from effector and memory cells. Differences in immune responses exist between biological sexes, however, how biological sex influences the timing and transcriptional programs of CD8+ T cell responses during chronic versus acute viral infection remains unknown. Here, we show that male and female CD8+ T cells exhibit transcriptional differences in their early responses during chronic but not acute viral infection in vivo. Using single-cell RNA-sequencing analyses, we show that female CD8+ T cells adopt an early exhaustion-like program compared to males. Moreover, we found sex-related differences in single-cell gene expression dynamics and fundamental cellular processes early after chronic infection. These findings reveal new insights into sex-related differences in CD8+ T cell exhaustion development and early T cell responses that may contribute to sex differential immune responses.

overall_design: CD8+ T cells were transferred from CD45.1 P14 donor mice to CD45.2 C57BL/6J recipient mice, including female-female, male-male, and female-male transfers. Recipients were infected with LCMV-Armstrong or LCMV-clone 13 for 4, 7, 28, or 40 days. CD8+ T cells were isolated, sorted with FACS, and analyzed using scRNA-seq.

first: Nyambura

last: Kahia

first: Sean

last: Robertson

first: Megan

last: Rodriguez

first: Paul

last: Layug

first: Harman

last: Vats

first: Victor

last: Spicer

first: Darien

last: Yeung

first: Arzu

last: Ozturk-Aptekmann

first: Janilyn

last: Arsenio


title: The FGF4–integrin β1 axis restores directed collective migration to accelerate diabetic wound regeneration.

first: Zhiming

summary: This dataset was generated to investigate the mechanisms underlying the pro-healing effects of Fibroblast Growth Factor 4 (FGF4) on diabetic wounds. We performed RNA sequencing on wound tissues from streptozotocin (STZ)-induced diabetic mice. The mice received daily topical applications of either recombinant FGF4 (rFGF4) or PBS vehicle control. Wound tissues were harvested on day 7 post-wounding for transcriptomic analysis.

overall_design: On day 7 following skin wounding, transcriptomic analysis via RNA sequencing was carried out on cutaneous tissues from streptozotocin (STZ)-induced diabetic mice that received either PBS (control) or recombinant FGF4 (rFGF4) treatment.

first: Jian

last: Sun

first: Zhifeng

last: Huang

first: Jie

last: Zhou

first: Shuodan

last: Ding


title: Decoding the Cell-Type and Spatial Roles of H19 in Cholestatic Liver Injury Through Single-Nucleus and Spatial Transcriptomics

status: Public on Apr 30 2026

city: Richmond

first: Grayson

middle: Welch

last: Way

email: waygw@vcu.edu, waygw@outlook.com

state: Virginia

address: 1217 E Marshall Street Room 534

department: Microbiology and Immunology

institute: VCU

summary: Despite recent advances, Primary Sclerosing Cholangitis (PSC)-a chronic obstructive biliary disease-still lacks effective therapies to prevent disease progression or the need for liver transplantation. Long non-coding RNA H19 (H19) has been implicated in promoting PSC disease progression. However, the underlying cell-specific and molecular mechanisms by which H19 contributes to PSC pathogenesis remain incompletely understood. Here we used single nucleus RNA sequencing (snRNAseq) and spatial transcriptomics to elucidate the cell- and spatial-specific expression alterations associated with H19 in the Mdr2KO PSC mouse model.

overall_design: Age- and sex-matched (female) WT, H19KO, Mdr2KO, and Mdr2KO/H19KO (DKO) mice were analyzed using single nucleus RNA sequencing (snRNAseq). Mdr2KO and DKO mice were also analyzed with GeoMx Digital Spatial Profiler (DSP) with the whole transcriptome atlas (WTA) spatial transcriptomics to elucidate the cell and spatially specific effects of H19 expression in cholestatic liver injury.

middle: W

first: Huiping


title: Single-cell RNA sequencing of differentiated human iPSC organoid-derived kidney tubuloids (iPSCod tubuloids)

city: Utrecht

first: Carla

last: Pou Casellas

address: Uppsalalaan 8

country: Netherlands

institute: Hubrecht Institute

summary: Kidney organoids generated from induced pluripotent stem cells (iPSC) have proven valuable for studies of kidney development, disease, and therapeutic screening. However, specific applications have been hampered by limited expansion capacity, immaturity, off-target cells, and inability to access the apical side. Here, we apply recently developed tubuloid protocols to purify and propagate kidney epithelium from d7+18 (post nephrogenesis) iPSC-derived organoids. The resulting ‘iPSC organoid-derived (iPSCod)’ tubuloids can be exponentially expanded for at least 2.5 months, while retaining expression of important tubular transporters and segment-specific markers. This approach allows for selective propagation of the mature tubular epithelium, as immature cells, stroma, and undesirable off-target cells rapidly disappeared. iPSCod tubuloids provide easy apical access, which enabled functional evaluation and demonstration of essential secretion and electrolyte reabsorption processes. In conclusion, iPSCod tubuloids provide a different, complementary human kidney model that unlocks opportunities for functional characterization, disease modeling, and regenerative nephrology.

overall_design: scRNA-seq of FAF-differentiated human iPSCod kidney tubuloids (1 sample from a bulk tubuloid culture)

first: Fjodor

last: Yousef Yengej

first: Carola

last: Ammerlaan

first: Maarten

middle: B

last: Rookmaaker

first: Marianne

last: Verhaar

first: Hans

last: Clevers


title: Single cell RNA-seq analysis of PBMCs from mouse models of mevalonate kinase deficiency

city: Sydney

first: Michael

last: Rogers

state: New South Wales

address: 384 Victoria Street

country: Australia

institute: Garvan Institute of Medical Research

summary: The single cell RNA sequencing data here were used in the publication "NK cell dysfunction and interferon gamma production underlie autoinflammation in mevalonate kinase deficiency". This study sought to identify changes in immune cell populations in peripheral blood of MvkV377I/del91 mutant mice (a genetic model of mevalonate kinase deficiency described in; Munoz et al. 2022, J Clin Invest 132(19):e160929. doi: 10.1172/JCI160929).

overall_design: PBMC were isolated from female wildtype (Mvk+/+) and MvkV377I/Δ91 mice, purified by fluorescence-activated cell sorting (FACS) and analysed by scRNA-seq.

first: Oliver

last: Skinner

first: Marcia

last: Munoz

first: Ryan

last: Chai

first: Andrew

last: McCorkindale


title: Endothelin-1 overexpression in mice increases vascular Vegfa164 and Vegfa188 alternative splice isoforms via enhanced Khdrbs3 expression

city: Montreal

first: Pierre

last: Paradis

address: 3755 ch. de la Côte-Sainte-Catherine

institute: Lady Davis Institute for medical research, Jewish General Hospital, McGill University

summary: Transgenic mice with tamoxifen-inducible endothelium-restricted human endothelin-1 overexpression (ieET-1) exhibited blood pressure (BP) elevation after 3 weeks and 3 months induction. Vascular injury was observed only after a 3-month exposure to human ET-1 overexpression. It is unknown whether 3-week or 3-month exposure to ET-1 overexpression results in gene dysregulation. We aimed to identify differentially expressed (DE) microRNAs and total RNA in mesenteric arteries of ieET-1 mice after 3-week and 3-month induction of human ET-1 overexpression.

overall_design: Ten to 12-week-old male ieET-1 mice and control ieCre mice expressing a tamoxifen-inducible Cre recombinase under the control of endothelium-specific Tie2 promoter were treated with tamoxifen (1 mg/kg/day, s.c.) for 5 days and sacrificed 16 days or 3 months later. RNA was extracted from mesenteric arteries for small and total RNA-sequencing using Illumina HiSeq-2500 and further studied using a systems biology approach.

first: Olga

last: Berillo

first: Suellen

last: Coelho

first: Nathanne

last: Dos Santos Ferreira

first: Chantal

last: Richer

first: Daniel

last: Sinnett

first: Ernesto

last: Schiffrin


title: Transcriptional profiling of SARS-CoV-2-infected Calu-3 cells.

city: New York

first: Stuart

last: Sealfon

address: One Gustave L. Levy Place

department: Department of Neurology

institute: Icahn School of Medicine at Mount Sinai

summary: To explore the effects of SARS-CoV-2 proteins on expression of host genes, Calus-3 cells were mock-infected or infected cells with SARS-CoV-2 WT or the 12 mutants. At 24 h post-infection RNA were isolated from the mock or virus-infected cells for deep sequencing.

overall_design: Calus-3 cells were mock-infected or infected cells with SARS-CoV-2 WT or the 12 mutants in tripicates. At 24 h post-infection, the infected cells were collected in trizol and  total RNA isolation was perfermed using the Zymo Direct-zol RNA micro prep Kit according to manufacturer's instruction. The isolated RNAs were submtted for deep sequencing


title: BRD2 upregulation as a pan-cancer adaptive resistance mechanism to BET inhibition [ChIP-seq]

status: Public on Apr 29 2026

city: Davis

first: Chang-il

last: Hwang

state: CA

address: One Shields Ave

department: Microbiology and Molecular Genetics

institute: University of California Davis

summary: Bromodomain and extraterminal motif (BET) inhibitors, such as JQ1, are promising cancer therapeutics that target epigenetic regulators, particularly BRD4. However, resistance to BET inhibitors (BETi) limits their clinical utility, necessitating a better understanding of adaptive mechanisms. We identified BRD2 upregulation as a conserved response to BET inhibition across multiple cancer types and hypothesized that BRD2 compensates for BRD4 loss, sustaining essential transcriptional programs during treatment. Consistent with this, BRD2 knockdown sensitized cancer cells to BETi in vitro, and combining BRD2 depletion and JQ1 treatment significantly impaired tumor growth in vivo. At the chromatin level, BRD2 and BRD4 ChIP-seq analysis of pancreatic cancer cells showed consistent BRD4 loss from chromatin after JQ1 treatment, while BRD2 displacement differed by sensitivity. Resistant cells maintained higher BRD2 occupancy than sensitive cells, suggesting a link between BRD2 retention and drug response. To dissect the underlying mechanism of BRD2 upregulation upon BET inhibition, we analyzed co-expression networks and observed that NFYA is co-expressed with BRD2 across diverse tissues and cancer types. Consistently, NFYA binds the BRD2 promoter. NFYA depletion abrogated BRD2 upregulation upon BETi treatment, indicating that NFYA is required for BRD2 induction following BET inhibition. Collectively, our findings establish BRD2 as a critical mediator of adaptive resistance to BETi in pan-cancer and identify NFYA as a novel transcriptional regulator of this process. Co-targeting BRD2 or its regulatory network offers a rational strategy to enhance the durability and efficacy of BET-based therapies.

overall_design: Comparative chromatin immunoprecipitation sequencing (ChIP-seq) of BRD2 and BRD4 across three murine KPC-derived PDAC lines (mT3-2D, mT19-2D, mT23-2D) under DMSO or JQ1 (1 µM, 24 hours).

first: Suyakarn

last: Archasappawat


title: DNA repair drives cisplatin-induced neuronal death

status: Public on Apr 28 2026

first: Jeroen

last: van den Berg

state: Utrecht

summary: Cisplatin and similar alkylating chemotherapy agents are the cornerstone treatments for many types of cancers. While effective, these drugs induce long-term side-effects in post-mitotic tissues including the nervous system. There are no known effective pharmacological interventions for chemotherapy-induced neurotoxicities, in part due to our limited understanding of how neurons and other non-dividing cells respond to DNA damage. Here, we show that nucleotide excision repair (NER) is responsible for cisplatin adduct removal in human neurons. However, contrary to its protective role in dividing cells, NER drives neuronal cell death in response to cisplatin. Through DNA repair synthesis, NER exhausts low levels of deoxynucleoside triphosphate (dNTP) pools found in post-mitotic neurons. dNTP pools are first consumed to resolve transcription blocking lesions through transcription-coupled NER. When dNTPs become exhausted, toxic double-strand breaks accumulate across the genome primarily because of incomplete global-genome NER. Supplementation with deoxynucleosides (dN) or genetic upregulation of dNTP production protects neurons from cisplatin-induced cell death. These results identify low levels of endogenous dNTP pools as a vulnerability of post-mitotic cells to DNA damage and suggest nucleoside supplementation as a strategy to protect patients from chemotherapy-induced neurotoxicity.

overall_design: i3Neurons were treated with 20 µM cisplatin for 24 hours with 20 µM EdU added for the indicated times (either 24 hours or hours 1-7 or 17-24 of cisplatin treatment). Neurons were harvested as single cells by incubating with accutase for 20 minutes and resuspending by repeated pipetting. Cells were washed with PBS, resuspended in 1 mL PBS, and then fixed by dropwise addition of 4 mL ice cold methanol under mild vortexing. Fixed cells were stored overnight at -20°C. The next day, the methanol solution was removed, and cells were resuspended in storage buffer (10% DMSO, 20 mM HEPES pH 7.5, 150 mM NaCl, 2 mM EDTA, EDTA-free protease inhibitors) and kept at -20°C until processing.

first: Willian

last: Nathan

first: Andre

last: Nussenzweig


title: Longitudinal spatial transcriptomics of murine IL10KO colitis

city: Stockholm

first: Jennifer

last: Fransson

address: Karolinska Institutet

country: Sweden

institute: Karolinska Institutet

summary: In order to describe in detail the processes involved in chronic colitis, we performed spatial transcriptomics at multiple time points in a IL10KO colitis mouse model. These data were compared to bulk RNAseq and scRNAseq (GSE255423) results from the same mice within the same study.

overall_design: Colon tissue was collected from WT mice at age 6 weeks and from IL10 KO at ages 10 and 14 weeks. One mouse collected at week 14 showed more severe colitis with a rectal prolapse.

first: Chiara

last: Sorini

first: Eduardo

last: Villablanca


title: Unfolded Protein Response governs an Alternative Splicing program conserved from healthy to malignant cells

city: London

first: Eleni

last: Maniati

address: John Vane Science Centre, Charterhouse Square

department: Barts Cancer Institute

institute: Queen Mary University of London

summary: The unfolded protein response (UPR) is a critical adaptive program triggered upon cellular stresses that profoundly reshapes the transcriptome and translatome. In the very first minutes of cellular stress, translation blockage, RNA decay and RNA granules formation prompt the synthesis of proteins essential to the stress response. Due to the dynamic nature of these processes and ribosome stalling, investigating translation upon stress has proven to be challenging; therefore, our understanding of these mechanisms and translatome rewiring upon stress remains limited. Here, we exploited O-Propargyl-puromycin (OPP) labelling of de novo peptides followed by LC-MS/MS to identify de novo proteins translated upon endoplasmic reticulum stress. Our approach combined to transcriptomic analyses revealed the synthesis of core splicing factor proteins and a profound reshaping of the splicing landscape upon ER stress. We identified a signature of 8 splicing events systematically occurring in eukaryotic cells exposed to ER stress. Using pharmacological, genetic, phosphoproteomic and sequencing approaches, we demonstrated that this specific ERsplice signature is driven by PERK activation and is dependent on splicing factors’ phosphorylation. Our study unveils a new role for ER stress and PERK in splicing regulation, and provide a molecular signature of ER stress through an ERsplice signature conserved from healthy to malignant tissues.

overall_design: RNASeq analysis was performed on the Oci AML3 and the HEK293T cell lines to examine the transcriptional changes in response to ER stress induction by treatment with Tunicamicin. Oci AML3 cells were examined at 4h and 24h after Tunicamicin treatment and DMSO treated cells as well as untreated cells were used as controls. HEK293T cells were examined at 24h and DMSO treated cells were used as controls. N = 3 replicates per experimental group.

first: Celine

last: Philippe

first: Kevin

last: Rouaoult-Pierre


title: BRD2 upregulation as a pan-cancer adaptive resistance mechanism to BET inhibition [RNA-seq]

overall_design: Comparative RNA-seq profiling across three murine KPC-derived PDAC lines (mT3-2D, mT19-2D, mT23-2D) under DMSO or JQ1 (1 µM, 24 hours).


title: Longitudinal bulk RNA-seq of murine Il10KO colitis

summary: In order to describe in detail the processes involved in chronic colitis, we performed bulk RNA-seq at multiple time points in murine Il10KO colitis. These data were compared to scRNAseq and spatial transcriptomics results from the same mice within the same study. Bulk data were analyzed by identifying differentially expressed genes between time points and treatment groups.

overall_design: Distal colon tissue was collected from BALB/c wild-type at 6 weeks of age and Il10KO mice at 2 week intervals from 6 weeks to 14 weeks of age. Bulk RNA-seq was performed on tissue samples. n = 3 mice per time point and genotype


title: Longitudinal spatial transcriptomics of murine T cell transfer colitis

summary: In order to describe in detail the processes involved in chronic colitis, we performed scRNA-seq at multiple time points in a CD45RBhi T cell transfer colitis mouse model. These data were compared to bulk RNAseq and scRNAseq results from the same mice within the same study. Spatial trancriptomics were analyzed by performing NMF to identify spatial patterns of gene expression.

overall_design: T cell transfer colitis was induced in Rag2 KO mice. Distal colon tissue was collected at days 0, 30 and 50. One mouse collected at day 50 was treated with anti-IL-12p40 starting from day 14.


title: Longitudinal scRNA-seq of murine Il10KO colitis

summary: In order to describe in detail the processes involved in chronic colitis, we performed scRNA-seq at multiple time points in murine Il10KO colitis. These data were compared to bulk RNAseq and spatial transcriptomics results within the same study. scRNAseq data were analyzed by annotating cell clusters and comparing proportions and gene expression programs over time.

overall_design: Distal colon tissue was collected from wild-type at 6 weeks of age and from Il10KO mice at intervals of 14 days from 6 weeks to 14 weeks of age. Colons from 3 animals at each time point were pooled and cells were sorted by FACS to separate epithelial (EpCAM+/CD45-), immune (EpCAM-/CD45+) and stroma (EpCAM-/CD45-) populations. Cells were processed using the 10X Chromium system for gene expression and Feature Barcodes.


title: Longitudinal scRNA-seq of murine T cell transfer colitis

summary: In order to describe in detail the processes involved in chronic colitis, we performed scRNA-seq at multiple time points in CD45RBhi T cell transfer colitis mouse models. These data were compared to bulk RNAseq and spatial transcriptomics results from the same mice within the same study. scRNAseq data were analyzed by annotating cell clusters and comparing proportions and gene expression programs over time.

overall_design: T cell transfer colitis was induced in Rag2 KO and SCID mice. Distal colon tissue was collected at intervals of 10 (Rag2 KO) or 7 (SCID) days. A group of mice were treated with anti-IL-12p40 starting from day 14 (Rag2 KO) or day 10 (SCID). Colons from 3 animals were pooled and cells were sorted by FACS to separate epithelial (EpCAM+/CD45-), immune (EpCAM-/CD45+) and stroma (EpCAM-/CD45-) populations. Cells were processed using the 10X Chromium system for gene expression and Feature Barcodes.


title: Longitudinal bulk RNA-seq of murine T cell transfer colitis

summary: In order to describe in detail the processes involved in chronic colitis, we performed bulk RNA-seq at multiple time points in CD45RBhi T cell transfer colitis mouse models. These data were compared to scRNAseq and spatial transcriptomics results from the same mice within the same study. Bulk data were analyzed by identifying differentially expressed genes between time points and treatment groups.

overall_design: T cell transfer colitis was induced in Rag2 KO and SCID mice. Distal colon tissue was collected at intervals of 10 (Rag2 KO) or 7 (SCID) days. A group of mice were treated with anti-IL-12p40 starting from day 14 (Rag2 KO) or day 10 (SCID). Bulk RNA-seq was performed on tissue samples. n = 2-3 mice per time point and treatment group


title: EBNA1 inhibitors reveal CDC7 and POU2F1 as direct functional targets in EBV+ epithelial cancers

status: Public on Apr 27 2026

city: Philadelphia

first: Priyankara

last: Wickramasinghe

state: PA

address: 3601 Spruce Street

department: Bioinformatics

institute: The Wistar Institute

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

overall_design: Refer to individual Series


title: EBNA1 inhibitors reveal CDC7 and POU2F1 as direct functional targets in EBV+ epithelial cancers [RNA-Seq]

summary: Epstein-Barr virus (EBV) latent infection is ubiquitously associated with nasopharyngeal carcinoma and gastric cancer, expressing very few viral protein components (EBNA1 and LMP1/2A). We previously showed that EBNA1 inhibitor VK1727 blocked cell cycle progression and growth of EBV+ tumors in vivo. However, the underlying molecular mechanism requires more evidence. In this study, we employed VK1727 to remove EBNA1 binding to viral and cellular genomes in three EBV+ epithelial tumors (PDX C15, C666-1 and SNU719). Then we integrated EBNA1 ChIP-seq and transcriptomic analysis to identify direct gene targets of VK1727, which involve in cell cycle progression and cell proliferation. Our analysis characterized a cell cycle dependent kinase CDC7 and a stem cell transcription factor POU2F1. Further analysis illustrated that EBNA1 binding to CDC7 promoter and POU2F1 intron promotes RNA Pol II-pS5 to initiate transcription of these two genes. Moreover, our results revealed CDC7 inhibitor Simurosertib is epistatic with VK1727 in reduction of EBV copy number, induction of cell cycle arrest, and inhibition of cell proliferation in EBV+ epithelial cancer. While POU2F1 knockdown reduced copy number of EBV, decreased expression of viral genes and inhibited proliferation of SNU719 cells. Our study revealed two functional gene targets of VK1727 in EBV+ epithelial cancers, which provides two potential biomarkers for following therapeutical research.

overall_design: Three EBV+ tumor models were treated with EBNA1 inhibitor VK1727 on 3-5 days. Then we integrated RNA-seq and EBNA1 ChIP-seq to identify direct targets of EBNA1 inhibitors in three EBV+ tumors.

first: Songtao

last: HE

first: Niseno

last: Terhuja

first: Leena

last: Yoon

first: Bhanu Chandra

last: Karisetty

first: Paul

last: Lieberman


title: A pivotal Wnt antagonist role promoting digit joint specification by constraining Wnt activity

status: Public on Apr 24 2026

city: Frederick

first: Susan

last: Mackem

state: MD

address: 1050 Boyles St. Building 560, Room 21-08

institute: NCI-Frederick

summary: Bmps and Wnts play opposing roles in several contexts during chondrogenesis and joint formation. Using genetic and genomic approaches, we found instead that canonical Wnts can cooperate with Bmps to enhance pSmad1/5 activity and initiate chondrogenic commitment in digit tip progenitors.   5’HoxdD/D mutant digits are characterized by elevated Bmp and pSmad1/5 activity and subsequent joint loss.  We show that expressing stabilized bcatenin (bcatCA) in interdigit mesenchyme rescues 5’HoxdD/D digit joint loss non-autonomously, by inducing secreted Wnt antagonists and normalizing digit tip pSmad1/5 levels. Indeed, genetic removal of Dkk2 in 5’HoxdD/D prevented joint rescue by bcatCA. Furthermore, elevating Wnt activity with Gsk3b antagonists in limb bud culture stabilized pSmad1/5 levels and enhanced Bmp activity.  Elevated pSmad1/5, as seen in 5’HoxdD/D, accelerates chondrogenic commitment, impeding a switch of phalanx forming region (PFR) cells in the digit tip to interzone (joint progenitor) fate.  We propose that, before progenitors transit into PFR, Wnt antagonists cooperate with Fgfs to prevent precocious pSmad1/5 accumulation by stabilizing Gsk3b to promote Smad-linker phosphorylation and Smad1/5 degradation.  Consequently, Wnt antagonists play a key role in modulating the pace of initial commitment of digit progenitors to chondrogenesis, together with Fgfs, and maintain mesenchymal plasticity to balance digit phalanx and joint formation.

overall_design: Comparison of RNAseq profiling between isolated interdigital tissues of control, 5'HoxdD/D and 5'HoxdD/D;bCatCA were used to look for the bCatCA target gene which can restore digit joint formatoin in 5'HoxdD/D.

first: Bau-Lin

last: Huang


title: In vivo systematic detection of the outcomes of CRISPR/Cas9 mediated DNA repair in skeletal muscle stem cells [IDM-Seq long-read]

status: Public on Apr 23 2026

city: Hong Kong

first: Yang

last: Fu

address: Prince of Wales Hospital, N.T, H.K, 32 Ngan Shing St, Sha Tin

department: Department of Orthopaedics and Traumatology

country: Hong Kong

institute: The Chinese University of Hong Kong

summary: CRISPR/Cas9 has revolutionized genome editing with broad therapeutic applications, yet its repair patterns in vivo remain poorly understood. Here, we systematically profile CRISPR/Cas9 editing outcomes at 95 loci using our established CRISPR/Cas9/AAV9-sgRNA system in skeletal muscle stem cells (MuSCs). Through comprehensive characterization of the repair outcomes, our findings demonstrate that the general rules governing CRISPR/Cas9-mediated editing in vivo largely align with those observed in vitro. Additional to the anticipated small editing indels such as MMEJ mediated deletions and NHEJ mediated templated insertions, we uncover a prevalent occurrence of large on-target modifications, including large deletions (LDs) characterized by microhomology (MH) and large insertions (LIs). Notably, the LIs comprise not only exogenous AAV vector integrations but also endogenous genomic DNA fragments (Endo-LIs). Endo-LIs preferentially originate from active genomic regions, with their integration shaped by three-dimensional chromatin architecture. By disrupting key components of the NHEJ and MMEJ repair pathways in vivo, we identify their distinct roles in regulating the large on-target modifications. Together, our work systematically profiles the CRISPR/Cas9 repair outcomes in vivo and offers valuable guidance for improving the safety of CRISPR/Cas9-based gene therapies.

overall_design: Targeted deep sequencing was performed across three experimental cohorts: (i) 44 single-sgRNA and 51 dual-sgRNA target sites, along with their respective controls (Note that several single- and dual-sgRNA samples shared the same control data); (ii) one single-sgRNA and one dual-sgRNA target site evaluated across a multiple-dose treatment gradient; and (iii) enzyme knockout models versus control groups. Additionally, ATAC-seq and ChIP-seq assays were conducted to explore the chromatin features influencing indel formation.


title: In vivo systematic detection of the outcomes of CRISPR/Cas9 mediated DNA repair in skeletal muscle stem cells [control]


title: Proteostasis sustains T cell differentiation potential and tumor-infiltrating lymphocyte function [RNA-seq]

status: Public on Apr 22 2026

city: La Jolla

first: Ananda

last: Goldrath

address: 9500 Gilman Drive

department: Molecular Biology

institute: University of California, San Diego

summary: CD8+ tumor-infiltrating lymphocytes (TIL) often fail to restrain tumor growth due to differentiation to T cell exhaustion. In healthy tissues, tissue-resident memory T cells (TRM) survey tissues and sustain protective capacity for years, and tumors that contain TIL with TRM-features are associated with better patient prognosis. We identified protein homeostasis (proteostasis) significant in distinguishing TRM and progenitor-exhausted TIL (TPEX) from terminally-exhausted TIL (TEX) by identifying multiple E3 ubiquitin ligases that maintain T cell differentiation potential. Sustained ligase-expression in TIL enhanced T cell accumulation, preserved stem-like TCF1+ populations, and improved anti-tumor function, whereas ligase loss-of-function impaired TIL and altered T cell differentiation in acute infection. TEX experience a loss of proteostasis, marked by unfolded protein accumulation despite functional proteasomes. Enforced ligase expression rescued this unfolded protein accumulation in TIL and improved immunotherapy responses, demonstrating the role of proteostasis in maintaining differentiation potential and identifying new avenues for advancing cancer immunotherapies.

overall_design: Recipient mice were injected intradermally with 1 × 10^6 MC38-GP33 adenocarcinoma cells. Congenically distinct P14 T cells were activated and transduced to generate EV and Neurl3 OE P14 T cells, which were co-transferred into recipients on d5 post-activation cells were mixed at a 1:1 ratio and a total of 5×10^5 P14 cells was transferred by intravenous (i.v.) injection into CD45 congenic recipients with d6 tumors. The mice were monitored three times per week, and the mice were sacrificed 6 days after the adoptive T cell transfer. For each replicate, cells from 2-3 mice were pooled per tissue and then 5,000 P14 sorted for bulk RNA-seq.

first: Nicole

last: Scharping


title: Proteostasis sustains T cell differentiation potential and tumor-infiltrating lymphocyte function [CITE-seq]

overall_design: Congenically distinct P14 T cells were activated and electroporated with complexed tracrRNA, Cas9, and crRNA to generate CRISPR control and KO P14 T cells, which were co-transferred into recipients then infected with LCMV Armstrong. On day 5 of infection, P14 T cells from IEL, liver, and spleen, were profiled by CITE-seq.

first: Maximilian

last: Heeg

first: Alexander

last: Monell

first: Giovanni

last: Galletti


title: Intracellular iron homeostasis-regulated epigenetic reprogramming contributes to -7/del(7q) leukemia

status: Public on Apr 21 2026

city: Chengdu

first: Yiman

last: Peng

state: Sichuan

address: No.1, Keyuan 4th Road, Gaopeng Avenue, Chengdu, Sichuan, China

department: State Key Laboratory of Biotherapy, West China Hospital, Sihcuan University

institute: Sichuan University

summary: Chromosome copy number variations are poorly understood drivers of human malignancies. -7/del(7q) is common in acute myeloid leukemia, confers a poor prognosis, and is thought to harbor several tumor suppressors. Previously, we identified the histone methyltransferase KMT2C as a tumor suppressor in this region. Here, through a differentiation CRISPR screen in hematopoietic stem and progenitor cells, we find that the mitochondrial iron transporter ABCB8 is essential for their differentiation. ABCB8 deficiency accelerates leukemogenesis in vivo and disrupts iron homeostasis, reducing cytoplasmic iron availability and impairing iron-dependent enzymes, including the histone demethylase KDM6A. Consequently, ABCB8 loss elevates H3K27me3 levels, repressing differentiation genes in an iron- and KDM6A-dependent manner. Notably, ABCB8 and KMT2C, neighboring genes on 7q, cooperatively regulate H3K27me3 to suppress leukemogenesis. Our findings reveal ABCB8 as a tumor suppressor in -7/del(7q) acute myeloid leukemia and uncover an epigenetic collaboration between neighboring tumor suppressors, driven by iron-mediated chromatin remodeling.

overall_design: Various mouse HSPC models were applied to investigate the functions of ABCB8 and other genes function in -7/del(7q) leukemia

first: Jianan

last: Zheng

first: Xintong

last: Deng

first: Lanxin

last: Zhang

first: Zhongwang

last: Wang


title: The imbalance of Th17/Treg cells induced by prenatal chronic stress exposure is associated with activation of the PI3K/Akt/NF-κB signaling pathway in offspring

city: Yinchuan

first: Ye

last: Li

address: School of Public Health and Management, Ningxia Medical University, Yinchuan 750004, China

institute: Ningxia Medical University

summary: Maternal immune dysregulation, caused by gestational psychological stress, infection, and other perturbations, results in altered offspring immune development and increases risk for immune related disorders. However, the number of studies reporting the effects of prenatal stress on immune system of offspring is very limited. In this study, we examined whether prenatal stress stimuli, based on the CUMS model, may activate the PI3K/Akt/NF-κB signaling pathway and cause an imbalance of Treg/Th17 in the offspring's spleen. Through the establishment of CUMS model, we discovered that prenatal stress increased the plasma levels of corticosterone, IL-1β and IL-6 in the rats that were exposed to it, as well as the serum levels of IL-6, TNF-α and TGF-β in the offspring. We also discovered a correlation between the levels of cytokines in the female rats and the offspring. Additionally, the outcomes of the transcriptome sequencing and PCR experiment demonstrated that the differentially expressed mRNAs in offspring exposed to prenatal stress may cause an imbalance of Th17/Treg via activating the Gng3-related PI3K/Akt/NF-B pathway.

overall_design:
Achronic mild stress stimulation model (CUMS) was established and high-throughput RNA sequencing (RNA-seq) was performed to examine the spleen tissue transcriptome of offspring to investigate the pathogenetic effect of PI3K/AKT/NF-κB pathway in the pathogenesis of chronic stress induced MIA damaging the balance of offspring Th17/Treg imbalance.
The rats in the PM group were exposed to the procedure of chronic unpredictable mild stress (CUMS) to establish a prenatal maternal stress model(21). The following nine stressors, which lasted 21 days, were a part of the CUMS protocol: ①crowding environment (7-8 rats in each cage, 24 h), ②humid sawdust (60%–70% humidity, 24 h), ③shaking stress (one time per second, 30 min), ④tilting cage (tilt 45°, 24h), ⑤restraint stress (2h), ⑥fasting and water deprivation (24h), ⑦swimming in ice water (5min).
The day of birth was designated postnatal day 0 (PND 0). At PND 21, male and female offspring were weaned and placed in separate cages. 8 offspring from the PC group were randomly chosen as group C, while 8 offspring from the PM group were randomly chosen as group M. The sample tissue was spleen tissue from these M and C groups.

first: Guixiang

last: Yao


title: Gene expression profile at single cell level of muscle-derived cells from Oncorhynchus mykiss white muscle

city: Rennes

first: Sabrina

last: Jagot

address: All Henri Fabre

department: PHASE

country: France

institute: INRAE

summary: Our research aimed to elucidate the cellular and molecular dynamics of muscle-derived cells during the decline of muscle hyperplasia in trout

overall_design: Single cell RNA seq study of muscle-derived cells (MDC) from white muscles of Oncorhynchus mykiss following the decline of hyperplasia growth. 12 MDC sc-RNA seq samples were collected and processed from animals weighting 10 g, 100 g, 500 g, 1k g and 1.5 kg. Mononucleated cells were isolated from white muscle juvenile trout (10 g to 1.5 kg body weight) as previously described (Gabillard et al., 2010). Briefly, 20 to 80 g of white muscle were mechanically dissociated with scalpels and enzymatically digested by collagenase and trypsin prior to filtration. In order to remove as much debris and red blood cells as possible from cell suspension, a 20%-60% Percoll gradient was applied. Cells were resuspended in Dulbecco’s modified Eagle’s medium (DMEM) containing 10% fetal bovine serum (FCS) and 1% antibiotic–antimycotic solution and conserved at 4°C, overnight (ON). Cells were washed 3 or 4 times with DMEM plus 1% of antibiotics and filtered using 40 µm Flowmi® Cell Strainers. After ensuring a cell viability greater than 70% and a concentration at 700 to 800 cells per µL, cell suspensions (~12,000 cells per reaction) were loaded onto the Chromium system (10X Genomics). Following the instructions of the manufacturer, cDNA amplification and scRNA-seq libraries were constructed using Single-Cell 3′ Gene expression kit v3.1 (10X Genomics). The libraries were sequenced using the Illumina Novaseq 6000 on a flowcell S4 200 cycles v1.5 (28 cycles for Read 1, 150 cycles for Read 2, 10 cycles for i7 index and 10 cycles for i5 index). Reads obtained from scRNA-seq were mapped on the Oncorhynchus mykiss reference genome (USDA_OmykA_1.1, NCBI ReSeq Assembly: GCF_013265735.2). Count matrices were generated using CellRanger v7.0.1 (10X Genomics).

first: Candice

last: Babarit

first: Nathalie

last: Sabin

first: Jean-Charles

last: Gabillard

first: Karl

last: Rouger


title: H3K9 di-methylation dynamics underlies mouse minor zygotic genome activation [ChIP-seq of mESC]

status: Public on Apr 19 2026

city: Suita-shi, Osaka

first: Ryo

last: Maeda

address: Yamadaoka 1-3

institute: The University of Osaka

summary: Minor zygotic genome activation (ZGA) is crucial for early development and totipotency acquisition, yet the regulatory mechanisms driving minor ZGA genes remain elusive. Here we show that dynamic regulation of H3K9me2 is essential for minor ZGA. H3K9me2 levels at minor ZGA gene loci are reduced at early 2-cell and are re-established by morula. Maternal depletion of the H3K9 demethylases KDM3A and KDM3B leads to increased H3K9me2 and impaired minor ZGA in early 2-cell, followed by developmental arrest at 2- to 4-cell. In mESCs, H3K9 at minor ZGA loci is highly di-methylated; combined loss of the H3K9 methyltransferases G9a and SETDB1 leads to synergistic de-repression of minor ZGA genes. Mechanistically, SETDB1 specifically targets Dux, while G9a broadly represses minor ZGA genes through H3K9 di-methylation linked to lamina-associated heterochromatin formation. These findings establish H3K9me2 dynamics as a key regulator for minor ZGA, highlighting the indispensable role of epigenetic control in early embryogenesis.

overall_design: Epigenome profiling by high throughput sequencing

first: Makoto

last: Tachibana


title: In vivo systematic detection of the outcomes of CRISPR/Cas9 mediated DNA repair in skeletal muscle stem cells [sgRNA]

first: Yang

last: Fu


title: Ribosome decoding memory directs translational re-coding of codon repeats

status: Public on Apr 20 2026

city: Ithaca

first: Saori

last: Uematsu

address: 526 Campus Road, Cornell University

department: Division of Nutritional Sciences

institute: Cornell University

summary: During mRNA translation, ribosome dynamics at individual codons critically shape the quality and quantity of protein products. Long runs of consecutive codons are generally thought to impede elongation by depleting cognate tRNAs. However, in Huntington’s disease, ribosomes translate hundreds of consecutive CAG codons without catastrophic stalling. Here, we systematically profile ribosome behavior across repeats of all 20 amino acids encoded in the human genome. For proline and lysine repeats – commonly considered difficult to decode – we find that ribosomes accelerate after an initial phase of slow decoding, a phenomenon we term adaptive decoding. Remarkably, codon-specific decoding memory enables iterative translation of arginine repeats, generating internally expanded protein products. In contrast, acidic amino acid repeats trigger ribosomal bypassing and produce internally truncated proteins. Contrary to prevailing assumptions, decoding inertia acquired during repeat translation constraints frameshifting. Disrupting the decoding memory of CAG repeats by inserting proline codons is beneficial in reducing polyglutamine synthesis and aggregation. These findings uncover an adaptive dimension of ribosome decoding that contributes to the synthesis of physiological and pathological amino acid repeats.

overall_design: Ribo-seq of HEK293 cells transfected with mRNA reporters that contain various homopolymeric repeats; Ribo-seq of HEK293 cells under normal conditions, Arg starvation, and SAMD9 activation


title: Genetic regulatory axis between AGR2 and ESR1 promotes breast cancer progression

city: Kuala Lumpur

first: M. Aiman

last: Mohtar

state: (select)

address: UKM Medical Molecular Biology Institute (UMBI)

country: Malaysia

institute: Universiti Kebangsaan Malaysia

summary: AGR2 has emerged as a key player in tumorigenesis and metastasis, exhibiting upregulation in various types of cancer and contributing to their malignant progression. Intriguingly, despite its canonical residence within the ER, this enigmatic protein possesses the ability to venture beyond cellular boundaries and manifest tumorigenic properties in the extracellular environment. This study aimed to first define the global transcriptome that is maintained by a functional AGR2 system in breast cancer cells and find potential constituents for this cancer associated process.

overall_design: To gain further insights into the role of AGR2 in breast cancer progression and identify potential modulators involved in AGR2 signaling and secretion, we employed a loss-of-function approach using CRISPR/Cas9 genome editing. The bone metastatic 1833-BoM cell line derived from a triple-negative breast cancer cell line was selected as the experimental model, and lentiviral delivery of CRISPR-Cas9 was utilized to target AGR2 using two different sgRNAs. Pools of lentivirally transduced CRISPR-Cas9 knockout (KO1 and KO2) of 1833-BoM cells and non-targeting control (NTC) were subjected to RNA-Seq to profile and quantify global transcriptome changes. We compared the global transcriptome of AGR2-targeted 1833-BoM breast cancer cells derived from two sgRNAs targeting AGR2 (AGR2 KO1 and AGR2 KO1) with non-targeting control sgRNA (NTC).

first: Syazalina

last: Zahari

first: Saiful Effendi

last: Syafruddin