title: Treatment of cholangiocarcinoma using humanized monoclonal antibodies targeting Claudin-1 (RNA-Seq of HuCC-A1 CDX tumors short treatment)

first: Frank

last: Jühling

summary: Cholangiocarcinoma (CCA) is an adenocarcinoma of the hepatobiliary system showing an alarming rise in incidence and mortality with unsatisfactory treatment options. Claudin-1 (CLDN1) is a transmembrane protein expressed in tight junctions and exposed on the cell surface in liver fibrosis and cancer. Using single cell RNA-sequencing (scRNA-Seq) and spatial transcriptomics of CCA patient tissues, we show that CLDN1 expression is highly upregulated in cancer cells and is associated with stemness and cell fate. Gain-of-function studies in CCA orthotopic in vivo mouse models showed decreased survival and enhanced tumor growth, unraveling a functional role of CLDN1 as an oncogenic driver. Targeting exposed CLDN1 using highly specific CLDN1 monoclonal antibodies (mAbs) robustly inhibited tumor growth across CCA CDX and PDX mouse models and patient-derived CCA organoids including tumors with medium or low CLDN1 expression. Moreover, antibody treatment markedly inhibited tumor cell migration, invasion, and extrahepatic metastasis. Mechanistically, targeting exposed CLDN1 on CCA tumors inhibited Notch1, FAK/SRC, and Hippo-YAP signaling, resulting in decreased cancer cell stemness, EMT and extracellular matrix remodeling. In conclusion, these results uncover CLDN1 as a previously undiscovered CCA driver and therapeutic target, paving the way for the clinical development of CLDN1 mAbs to improve the dismal outcome of patients with advanced CCA.

overall_design: To investigate the early mechanism of action of the CLDN1 mAb, fresh tumor tissues from mice bearing established HuCC-A1-xenograft tumors treated with an anti-CLDN1 mAb or vehicle control for 48h were harvested and analyzed using RNA-Seq .

first: Zeina

last: Nehme

first: Thomas

last: Baumert


title: RBM5 is essential for the maintenance of leukemia stem cells by regulating a leukemic transcription program in cooperation with MYC [scRNA-seq]

status: Public on Jun 08 2026

city: Suzhou

first: Peng

last: Xu

state: Jiangsu

address: Office3625 Building703, RENAI ROAD No.199, INDUSTRIAL PARK DISTRICT

department: Suzhou Medical College

country: China

institute: Soochow University

type: Expression profiling by high throughput sequencing

summary: Acute myeloid leukemia (AML) represents a type of malignant hematological disease that is caused by the dysregulated developmental program of leukemia stem cells (LSCs). RBM5 was recently reported as a key regulator in maintaining the survival of human leukemia cells via non-canonical transcriptional activation of HOXA9. However, its function in LSCs and the broad genome-wide transcriptional targets remain elusive. Here, we report that RBM5 is required for murine leukemogenesis and maintains self-renewal of LSCs in vivo, but dispensable for normal hematopoiesis. RBM5 is highly expressed in LSCs, and its deficiency results in specifically defective LSC function with the inhibition of self-renewal gene expression and induction of myeloid differentiation program. Gene expression, chromatin accessibility, and direct genome-wide RBM5 binding further identify the direct transcriptional targets of RBM5 in primary leukemia cells including several stemness genes Hoxa9 and Myc. Forced expression of both HOXA9 and MYC rescued the RBM5 depletion effects on colony formation and self-renewal gene expression program. Thus, our study shows that RBM5 regulates the AML LSC program through transcriptional regulation and provides a rationale to therapeutically target RBM5 in myeloid leukemia.

overall_design: The functional assay clearly indicates that Rbm5 is required for the maintenance of mouse primary leukemia cells while dispensable for the normal hematopoietic stem and progenitor cells (HSPCs). We sought to explore the underlying molecular mechanism to better interrogate the role. We hypothesized that RBM5 might control the MLL-fusion self-renewal gene signature in LSCs. To identify the gene expression profile in this heterogenetic cell population, we performed high-resolution single-cell RNA-sequencing (scRNA-seq) in wild-type (WT) and Rbm5 knockout (KO) MLL-AF9 primary leukemia cells from the same endpoint after primary transplantation, together with corresponding normal c-Kit+ HSPCs


title: RBM5 is essential for the maintenance of leukemia stem cells by regulating a leukemic transcription program in cooperation with MYC [bulk RNA-seq]

overall_design: To obtain genome-wide insights into how RBM5 regulates the MLL self-renewal gene program, we further performed genome-wide transcriptome analysis by bulk RNA-sequencing in wild type (WT) and Rbm5 knockout (KO) MLL-AF9 primary leukemia cells derived from bone marrow samples


title: Nanostring-Based Gene Expression Profiling of Melanoma Lymph Node Metastases

city: Melbourne

first: Andrea

last: Di Pietro

state: VIC

address: 305 Grattan Street

department: Cancer Immunology program

country: Australia

institute: Peter MacCallum Cancer Centre

summary: This study investigates gene expression profiles in metastatic melanoma lymph node samples using the Nanostring nCounter platform. Samples were obtained from patients who were treatment-naïve, resistant, or responsive to immune checkpoint inhibitor (ICI) therapy. We applied both the PanCancer Immune Profiling Panel and a custom tissue-resident memory (TRM) T cell panel to assess immune cell composition and activation states. The dataset reveals transcriptional signatures associated with ICI response, including enrichment of TRM-associated genes and interferon-stimulated pathways in responders, and immunosuppressive features in resistant tumors. These data provide insights into the role of tumour-resident T cells and the tumour immune microenvironment in shaping response to immunotherapy.

overall_design:
Gene expression profiling was performed on formalin-fixed paraffin-embedded (FFPE) lymph node metastases from 32 patients with stage III/IV melanoma. Samples were stratified into three clinical groups based on ICI treatment status: treatment-naïve (n=13), ICI-resistant (n=5), and ICI-responsive (n=6). Total RNA was extracted from 10 μm sections and analysed using the NanoString nCounter platform. Two panels were used: the PanCancer Immune Profiling Panel (v1.1) and a custom tissue-resident memory (TRM) T cell panel. Data were normalised and quality-controlled using NanoString nSolver and further analysed to identify differentially expressed genes and pathway enrichment associated with treatment response.
***Raw data files are being made available in European Genome-phenome Archive (EGA - https://ega-archive.org) for controlled access due to privacy concerns***

first: Angela

last: Pizzolla

first: Sean

last: Macdonald

first: Thu

last: Ngoc Nguyen

first: Patrick

last: Crock

first: Niko

last: Thio


title: Stag2 dependent chromatin remodeling enforces the erythroid-specific Gata1 cistrome

city: New York

first: Varun

middle: Saichandan

last: Sudunagunta

state: NY

address: 650 W 168th, Black Building, 1110B

department: Division of Hematology/Oncology, Department of Medicine

country: USA

institute: Columbia University Vagelos College of Physicians and Surgeons

type: Genome binding/occupancy profiling by high throughput sequencing

summary: The transcription factor GATA1 has pleiotropic hematopoietic functions, particularly in erythroid and megakaryocytic ontogeny. While mechanistic investigations have uncovered many facets of GATA1 biology, how GATA1 co-regulates divergent cell fates remains incompletely characterized. We previously described that loss of Stag2, a member of the cohesin complex and a recurrent mutational target in myelodysplastic syndrome (MDS) and myeloid leukemia of Down Syndrome, results in altered chromatin accessibility, transcription factor function, and cell differentiation. Hence, we hypothesized that chromatin accessibility determines GATA1 cistrome specificity and lineage fate decisions. To understand the connection between chromatin accessibility and GATA1, we comprehensively studied erythropoiesis in Stag2∆ mice. Defects in Stag2-deficient hematopoiesis included reduced numbers of erythroid progenitors (EryPs), impaired terminal erythroid differentiation, increased number of MkPs, and increased megakaryocytes. RNA- and ATAC-sequencing of EryPs revealed altered patterns of Gata1 target gene expression with altered accessibility in conjunction with loss of expression of erythroid targets and gain of megakaryocyte targets. Despite unchanged Gata1 expression, Gata1 occupancy was reprogrammed from erythroid to megakaryocyte targets with Fli1 motifs enriched at Stag2∆ Gata1 binding sites. Functionally, we observed that Stag2-deficient EryPs have diminished erythroid output and augmented megakaryocyte output in orthogonal differentiation assays, which was partially reversed with Fli1 knockdown. Human models and primary MDS patients recapitulated the essential phenotypic and molecular features of our in vivo murine MDS model. Collectively, this study establishes chromatin accessibility as a determinant of transcription factor binding specificity, revealing an accessibility-driven Gata1 retargeting mechanism underlying MDS dyserythropoiesis.

overall_design:
CUT&RUN: CUT&RUN was performed on EryPs from Stag2 WT and KO (∆) mice 6-8 weeks after pIpC administration to determine the consequences of Stag2 loss on Gata1 chromatin occupancy.
HSPC 10X Multiome: Single nuclei were extracted from lineage negative HSPCs from Stag2 WT and KO (∆) mice at 6-8 weeks after the last dose of pIpC. Multi-ome libraries were prepared using the 10x Genomics platform.
Ter119+ 10X Multiome: Single nuclei were extracted from Ter119+ erythroblasts from Stag2 WT and KO mice at 6-8 weeks after the last dose of pIpC. Multi-ome libraries were prepared using the 10x Genomics platform.
HiC: HiC was performed on EryPs from Stag2 WT and KO mice 6-8 weeks after pIpC administration to determine the consequences of Stag2 loss on 3D chromatin architecture.
CUT&RUN: CUT&RUN was performed on EryPs from Stag2 WT and KO mice 6-8 weeks after pIpC administration to ascertain the genomic occupancy of Stag2.

middle: S

first: Edna

middle: M

last: Stewart

first: Yi

last: Chen

first: Aaron

middle: D

last: Viny


title: Characterization of cholangiocarcinoma cell line-derived xenograft (CDX) tumors

city: Strasbourg

address: 3 Rue Koeberlé

country: France

institute: Université de Strasbourg, Inserm, Institut de Recherche sur Les Maladies Virales et Hépatiques UMR_S1110

overall_design: To investigate the characteristics of tumors with high or low response to the CLDN1 mAb, fresh tumor tissues from mice bearing established HuCC-A1, EGI-1 or HuCC-T1-xenograft tumors were harvested and analyzed using RNA-Seq .

middle: F


title: Systematic investigation reveals extensive Epstein-Barr virus transcriptional regulation of the human genome [ChIP-seq]

city: Cincinnati

first: Matthew

last: Weirauch

state: Ohio

address: 3333 Burnet Avenue

department: Center for Autoimmune Genomics and Etiology (CAGE)

institute: Cincinnati Children's Hospital Medical Center

summary: We systematically investigate interactions between Epstein-Barr virus (EBV) transcriptional regulators (vTRs) and the human genome. Starting with 16 known and candidate vTRs, we identify nine whose introduction into human cells results in substantial alterations to host gene expression. Genome-scale determination of vTR genomic binding events and alterations to chromatin accessibility reveals a detailed map of EBV's functional interactions with the human genome, including >100,000 vTR binding events impacting almost a quarter of all human genes. BMRF1 emerges as a potent regulator, impacting >7,000 genes and altering >37,000 chromatin regions. Our results provide new evidence that EBV RTA interacts with and stabilizes the binding of human RBPJ. Network analysis reveals that many human genes are targeted by multiple EBV vTRs, highlighting the vast coordinated impact of EBV on human gene expression. This study provides a valuable, extensive resource for examining EBV-induced alterations to human gene regulation, with data available on multiple platforms.

overall_design: We performed anti-GFP ChIP-seq on Flp-In-293 cell lines that had been transfected with one of nine Epstein-Barr virus transcriptional regulators or a control. For 3 cell lines, we also performed anti-RBPJ ChIP. Experiments were performed in triplicate.

first: Leah

last: Kottyan


title: Rooting trait differences in Poplar and genome-wide identification and analysis of the WUSCHEL-related homeobox (WOX) gene family

status: Public on Jun 09 2026

city: Kunming

first: Xiaolin

last: Zhang

address: qingyun street

institute: southwest forestry university

summary: Plant propagation requires adventitious root production, and the inability to root cuttings prevents some tree species from being widely used and propagated on a big scale. Studies on the differences in adventitious root production ability between species that are easily rooted and those that are difficult to root are few, despite the fact that many studies have been done to examine the developmental mechanisms of adventitious roots. To attempt to address this problem, we examined the transcriptomes of Populus davidiana (difficult-to-root) and Populus yunnanensis (easy-to-root) spikes at various intervals following cutting. We discovered that the number of differential genes was significantly greater in the 96- and 120-hour groups than in the 0- and 48-hour groups. The majority of growth hormone and cytokinin-related genes were up-regulated in P. yunnanensis, while they were down-regulated in P. davidiana.

sample_organism:
Populus yunnanensis
Populus davidiana

platform_organism:
Populus yunnanensis
Populus davidiana

overall_design: Annual branches of P. yunnanensis and P. davidiana in good growth condition were selected, and all the buds and leaves were removed, and 15-cm-long cuttings were intercepted.

first: ChengZhong

last: He

first: Dan

last: Zong

first: Tingting

last: Yang


title: Systematic investigation reveals extensive Epstein-Barr virus transcriptional regulation of the human genome [RNA-Seq]

overall_design: We performed RNA-seq on Flp-In-293 cell lines that had been either transiently or stably transfected with one of 16 potential Epstein-Barr virus transcriptional regulators or a control. Experiments were performed in triplicate.


title: Tumor-resident T cells and dendritic cells form an in situ archetype for immunotherapy response in melanoma [scTCR-seq]

summary: Tumor-resident (TR) T cells participate in immunosurveillance of melanoma, but their role in determining response to immune checkpoint inhibitors (ICI) has not been comprehensively explored. We performed spatial and single-cell profiling on 32 metastatic melanoma lymph node samples, from treatment-naïve, ICI-resistant, or ICI-responsive patients. In responders, we found enrichment for early differentiation (TCF1+) CD8+ and CD4+ TR which co-localized with melanoma cells. CD8+ TR were hyperexpanded, and both CD8+ and CD4+ TR upregulated cytotoxicity-related gene expression, suggesting functional anti-tumor immunity. Conversely, ICI-resistant tumors displayed chronic IFN-γ responses within the tumor microenvironment to potentiate T cell exhaustion. In ICI-responsive melanoma tumors, CD8⁺ TR interact with CD4⁺ TR cells (via the CCL4-CCR5 axis) and engage with type-3 dendritic cells (DC3) (via IL15-IL15R interaction). This intratumoral immune triad (CD8⁺ TR – CD4⁺ TR – DC) is exclusive to responders. This study illustrates the role of TR cells and their crosstalk with DCs in effective ICI responses.

overall_design:
In our study, we analyzed tumor samples from patients with stage III/IV melanoma who were either untreated, resistant or responsive to ICI treatment. We performed detailed TCR clonotype studies by using single-cell TCR-Seq. For this experiment we used n=4 samples from untreated patients,  n=4 samples from ICI-resistant patients, and n=4 samples from ICI-responder patients.

***************************************************************
Raw files for human/patient samples are being made available in European Genome-phenome Archive (EGA - https://ega-archive.org) for controlled access to the personally identifiable sequence data.
***************************************************************

first: Sara

last: Alei

first: David

last: Yoannidis

first: Timothy

last: Semple


title: Tumor-resident T cells and dendritic cells form an in situ archetype for immunotherapy response in melanoma [bulk RNA-seq]

first: Andrea

last: Di Pietro

overall_design:
In our study, we analyzed tumor samples from patients with stage III/IV melanoma who were either untreated, resistant or responsive to ICI treatment. We performed whole tissue transcriptomics and gene enrichment analyses by using bulk-RNA sequencing. For this experiment we used n = 14 samples from untreated patients,  n = 10 samples from ICI-resistant patients, and n = 5 samples from ICI-responder patients.

***************************************************************
Raw files for human/patient samples are being made available in European Genome-phenome Archive (EGA - https://ega-archive.org)  for controlled access to the personally identifiable sequence data.
***************************************************************

first: Angela

last: Pizzolla

first: Sean

last: Macdonald

first: Stuart

last: Bencraig


title: Tumor-resident T cells and dendritic cells form an in situ archetype for immunotherapy response in melanoma [scRNA-seq]

overall_design:
In our study, we analyzed tumor samples from patients with stage III/IV melanoma who were either untreated, resistant or responsive to ICI treatment. We performed detailed transcriptomics studies by using single-cell RNA-Seq. For this experiment we used n=4 samples from untreated patients,  n=4 samples from ICI-resistant patients, and n=4 samples from ICI-responder patients.

***************************************************************
Raw files for human/patient samples are being made available in European Genome-phenome Archive (EGA - https://ega-archive.org)  for controlled access to the personally identifiable sequence data.
***************************************************************

first: Patrick

last: Crock

first: Niko

last: Thio


title: P5CS regulates translation by functioning as non-canonical RBP [LACE-seq]

city: Nanjing

first: Shan

last: Gao

address: No. 2 Sipailou, Xuanwu District

institute: Southeast University

summary: P5CS is the rate-limiting enzyme in the proline biosynthetic pathway, while whether P5CS mediates function beyond enzyme activity remains completely unknown. Here, we reveal that P5CS functions as a non-canonical RNA-binding protein and inhibits the growth and metastasis of cancer cells by suppressing translation initiation in an enzyme activity-independent manner.  To explore the underlying mechanism of P5CS in translation regulation, Ribo-seq, RIP-seq and LACE-seq were performed to investigate the downstream targets of P5CS.

overall_design: RNA binding-sites analysis of LACE-seq data for Anti-P5CS and Anti-IgG in NCI-H1299 cells.

first: Qingqing

first: Shuwen

last: Cheng


title: XPO1 R749Q Mutation Drives Endometrial Cancer Progression by Activating HIF-1/2α–AXL–PI3K/MAPK Signaling

city: 上海

first: zeheng

last: Lv

address: 2699 Pudong New Area High Tech West Road

institute: Tongji university

summary: The tumor driver gene XPO1 (exportin-1) exhibits high-frequency mutations in endometrial cancer (approximately 6%), with two hotspot mutation sites identified as E571K and R749Q. However, the molecular mechanisms by which XPO1 mutations influence the initiation and progression of endometrial cancer remain unclear. Here, we we discovered an unexpected role of XPO1 R749Q in regulating AXL expression in EC.This study reveals that the XPO1 R749Q mutation drives malignant transformation in endometrial cancer, including enhanced proliferation, migration, and invasion, by activating the PI3K-Akt and MAPK signaling pathways through the HIF1α/HIF2α-AXL axis. Importantly, the oncogenic effects mediated by the XPO1 R749Q mutation can be effectively suppressed by the AXL inhibitor cabozantinib and the XPO1 inhibitor KPT-330. These findings elucidate the molecular mechanism by which the XPO1 R749Q mutation contributes to endometrial carcinogenesis and provide a compelling therapeutic rationale for targeting the XPO1 R749Q-mutant subtype of endometrial cancer with cabozantinib and KPT-330

overall_design: To study the biological function of XPO1 R749Q in EC, we generated  XPO1 R749Q  knockin cell lines using CRISPR/Cas9 methods. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells. Comparative gene expression profiling analysis of RNA-seq data for ishikawa cells and its XPO1 R749Q  knockin derivatives.


title: Single cell multiomics unravel the transcription networks controlling the different EMT tumor states [multiome]

city: Brussels

first: Gabriel

middle: Sölvi

last: Windels

address: 808, route de Lennik

department: Faculty of Medicine

country: Belgium

institute: Université Libre de Bruxelles (ULB)

summary: Epithelial-to-mesenchymal transition (EMT) is a process by which cells lose their epithelial characteristics and acquire mesenchymal traits. In cancer, EMT is associated with tumor initiation, progression, invasion, metastasis and resistance to therapy. Recent studies demonstrated that EMT is not a binary switch, but presents intermediate states associated with different tumor functions. The gene regulatory networks (GRNs) controlling the different EMT states remain elusive. Here, using multi-OMIC approaches combining single cell RNA-seq and single cell ATAC-seq, we define the transcriptomic and chromatin landscape associated with the distinct EMT states in mouse skin squamous cell carcinoma (SCC) exhibiting EMT. Using CRISPR/Cas9-mediated loss of function studies combined with functional characterization in vitro and in vivo, we unravel the cellular and molecular mechanisms regulated by Pitx1, Klf5, Nfatc1 and Creb3l1, transcription factors (TFs) controlling specific EMT states. Altogether, our results identify the transcriptional and chromatin landscape of the distinct EMT tumor states and uncover novel key TFs controlling these states and their transition, providing potential novel targets for anti-cancer therapy.

overall_design: To induce tumorigenesis on Lgr5CreER/ KrasLSL-G12D/p53fl/fl/Rosa26-YFP+/+ (LKPR), Tamoxifen was diluted at 25 mg/ml in sunflower seed oil, 10% EtOH (Sigma). Four daily intraperitoneal (IP) injections of 2.5 mg tamoxifen were administered at P28 to LKPR mice. After 7-9 week after Tamoxifen injection tumour appearance and size were detected by daily observation and palpation. Mice were euthanized when tumour size was reached or when mice presented signs of distress. Skin tumours from LKPR mice were dissected, rinsed and digested in collagenase type I (Sigma) at 3,5mg/ml in HBSS (Gibco) for 1h at 37°C on a rocking plate protected from the light. Collagenase was blocked by the addition of EDTA (5mM) and then the cells were rinsed 1 time in PBS supplemented with 10% FBS and the cell suspension were filtered through a 70-μm cell trainer (BD Bioscience). For the wash next and antibody incubation, cells were resuspended in PBS supplemented with 2% FBS (FACS buffer).  Cells were incubated with BV711- conjugated anti-EPCAM (rat, clone G8.8, BD Bioscience Cat#563134, dilution 1:100), PE-conjugated anti-CD45 (rat, clone 30-F11, BD, Cat#553081, dilution 1:100) and PE-conjugated anti-CD31 (rat, clone MEC 13.3, BD, Cat#553373, dilution 1:100) antibodies for 30 min at 4 °C protected from light. For cell sorting, cells were also filtered through a 40-μm cell trainer (BD Bioscience). Living single tumour cells were selected by forward and side scatter, doublet discrimination and Hoestch exclusion. Profile of the tumors was analyzed following viability and profile of YFP, Lin- (CD45/CD31) and EPCAM expression. Once screened, YFP+ LIN- tumor cells were sorted for 10X Multiome experiment using FACSAria and FACSDiva software (BD Bioscience). After FACS isolation, 200.000 cells were collected in PBS, 0,04% filtered BSA using low binding 1.5 ml tubes (Eppendorf). For nuclei isolation, buffers were prepared following manufacturer’s instructions (adapted from protocol CG000365 Rev C, 10x Genomics). Sorted cells were centrifuged at 300g, 5 min at 4ºC and supernatant was carefully removed. Chilled lysis buffer (100 μl) was added, pipette mixed 10 times and incubated on ice for 3 minutes and 30 seconds. Wash buffer (800 μl) was added to the lysed cells and pipette mixed 5 times. Lysed cells were centrifuged at 500g, 5 min at 4ºC, followed by a second washing step. Nuclei were resuspended in nuclei buffer, counted and loaded on Chromium Next GEM Single Cell Multiome, ATAC + Gene Expression microfluidic chips (10x Genomics) was employed for Multiome. The libraries were prepared using the Chromium Single Cell 3′ Library Kit (V2-chemistry, 10x Genomics), quantified using a low coverage Illumina NextSeq 550 run and sequenced on an Illumina NovaSeq.

first: Andrea Pérez

last: González

first: Gabriel Solvi

first: Kevin

last: Bévant

first: Justine

last: Lengrand

first: Sophie

last: Lemaire

first: Virginie

last: Moers

first: Samuel

last: Scozzaro

first: Ulysse

last: Debroux

first: Christine

last: Dubois

first: Sebastiaan

last: Vanuytven

first: Cédric

last: Blanpain


title: Oxytocin is required for normal milk fat production

city: Boston

first: NORC

last: Boston

state: MA

address: 3 Blackfan Circle, CLS0733

institute: Beth Israel Deaconess Medical Center

summary: We used single-nucleus RNA-seq to examine the heterogeneity of lactating mammary glands (MGs) and the transcriptional profiles of mammary epithelial cells (MECs) in control and adipocyte-specific oxytocin receptor knockout (OxtrΔAd) mice. Our analysis identified all expected MG cell types, including MECs, myoepithelial cells, adipocytes, adipose progenitors, hormone-sensing progenitors, vascular, and immune cells. Notably, OxtrΔAd MGs exhibited a profound metabolic shift in MECs, characterized by reduced mTOR signaling, increased autophagy, and decreased lipid synthesis. These findings underscore the essential role of OXT-driven adipose lipolysis in supporting lactation.

overall_design: On postnatal day 1 (P1), litter sizes were standardized to 4-5 pups per cage. Inguinal white adipose tissue (iWAT) was harvested from lactating Oxtrflox and OxtrΔAd dams on postnatal day 11 (P11).

first: Li

last: Erwei

first: Rosen

last: Evan


title: Single cell multiomics unravel the transcription networks controlling the different EMT tumor states [bulk RNA-seq]

overall_design: To analyze the EPCAM profile and perform cell sorting for bulk RNA sequencing on the generated CRISPR/Cas9 cell lines, cells were washed in PBS and detached from the cell culture plate with trypsin. Cells were resuspended and washed with PBS supplemented with 2% FBS and incubated with anti-EPCAM (rat, clone G8.8, Biolegend 118218, dilution 1:200) 30 min at 4ºC protected from the light. After antibody staining, cell suspensions were washed with PBS supplemented with 2% FBS and centrifuged. Cells were then resuspended in 7-AAD (BD, 559925, dilution 1:40) and filtered through a 40-μm cell strainer (BD Bioscience). Living single mCherry+ YFP+ EPCAM+ or mCherry+ YFP+ EPCAM- tumor cells were selected by forward and side scatter, doublet discrimination and Hoechst exclusion. RNA was extracted from FACS-isolated cells or culture cell lines using RNeasy micro kit (QIAGEN) according to the manufacturer’s recommendations. RNA quality was evaluated by Bioanalyzer 2100 (Agilent) before sequencing. Indexed cDNA libraries were obtained using Ovation Solo RNA-seq Systems (NuGen) according to the manufacturer’s recommendations. The multiplexed libraries (11 pM or 18 pM) were loaded onto flow cells and sequences were produced using a HiSeq PE Cluster Kit v4 and TruSeq SBS Kit v3-HS (250 cycles) on a Novaseq 6000 (Illumina). Approximately 20 million paired end reads per sample were generated and quality checks were performed with FastQC.


title: Ferroportin inhibition in colon macrophages shapes the microbiome and promotes mucosal healing

city: Newark

first: Alexander

last: Lemenze

state: New Jersey

address: 185 South Orange Ave

institute: Rutgers

summary: Inflammatory bowel diseases (IBD) are complex inflammatory disorders marked by microbial dysbiosis and dysregulated iron homeostasis. Iron homeostasis is controlled by endogenous hepcidin, which inhibits iron export through ferroportin (Fpn) to promote mucosal healing via nutritional immunity against tissue-infiltrating bacteria. However, the relevant site of Fpn activity is unknown, and the clinical potential of this pathway in IBD remains unexplored. Using unbiased profiling approaches, we demonstrate that functional Fpn is specifically expressed by discrete intestinal macrophage subsets in both mice and humans. While systemic Fpn inhibition and intestinal inflammation both cause iron deficiency, we identified that colon-specific hepcidin delivery can target Fpn on colon macrophages without disrupting iron homeostasis. Further, colon macrophage Fpn inhibition significantly accelerated recovery in a pre-clinical model of intestinal inflammation and modulated microbiome composition. Altogether, these findings outline a model where bacteria critically depend on macrophage-derived iron and impair mucosal healing in IBD. Our identification of a tissue-specific therapeutic window for Fpn inhibition reveals a novel therapeutic strategy to promote mucosal healing in IBD.

overall_design: Colon lamina cells from healthy mice were selected for Live/CD45+/Ly6G-/Fpn+ macrophages (including CD11b+/F480+, CD11b-/F480+, and F480-/CD64+/CD11b+) by FACS sorting. Cells from 12 mice were pooled. These isolated cells were then subjected to scRNAseq.

first: Bhupendra

last: Singh Rawat

first: Nicholas

last: Bessman


title: ATR inhibition affects RNA Polymerase II transcription during S-phase

city: Birmingham

first: Marco

last: Saponaro

address: Vincent Drive

department: Institute of Cancer and Genomic Sciences

country: United Kingdom

institute: University of Birmingham

summary: Transcription and replication are the key processes in cell growth and division that utilize DNA as their template. Concurrently, conflicts between the two processes increase genome instability levels. Evidence in the literature indicate that transcription and replication can however coexist, suggesting the requirement for cellular mechanisms to avoid reciprocal interference. To identify factors important in this regulatory process, we performed a screening of known DNA damage response proteins. Among the factors assessed, we found that specifically inhibition of ATR affected cells’ ability to replicate long transcribed genes, impacting also on cells’ ability to transcribe these genes. However, ATR activity was also required later during S-phase the control transcription activity on all genes. Dissecting which of ATR’s roles is important for this process, we uncovered that SMARCAL1 is likewise required to regulate genes transcription later during S-phase. Altogether, we have uncovered how DNA damage response factors are required to support the replication of transcribed regions, but also how their role extends to regulate also genes transcription levels during S-phase.

first: Jianming

last: Wang


title: Effect of depletion of galanin on gene expression in myeloid-derived suppressor cells

city: Cleveland

first: Lizhi

last: Pang

state: OH

address: 9500 Euclid Avenue

department: Department of Cancer Biology

institute: Cleveland Clinic

summary: To investigate the mechanism of glioblastoma (GBM) cells-derived galanin (GAL) in the regulation of myeloid-derived suppressor cells (MDSCs) biology, we treated mouse bone marrow-derived MDSCs with GBM cell-derived conditioned medium (CM) and GAL recombinant protein. We then performed gene expression profiling analysis using data obtained from RNA-seq.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for MDSC treated with or without cancer cell-derived CM, as well as MDSC treated with or without GAL protein.

first: Pang

last: Lizhi

first: Peiwen

last: Chen


title: Combining multiple omics with molecular dynamics reveals SCP2-mediated intestinal toxicity of Aflatoxin B1

city: Fuzhou

first: Peichun

last: Ye

address: No.1 Xuefu North Road, Fuzhou, Fujian, China

institute: Fujian Medical University

summary: This study aims to explore the mechanism of AFB1-induced toxicity damage in SW480 cells through the epigenetics, proteomics, and metabolomics, and experimental verification.

overall_design: AFB1 exposure induces ROS accumulation, mitochondrial dysfunction, and influence of lipid metabolism in SW480 cells.

first: Mengting

first: Jiaxin

last: Wen

first: Yiyan

last: Qiu

first: An

last: Zhu


title: Wnt and Nodal asymmetries stratify mouse laterality phenotypes in the absence of node flow

city: Paris

first: Sigolène

last: Meilhac

address: 24 boulevard du Montparnasse

institute: Institut Imagine, Institut Pasteur

summary: Left-right symmetry breaking in mice is considered to occur via node leftward fluid flow. The molecular cascade within the node has been reconstructed at high resolution; however, its importance for organogenesis remains poorly understood. Here we show in mutants for the motile cilium component CCDC40 that 70% of mice develop normal situs at birth despite abrogation of node flow. The discrete morphospace output, including situs inversus totalis and heterotaxy with left isomerism, supports an innovative model of symmetry-breaking, in which node flow only biases asymmetry orientation, while a distinct mechanism, potentially self-amplifying, generates it. Longitudinal, quantitative and paired transcriptomic analyses uncover the molecular signature of laterality clusters, highlighting WNT in addition to NODAL pathways. We identify asymmetry of cardiopulmonary progenitors, the disruption of which is associated with combined heart and lung defects in mutants. Functional pharmacological perturbation reinforces the importance of WNT, besides the node, in the establishment of asymmetry.

overall_design: Bulk RNA sequencing of left-right paired microdissected heart fields at stage E8.5i in Ccdc40 mutant embryos (Ccdc40lnks/lnks) and wild-type littermates (Ccdc40+/+)

first: Amaia

last: Ochandorena-Saa

first: Emeline

last: Perthame

first: Cécile

last: Rouillon

first: Nicolas

last: Cagnard

first: Christine

last: Bole-Feysot


overall_design: ATR inhibition affects RNA Polymerase II transcription during S-phase

first: Patricia

last: Rojas


title: Treatment of cholangiocarcinoma using humanized monoclonal antibodies targeting Claudin-1(PDX tumors)

first: Frank

last: Jühling

overall_design: Fresh tumor tissues from mice bearing established primary human cholangiocarcinoma tumors (PDX mouse model-P2-441) treated with an anti-CLDN1 mAb or vehicle control were harvested and analyzed using scRNA-Seq

first: Marion

last: Muller

first: Emilie

last: Crouchet

first: Laurent

last: Mailly

first: Thomas

last: Baumert


title: Treatment of cholangiocarcinoma using humanized monoclonal antibodies targeting Claudin-1

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

overall_design: Refer to individual Series


title: Treatment of cholangiocarcinoma using humanized monoclonal antibodies targeting Claudin-1 (CCA patient tissues)

summary: Cholangiocarcinoma (CCA) is an adenocarcinoma of the hepatobiliary system showing an alarming rise in incidence and mortality with unsatisfactory treatment options. Claudin-1 (CLDN1) is a transmembrane protein expressed in tight junctions and exposed on the cell surface in liver fibrosis and cancer. Using single cell RNA-sequencing (scRNA-Seq) and spatial transcriptomics of CCA patient tissues, we show that CLDN1 expression is highly upregulated in cancer cells and is associated with stemness and cell fate. Gain-of-function studies in CCA orthotopic in vivo mouse models showed decreased survival and enhanced tumor growth, unraveling a functional role of CLDN1 as an oncogenic driver. Targeting exposed CLDN1 using highly specific CLDN1 monoclonal antibodies (mAbs) robustly inhibited tumor growth across CCA CDX and PDX mouse models and patient-derived CCA organoids including tumors with medium or low CLDN1 expression. Moreover, antibody treatment markedly inhibited tumor cell migration, invasion, and extrahepatic metastasis. Mechanistically, targeting exposed CLDN1 on CCA tumors inhibited Notch1, FAK/SRC, and Hippo-YAP signaling, resulting in decreased cancer cell stemness, EMT and extracellular matrix remodeling. In conclusion, these results uncover CLDN1 as a previously undiscovered CCA driver and therapeutic target, paving the way for the clinical development of CLDN1 mAbs to improve the dismal outcome of patients with advanced CCA.

overall_design: Four patient-derived FFPE embedded intrahepatic CCA samples (20H07891, 20H18503, 22H01065 and 23H04104) were selected for spatial transcriptomic analysis using CosMx Spatial Molecular Imager (NanoString) based on histopathology, clinical data and Claudin-1 IHC staining

first: Marie

middle: A

last: Oudot

first: Mihaela

last: Onea


title: Treatment of cholangiocarcinoma using humanized monoclonal antibodies targeting Claudin-1(HuCC-A1 CDX tumors)

overall_design: To investigate the mechanism of action of the CLDN1 mAb, fresh tumor tissues from mice bearing established HuCC-A1-xenograft tumors treated with an anti-CLDN1 mAb or vehicle control were harvested and analyzed using RNA-Seq .


title: Treatment of cholangiocarcinoma using humanized monoclonal antibodies targeting Claudin-1(CCA organoids)

overall_design: To investigate the mechanism of action of the CLDN1 mAb, patient-derived organoids (HCM-CSHL-0433-C24 PDM217) treated with an anti-CLDN1 mAb or isotype control antibody control were harvested and analyzed using RNA-Seq .

first: Zeina

last: Nehme


title: FIR targets the genes in HeLa cell.

city: Chiba

first: Masaki

last: Fukuyo

address: 1-8-1 Inohana, Chuo-ku

department: Department of Molecular Oncology

country: Japan

institute: Chiba University

summary: To identify the  FIR target genes in HeLa cell line, this cell line was subjected to RNA-seq analysis.

overall_design: 1) HeLa were transfected with 25uM siRNAs (siGL2, siFIR, siFIRΔexon2),  4ug FLAG vectors (FLAG vector, FIR-FLAG, FIRΔexon2), (Lipofectamine 2000)

first: Kouichi

last: Kitamura

first: Tyuji

last: Hoshino

first: Atsushi

last: Okabe

first: Bahityar

last: Rahmutulla

first: Nobuko

last: Tanaka

first: Sohei

last: Kobayashi

first: Tomoaki

first: Takashi

last: Shida

first: Mashiro

last: Ueda

first: Toshinari

last: Minamoto

first: Hisahiro

last: Matsubara

last: Kaneda

first: Kazuyuki

last: Matsushita


title: single-cell analysis of PA14-treated control and roX2 depleted ISCs (PA14 treated)

city: Shanghai

first: Yonghao

last: Li

address: Siping Road No.1239

department: School of Life Sciences and Technology

institute: Tongji University

summary: To investigate if roX2 is involved in pathogen induced gene silencing, we perfomed the single-cell analysis.  We show that depletion of roX2 resulted in 2780 genes up-regulated, supporting a repressive role of roX2 in transcription.

overall_design: Single ISC population from PA14 treated control ISCs and that with roX2 depletion were used for the single-cell analysis.

first: K

middle: L


title: Single-cell analysis of Drosophila intestinal stem cells (ISCs) during ageing

summary: We investigated the transcriptional profile of midgut ISCs from differentially aged animals at the single-cell resolution. We found that the ISCs in old animals showing a decrease transcription than young animals.

overall_design: Drosophila single ISCs from differentially aged animals were isolated using FACS, and used to generate library and further 10X sequencing

first: Hui-Min

last: Wei

first: Kai-Le


title: Targeting mitochondrial ROS-CK2-SET-PP2A pathway with ceria nanoparticles to reverse Tau pathology in APOEε4-associated Alzheimer’s disease [RNA-seq]

status: Public on Jun 07 2026

city: seoul

first: Dakyung

last: Lee

address: 101 Daehakro

country: South Korea

institute: University

summary: In this study, we used triphenylphosphonium-conjugated ceria nanoparticles (Ceria-TPP) to target mitochondrial ROS in APOEε4 iPSC-derived neurons, and analyzed transcriptional changes using bulk RNA sequencing.

overall_design: We performed bulk RNA-seq on day 19 human iPSC-derived neurons (2D) from two genotypes, APOEε3 and APOEε4. At day 19, human iPSC-derived neurons (2D) received vehicle (APOEε3 and APOEε4) or Ceria-TPP (95 µM for 24 h; APOEε4 only). Transcriptomes were compared across APOEε3-Vehicle, APOEε4-Vehicle, and APOEε4-Ceria-TPP to assess APOE genotype effects and the impact of mitochondrial ROS-targeted treatment. All samples were treated with Aβ at 4 µM.

first: Jong Won

last: Han

first: Yubeen

last: Kim

first: June-Hyun

last: Jeong

first: Yunjung

first: Suk-Kyung

last: Shin

first: Seok Beom

last: Hong

first: Keuntae

first: Sieun

last: Choi

first: Rian

last: Kang

first: Jong-Chan

last: Park

first: Kangmin

last: Suh

first: Jinyoung

last: Chu

first: Nohyun

first: Sang Ihn

first: Dong-Sup

first: Il-Joo

last: Cho

first: Seok

last: Chung

first: Jong-Il

first: Taeghwan

last: Hyeon

first: Inhee

last: Mook-Jung


title: Single-cell transcriptomic atlas of adult dermatomyositis, cutaneous lupus erythematosus and healthy skin

first: Ksenia

last: Anufrieva

address: 60 Fenwood Rd

institute: Brigham and Women's Hospital

summary: Adult-onset dermatomyositis (DM) is a systemic autoimmune disease associated with an elevated risk of malignancy, yet the cellular and molecular features distinguishing cancer-associated DM from non-cancer DM remain poorly defined. Here, we conduct a comprehensive single-cell RNA sequencing analysis of adult-onset DM skin, including lesional and non-lesional samples, alongside cutaneous lupus erythematosus (CLE) and healthy control skin, to characterize immune and stromal cell states and disease-specific transcriptional programs. We identify distinct immune-stromal cell populations that differentiate cancer-associated DM from non-cancer-associated DM and CLE, including a vascular injury phenotype with hypoxia and metabolic reprogramming enriched in cancer-associated DM. These findings nominate cell-state-defining molecular features as potential biomarkers for cancer screening and therapeutic targeting in adult dermatomyositis.

overall_design: Skin biopsies from adult patients with DM and CLE, as well as healthy controls, were profiled using single-cell RNA sequencing across 44 unique biopsies — lesional DM (n=22, stratified by cancer association), lesional CLE (n=9), non-lesional (n=8), and healthy controls (n=5). For each sample, cells were dissociated from formalin-fixed paraffin-embedded (FFPE) skin sections and processed using the 10x Genomics Chromium Fixed RNA Profiling (Flex) platform with multiplexing of 16 samples per library using unique Probe Barcodes.

first: Kevin


title: Whole-genome bisulfite sequencing reveals dynamic DNA methylation changes in Vigna radiata under direct and pre-conditioned salt stress

city: Jinan

first: Zhi-Wei

last: Wang

address: No. 23788, Industrial North Road, Licheng District

institute: Shandong Academy of Agricultural Sciences

type: Methylation profiling by high throughput sequencing

summary: DNA methylation is an important epigenetic mechanism regulating gene expression and stress memory in plants. To investigate the role of DNA methylation in salt stress adaptation, we performed whole-genome bisulfite sequencing (WGBS) of mung bean (Vigna radiata cv. Weilv 9) leaves under two treatment regimes: T1 (pre-conditioned with 100 mM NaCl for 24 h, recovered for 48 h, then re-exposed to 100 mM NaCl) and T2 (direct exposure to 100 mM NaCl without preconditioning). Seedlings were grown hydroponically in half-strength Murashige and Skoog medium under controlled environmental conditions. Genomic DNA was extracted from the first fully expanded true leaves at 0, 6, and 48 h after the onset of the final salt treatment, with three biological replicates per condition. Bisulfite-converted DNA was sequenced to generate genome-wide methylation profiles. Comparative analysis revealed dynamic changes in CG, CHG, and CHH contexts, providing insights into the epigenetic basis of salt tolerance and stress priming in legumes.

overall_design: Whole-genome bisulfite sequencing (WGBS) of Vigna radiata cv. Weilv 9 leaves under two salt treatments: T1 (pre-conditioning + recovery + second NaCl exposure) and T2 (direct NaCl exposure). Samples were collected at 0 h, 6 h, and 48 h after the onset of the final salt treatment. Three biological replicates were included for each treatment and time point. Genomic DNA was subjected to bisulfite conversion and paired-end sequencing.


title: Transcriptome analysis of Vigna radiata leaves in response to direct and pre-conditioned salt stress [RNA-Seq]

summary: We investigated the adaptive responses of mung bean cultivar 'Weilv 9' to salt stress using RNA-seq. Two treatments were applied: T1 (pre-conditioned with 100 mM NaCl for 24 h, recovered for 48 h, then re-exposed to 100 mM NaCl) and T2 (direct exposure to 100 mM NaCl without preconditioning). Samples were collected at 0, 1, 3, 6, 12, 24, and 48 h after the onset of the final salt treatment from the first fully expanded true leaves (n=3 per time point per treatment). Plants were grown under controlled conditions (25°C, 12,000 lux, 16h/8h light/dark, 70% RH) in 1/2 MS nutrient solution. The 0 h time point in T2 represents naive control, while in T1 it reflects residual effects after recovery. Data aim to reveal transcriptional reprogramming under salt stress and preconditioning.

overall_design: RNA-seq of Vigna radiata cv. Weilv 9 leaves under two salt treatments (T1: pre-conditioned + recovery + second NaCl; T2: direct NaCl), sampled at 0, 1, 3, 6, 12, 24, 48 h after final NaCl exposure, with three biological replicates per time point per treatment.


title: ATAC-seq profiling of chromatin accessibility in Vigna radiata leaves under direct and pre‑conditioned salt stress

summary: Salinity is a major environmental constraint limiting crop productivity. Chromatin accessibility plays a crucial role in transcriptional regulation under stress conditions. In this study, we investigated genome-wide chromatin accessibility dynamics in mung bean (Vigna radiata cv. Weilv 9) leaves under salt stress using ATAC-seq. Two treatment groups were established: T1 (pre-conditioned with 100 mM NaCl for 24 h, recovered for 48 h, then re-exposed to 100 mM NaCl) and T2 (direct exposure to 100 mM NaCl without preconditioning). Seedlings were grown hydroponically in half-strength Murashige and Skoog medium under controlled environmental conditions. Nuclei were isolated from the first fully expanded true leaves at 0, 6, and 48 h after the onset of the final salt treatment, with three biological replicates per condition. Comparative ATAC-seq analysis revealed dynamic changes in chromatin accessibility associated with transcriptional reprogramming and stress memory. This dataset provides valuable insights into the epigenetic basis of salt tolerance and acclimation in legumes.

overall_design: ATAC-seq of Vigna radiata cv. Weilv 9 leaves under two salt treatments: T1 (pre-conditioning + recovery + second NaCl exposure) and T2 (direct NaCl exposure). Samples were collected at 0 h, 6 h, and 48 h after the onset of the final salt treatment. Three biological replicates were included for each treatment and time point. Nuclei were isolated and subjected to transposase-mediated fragmentation and sequencing.


title: Targeting mitochondrial ROS-CK2-SET-PP2A pathway with ceria nanoparticles to reverse Tau pathology in APOEε4-associated Alzheimer’s disease [scRNA-seq]

first: Dakyung

last: Lee

summary: In this study, we used triphenylphosphonium-conjugated ceria nanoparticles (Ceria-TPP) to target mitochondrial ROS in APOEε4 human iPSC-derived brain organoid, and profiled transcriptional changes via single-cell RNA-seq.

overall_design: We performed single-cell RNA-seq on day 60 human iPSC-derived brain organoids (3D) from two genotypes, APOEε3 and APOEε4. At day 60, brain organoids received vehicle (APOEε3 and APOEε4) or Ceria-TPP (150 µM for 24 h; APOEε4 only). Transcriptomes were compared across APOEε3-Vehicle, APOEε4-Vehicle, and APOEε4-Ceria-TPP to assess APOE genotype effects and the impact of mitochondrial ROS-targeted treatment.

first: Jong Won

first: Yubeen

first: June-Hyun

first: Yunjung

first: Suk-Kyung

first: Seok Beom

first: Keuntae


title: CUT&Tag of H3K18 lactylation in mouse embryonic stem cells treated with vitamin B6 for 7 days

city: Guizhou

first: Dengwang

last: Chen

address: No. 6, Xuefu West Road, Xinpu Subdistrict, Xinpu New District

institute: Department of Histology and Embryology, Zunyi Medical University

summary: Vitamin B6 (pyridoxine) is widely used as a first-line treatment for nausea and vomiting during pregnancy, yet its safety profile during embryonic development, particularly at supraphysiological doses, remains incompletely understood.

overall_design: To investigate the genome wide distribution of H3K18 lactylation (H3K18la) upon vitamin B6 induced metabolic reprogramming, we performed CUT&Tag on mESCs differentiated as embryoid bodies for 7 days in the presence or absence of 20 µM pyridoxine. The data show that vitamin B6 treatment enhances H3K18la enrichment at transcription start sites, particularly at genes involved in endoderm differentiation (e.g., Alkbh5).

first: Xinyue

last: Jiang

first: Jun

last: Tan


title: Single nucleus multiome (RNAseq and ATACseq) of male and female mouse pituitary

city: New York

first: Elena

last: Zaslavsky

address: 1 Gustave L. Levy Pl

institute: Icahn School of Medicine at Mount Sinai


title: Vitamin B6 Promotes Endoderm Differentiation of Mouse Embryonic Stem Cells via Glycolysis-H3K18 Lactylation Axis

overall_design: Here, we demonstrate that vitamin B6 treatment (20 μM) induces metabolic reprogramming in mouse embryonic stem cells (mESCs) by shifting energy metabolism from oxidative phosphorylation to glycolysis, as evidenced by decreased mitochondrial membrane potential, enhanced glucose consumption, elevated lactate production, and increased intracellular ATP levels, along with coordinated upregulation of key glycolytic enzymes (Hk2, Ldha, Pdk1, Pkm2) and downregulation of oxidative phosphorylation-related genes. Importantly, increased glycolysis and subsequent lactate accumulation promote histone lactylation, particularly at the H3K18 site. Transcriptomic profiling combined with CUT&Tag analysis revealed that vitamin B6 markedly enriches H3K18 lactylation at the promoter region of Alkbh5, a known N6-methyladenosine demethylase involved in endoderm differentiation. Inhibition of glycolysis by 2-deoxy-D-glucose suppresses vitamin B6-induced H3K18 lactylation, attenuates endoderm marker gene (Gata4, Gata6) upregulation, and restores ectoderm marker gene (Sox1, Sox3) expression, suggesting that the metabolic-epigenetic axis is essential for vitamin B6-mediated lineage specification. Collectively, our findings reveal that vitamin B6 promotes endoderm differentiation while suppressing ectoderm differentiation through a glycolysis-dependent H3K18 lactylation mechanism, providing new insights into the metabolic-epigenetic regulation of early embryogenesis and raising important considerations regarding the safety of high-dose vitamin B6 exposure during pregnancy.


title: Brain Transcriptomics Across Diverse Sleep-Wake Manipulations Reveals Multiple Homeostatic Pathways in Drosophila

city: Ann Arbor

first: Ravi

last: Allada

state: Michigan

address: 2800 Plymouth Rd

department: Michigan neuroscience Institute

institute: university of michigan

summary: Sleep is governed by two processes: a circadian process that times sleep and wake and a homeostatic process that drives sleep as a function of prior wake history. Discovered in the fruit fly Drosophila, the period (per) gene is a “universal” cornerstone of the circadian clock, robustly oscillating at the transcript level, in all organs and tissues and in essentially all animals.  We hypothesized that there may be a comparable factor (we term “sleeper”) for sleep homeostasis. To identify sleeper, we performed a wide-ranging transcriptomic analysis to identify genes whose expression tracks sleep-wake history in the Drosophila brain.  We use a variety of methods to manipulate sleep-wake and subsequent rebound including mechanical, thermogenetic, optogenetic, pharmacological and circadian/baseline across 7 datasets. Using a log2 fold change threshold of 1, we did not identify any gene that was sleep-wake dependent across all datasets, raising the possibility that genes identified with a single method of sleep manipulation are related to the nature of the manipulation and not to sleep. Nonetheless, we identified genes whose expression changed with sleep-wake in a consistent direction across at least 2 datasets. We did observe significant pairwise overlap in regulated genes across many of the datasets. Gene ontology analysis of genes associated with sleep and wake as well as with sleep rebound. These analyses highlight previous processes implicated in sleep homeostasis as well as provide potentially novel pathways. In addition, we also examine genes whose expression correlates with prior sleep-wake history and/or predicted subsequent sleep rebound across these datasets. Among significantly correlated genes we observed some that were correlated with recent (<3h) sleep history while others were correlated with much longer (>6h) time frames suggesting temporally distinct genetic pathways for integrating waking experience. This analysis also highlights specific GO pathways for sleep/wake/rebound. Applying a novel GPT based paper search algorithm, we call fl.ai, we identified several genes with implicated or demonstrated function in sleep regulation consistent with potential homeostatic function. Collectively, these studies inform the future design of studies on the nature of sleep homeostasis as well as provide unique molecular clues across diverse sleep-wake conditions.

overall_design: RNA-seq profiling was performed on whole-brain Drosophila samples subjected to mechanical sleep deprivation and thermogenetic TrpA1 activation, along with their respective controls. Mechanical sleep deprivation was conducted for durations of 3 h, 6 h, and 12 h, with three biological replicates for each time point. Thermogenetic TrpA1 activation was carried out at two temperatures (21 °C and 29 °C) using four wake-promoting lines (R21H11, R65H02, HC, and R60F09) and one sleep-promoting line (R85C10). Each of the five sleep/wake-promoting lines included its own control at 29 °C. Additionally, circadian profiling was performed for control datasets collected at six different circadian time points, each with three biological replicates.

first: Shiju

last: Sisobhan

first: Clark

last: Rosensweig

first: Aadish

last: Shah

first: Tomas

last: Andreani


title: Transcriptomic Profiling of Blood-Stage Plasmodium falciparum in Children with Severe Malarial Anemia

city: Albuquerque

first: Douglas

middle: Jay

last: Perkins

state: NM

address: MSC10 5550, 1 University of New Mexico

department: Center for Global Health

institute: University of New Mexico

summary: Malaria is a major global health threat, with millions of cases and hundreds of thousands of deaths reported annually, primarily in sub-Saharan Africa. Children under five years of age residing in holoendemic Plasmodium falciparum transmission regions are the most vulnerable to malaria, accounting for vast majority of cases and mortality. The major clinical manifestation of severe malaria in these children is severe malarial anemia [SMA, hemoglobin (Hb)<6.0 g/dL]. The molecular mechanisms underlying SMA pathogenesis, particularly the contribution to this disease process of P. falciparum gene activities at transcriptomic levels, remain largely unexplored. As such, the overall objective of the study was to profile the blood-stage Plasmodium falciparum transcriptome in children with SMA. To achieve this goal, we performed RNAseq on total RNA from peripheral blood samples of 60 pediatric malaria patients (3-36 months) with non-SMA (Hb≥6.0 g/dL, n=40) and SMA (n=20) at enrollment. The RNA reads were mapped to the P. falciparum reference genome (PfKE01). Diffentially expressed genes (DEGs) in SMA relative to non-SMA and relevant biological pathways in P. falciparum were identified. In addition, the performance of the expressed parasite genes in predicting SMA was assesed. These findings promote the identification of potential parasite-derived biomarkers and therapeutic targets for improving SMA management.

overall_design:
To compare transcriptomic profiling of blood-stage P. falciparum between children aged 0-59 months with SMA and nonSMA, children with P. falciparum infections (any density parasitemia) were stratified into two groups based on Hb concentrations: Hb≥6.0 g/dL (nonSMA, n=40), and Hb<6.0 g/dL (SMA, n=20).None of the children had any experimentally detected co-infectons (i.e., HIV-1 and bacteremia).
Total RNA isolated from peripheral blood of 60 malaria patients (40 non-SMA and 20 SMA) with RIN>8 were used for library construction and paied-end RNA sequencing. The sequence were then aligned to the reference genome of Plasmodium falciparum Kenya isolate pfKE01.

middle: J

first: Qiuying

last: Cheng

first: Ivy

last: Hurwitz

first: Christophe

middle: G

last: Lambert

first: Philip

last: Seidenberg

first: Kristan

last: Schneider

first: Benjamin

middle: H

last: McMahon

first: Collins

last: Ouma

first: Evans

last: Raballah

first: Samuel

middle: B

last: Anyona

first: Clinton

middle: O

last: Onyango

first: Anne

last: Ong'ondo

first: Nicholas

last: Ondiek

first: Everlyne

last: Modi

first: Joan

last: Ochieng

first: Vincent

middle: I

last: Omanje

first: Rodney

last: Mongare

first: Sharley

last: Wasena

first: Shamim

middle: W

last: Osata


title: Targeted Elimination of FAP⁺ Fibroblasts by BiTE-Engineered Extracellular Vesicles Prevents Epidural Fibrosis

city: Wuhan

first: Zheng

last: Zhang

address: Jiefang Road 1095

institute: Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology

summary: Epidural fibrosis (EF) is a frequent and debilitating complication that impairs recovery following spinal surgery, yet effective targeted therapies are lacking. Here we observe enrichment of FAP⁺ fibroblasts at surgical sites in patients after laminectomy. To therapeutically target this subset, we develop bispecific antibody–decorated extracellular vesicles (BsAb EVs), which redirect endogenous T cells to eliminate FAP⁺ fibroblasts in situ. In a preclinical model, BsAb EVs selectively eliminate pathogenic fibroblasts, reduce fibrotic collagen accumulation, and prevent the development of postoperative epidural fibrosis without detectable systemic toxicity under the tested conditions. Single-cell RNA sequencing reveals that FAP⁺ fibroblasts represent a transcriptionally distinct subset from α-SMA⁺ myofibroblasts, characterized by enhanced extracellular matrix remodeling and TGF-β production. Together, these findings highlight a critical stromal subset in EF pathogenesis and position BsAb EVs as a promising immunotherapeutic strategy for targeting pathogenic stromal cells in fibrotic and tissue-remodeling disorders.

overall_design: Bulk RNA sequencing was performed on paraspinal soft tissue tissues from 3 groups: No operation, SHAM, Laminectomy (4 biological replicates per group). For downstream differential expression and pathway analyses, three high-quality replicates per group were selected based on RNA integrity and sequencing metrics.

first: Wei

last: Xiong

first: Liang

last: Huang

first: Shanwei

last: Ye

first: Qian

last: Xu


title: Bispecific Antibody Engineered Extracellular Vesicles Redirect T Cells to Prevent Postoperative Epidural Fibrosis [scRNA-seq]

overall_design: To investigate how BsAb EVs therapy alters the cellular landscape at the postoperative site, we performed single-cell RNA sequencing (scRNA-seq) on epidural scar tissues collected one week after laminectomy from mice treated with BsAb EVs or wild-type (WT) EVs. This dataset is related to the bulk RNA-seq dataset GSE310366


title: Gene expression analysis of early Barrett's adenocarcinoma, Barrett's esophagus, normal gastric mucosa, and esophageal mucosa

city: Bunkyo-ku

first: Dai

last: Kubota

institute: The University of Tokyo

summary: The objective of this study was to identify genes and pathways early Barrett's adenocarcinoma through comprehensive gene expression analysis.

overall_design: RNA data from 13 early BACs, 11 BEs, 13 normal esophageal mucosae, and 10 normal gastric mucosae were included, as all 13 BAC cases before endoscopic submucosal ressection yielded good-quality RNA.

first: Yu

last: Takahashi


title: Relationship between environmental pollutant TBOEP and renal metabolism

city: Changzhou

first: Shuai

last: Chen

address: 68 Gehu Rd, Wujin District

institute: The Affiliated Changzhou NO.2 People’s Hospital of Nanjing Medical University

summary: Tris(2-butoxyethyl) phosphate (TBOEP) is a common organophosphorus compound widely used in industrial production as a plasticizer and flame retardant. In recent years, studies have shown that TBOEP may pose potential threats to human health, particularly its association with kidney metabolic function has attracted widespread attention. The kidneys, as the most important metabolic organ in the human body, play a crucial role in detoxification, synthesis, and decomposition of various biomolecules. After entering the human body, TBOEP is mainly metabolized and detoxified by the kidneys. However, TBOEP and its metabolites may interfere with the normal function of the kidneys, leading to metabolic disorders. Studies have shown that TBOEP exposure may affect the activity of enzymes in the kidneys, such as cytochrome P450 enzyme systems, which are involved in the metabolism of various endogenous and exogenous substances. In addition, TBOEP may also affect kidney metabolism by influencing gene expression. For example, TBOEP exposure may activate or inhibit genes related to lipid metabolism, glucose metabolism, and oxidative stress, thereby altering the metabolic state of the kidneys. These changes not only affect the function of the kidneys themselves but may also have a chain reaction on the health of other organs and systems through the interaction of the systemic metabolic network. Furthermore, TBOEP exposure may lead to kidney damage and dysfunction, which can further exacerbate metabolic disorders. For example, kidney damage can impair the excretion of metabolic waste products, leading to their accumulation in the body and further disrupting metabolic balance. In summary, as an environmental pollutant, the potential impact of TBOEP on kidney metabolic function cannot be ignored. Future research needs to further explore the toxicological mechanisms of TBOEP and its long-term effects on human health in order to develop effective prevention and intervention measures to protect public health.

overall_design: Once the HK2 cells reached confluency, they were stimulated with 20 μM TBOEP for 48 hours


title: Identification of the SARS-CoV-2 genome packaging signal in the nsp12-coding region

city: Daejeon

first: Jongmin

last: Lim

address: 291 Daehak-ro, Yuseong-gu,

department: Department of Bio and Brain Engineering

institute: KAIST

summary: Selective genome packaging is a critical step for RNA viruses, which must distinguish genomic RNA from other abundant transcripts. For SARS-CoV-2, the cis-acting packaging signal is thought to be recognized by the nucleocapsid (N) protein, but its identity and mechanistic basis for selective recognition remain undefined. Here we identify the packaging signal within the nsp12 polymerase-coding region. CLIP-seq maps N-bound sites and, together with virus-like particle assays, pinpoints a conserved segment with strong packaging activity. An orthogonal defective-interfering RNA approach confirms its role in genome selection. We further delineate two critical subregions, α and β, that engage the N C-terminal domain. Synonymous mutations in either subregion selectively disrupt packaging and reduce viral fitness. Notably, the α subregion encompasses the ribosomal frameshifting element, revealing its dual role in viral translation and assembly. These findings establish the mechanistic basis for SARS-CoV-2 genome packaging and offer a potential antiviral target.

overall_design: formaldehyde crosslinking and immunoprecipitation RNA-sequencing  (fCLIP) for N protein in SARS-CoV-2 infected Vero cells.

first: Youngran

last: Park

first: V

last: Narry Kim

first: Young-suk

last: Lee


title: Effects of an autophagy-related protein degrader on murine 4T1 breast cancer model

status: Public on Jun 06 2026

city: Singapore

first: Cheng

address: 70 Nanyang Drive

country: Singapore

institute: Nanyang Technological University

summary: We developed an targeted protein degrader that could degrade VPS34, a key factor for autophagy initiation, to inhibit autophagy pathway in tumor. We did bulk RNA-seq to investigate how such protein degrader modulated the gene expression regarding autophagy pathway and immune response.

overall_design: Following the injection of protein degraders for three times, tumors were collected from mice and homogenized, lysed, and processed for RNA bulk-seq.


title: Single cell multiomics unravel the transcription networks controlling the different EMT tumor states

city: Brussels

first: Cedric

last: Blanpain

address: Route de Lennik 808

institute: ULB

summary: Epithelial-to-mesenchymal transition (EMT) is a process by which cells lose their epithelial characteristics and acquire mesenchymal traits. In cancer, EMT is associated with tumor initiation, progression, invasion, metastasis and resistance to therapy. Recent studies demonstrated that EMT is not a binary switch, but presents intermediate states associated with different tumor functions. The gene regulatory networks (GRNs) controlling the different EMT states remain elusive. Here, using multi-OMIC approaches combining single cell RNA-seq and single cell ATAC-seq, we define the transcriptomic and chromatin landscape associated with the distinct EMT states in mouse skin squamous cell carcinoma (SCC) exhibiting EMT. Using CRISPR/Cas9-mediated loss of function studies combined with functional characterization in vitro and in vivo, we unravel the cellular and molecular mechanisms regulated by Pitx1, Klf5, Nfatc1 and Creb3l1, transcription factors (TFs) controlling specific EMT states. Altogether, our results identify the transcriptional and chromatin landscape of the distinct EMT tumor states and uncover novel key TFs controlling these states and their transition, providing potential novel targets for anti-cancer therapy.

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: To induce tumorigenesis on Lgr5CreER/ KrasLSL-G12D/p53fl/fl/Rosa26-YFP+/+ (LKPR), Tamoxifen was diluted at 25 mg/ml in sunflower seed oil, 10% EtOH (Sigma). Four daily intraperitoneal (IP) injections of 2.5 mg tamoxifen were administered at P28 to LKPR mice. After 7-9 week after Tamoxifen injection tumour appearance and size were detected by daily observation and palpation. Mice were euthanized when tumour size was reached or when mice presented signs of distress. Skin tumours from LKPR mice were dissected, rinsed and digested in collagenase type I (Sigma) at 3,5mg/ml in HBSS (Gibco) for 1h at 37°C on a rocking plate protected from the light. Collagenase was blocked by the addition of EDTA (5mM) and then the cells were rinsed 1 time in PBS supplemented with 10% FBS and the cell suspension were filtered through a 70-μm cell trainer (BD Bioscience). For the wash next and antibody incubation, cells were resuspended in PBS supplemented with 2% FBS (FACS buffer).  Cells were incubated with BV711- conjugated anti-EPCAM (rat, clone G8.8, BD Bioscience Cat#563134, dilution 1:100), PE-conjugated anti-CD45 (rat, clone 30-F11, BD, Cat#553081, dilution 1:100) and PE-conjugated anti-CD31 (rat, clone MEC 13.3, BD, Cat#553373, dilution 1:100) antibodies for 30 min at 4 °C protected from light. For cell sorting, cells were also filtered through a 40-μm cell trainer (BD Bioscience). Living single tumour cells were selected by forward and side scatter, doublet discrimination and Hoestch exclusion. Profile of the tumors was analyzed following viability and profile of YFP, Lin- (CD45/CD31) and EPCAM expression. Once screened, YFP+ LIN- tumor cells were sorted for 10X Multiome experiment using FACSAria and FACSDiva software (BD Bioscience). After FACS isolation, 200.000 cells were collected in PBS, 0,04% filtered BSA using low binding 1.5 ml tubes (Eppendorf). For nuclei isolation, buffers were prepared following manufacturer’s instructions (adapted from protocol CG000365 Rev C, 10x Genomics). Sorted cells were centrifuged at 300g, 5 min at 4ºC and supernatant was carefully removed. Chilled lysis buffer (100 μl) was added, pipette mixed 10 times and incubated on ice for 3 minutes and 30 seconds. Wash buffer (800 μl) was added to the lysed cells and pipette mixed 5 times. Lysed cells were centrifuged at 500g, 5 min at 4ºC, followed by a second washing step. Nuclei were resuspended in nuclei buffer, counted and loaded on Chromium Next GEM Single Cell Multiome, ATAC + Gene Expression microfluidic chips (10x Genomics) was employed for Multiome. The libraries were prepared using the Chromium Single Cell 3′ Library Kit (V2-chemistry, 10x Genomics), quantified using a low coverage Illumina NextSeq 550 run and sequenced on an Illumina NovaSeq.

first: Andrea Pérez

last: González

first: Gabriel Solvi

last: Windels

first: Kevin

last: Bévant

first: Justine

last: Lengrand

first: Sophie

last: Lemaire

first: Virginie

last: Moers

first: Samuel

last: Scozzaro

first: Ulysse

last: Debroux

first: Christine

last: Dubois

first: Sebastiaan

last: Vanuytven

first: Cédric


title: RIOK3 potentially regulates osteogenesis related pathways in ankylosing spondylitis and the differentiation of bone marrow mesenchymal stem cells

city: Hefei

first: shengqian

last: Xu

address: No. 218, Ji-xi Road

institute: the First Affiliated Hospital of Anhui Medical University

summary: Background: RNA-binding proteins (RBPs) are key effectors of gene expression andplay critical rolesininflammation, immune regulation,andmany rheumatic diseases. This study screened the differentially expressed RBPs between ankylosing spondylitis (AS) patients and the healthy control group through transcriptome sequencing and explored the potential biological function and mechanism of target RBP in AS patients. Methods: The differentially expressed genes (DEGs) in whole blood cells of 5 AS patients and 3 healthy people were obtained by RNA-seq, and the differentially expressed RBPs were obtained by overlapping the DEGs and the summarytable of RBPs. The selected target RBP (RIOK3) was verified by qRT-PCR in the peripheral blood mononuclear cells (PBMCs) of patients with AS and age_x001E_ and sex_x001E_ matched controls. Next, mouse bone marrow mesenchymal stem cells (mBMSCs) were transfected with siRNA targeting RIOK3 usingthelipofectaminetransfectiontechnique, and the molecular functions, biological processes, and signaling pathway enrichment analysis of DEGs regulated by RIOK3 were performed using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). The expression level of the selected genes in siRIOK3 mBMSCs was detected by qRT-PCR to further verify the regulatory role of RIOK3. Then, the RIOK3 stable knockdown transfected cell lines were constructed by lentivirus infection, and calcium deposits were observed byAlizarinredstaining after21daysof osteogenicinduction, and the expression of osteogenic genes ALP, OCN, and OPN were assessed by qRT-PCR. Results: RIOK3 was enriched in interferon-related pathway and innate immune-related pathway, which was an important immune regulatory factor and could effected the function of ribosomes. RIOK3knockdown will inhibited the expression of genes related to transcription and ribosomal function in mBMSCs, especially the transcription factors related to osteogenic differentiation, and will also effected the expression of β-interferon related pathway genes. RIOK3 knockdown effect was mainly co-expressed with HIF-1 signal pathway, MAPK signal pathway, and inflammatory response related pathway genes in the osteogenic differentiation of mBMSCs. The cellularexperimentalresults further confirmedthat RIOK3 knockdown will reduce the osteogenic differentiation ability of mBMSCs.  Conclusion: Collectively,RIOK3 may affect the differentiation of mBMSCs and participate in the occurrence and development of AS, especially pathological bone formation. Thisstudymay providenew perspectivefortheresearchofthe mechanism of AS and atheoreticalbasisforRIOK3asapotential target for AS therapy.

overall_design: To further explore the regulation of RIOK3 on mBMSC osteogenic differentiation, we established stable RIOK3-knockdown cell lines by transfecting cells with the lentivirus.We then performed gene expression profiling analysis on RNA seq data of RIOK3 knockout and blank control mBMSCs

first: Shengqian

first: Hexiang

last: Zong

first: Yuechen


title: Oxidative and glycolytic skeletal muscle-derived exosomes selectively coated miRNAs and participate in regulating myoblast proliferation and differentiation mediated by miR-4331-3p

city: chongqing

first: Jia

last: Luo

state: chongqing

address: tiansheng road

institute: Southwest University

type: Non-coding RNA profiling by high throughput sequencing

summary: The phenotypic characteristics and meat quality of skeletal muscle are collectively determined by the muscle cells, other cellular groups within it, and their intricate interactions with the extracellular microenvironment. Exosomes have the capacity to influence the development and microenvironment of skeletal muscle, thus playing a crucial role in its differentiation and maturation. In this study, we conducted an initial evaluation of the muscle fiber phenotypes in glycolytic skeletal muscle (Longissimus dorsi, HC-L) and oxidative skeletal muscle (Psoas major, HC-P) of Hechuan black pigs. The results revealed significant differences in terms of muscle fiber diameter, density, and type phenotypes (P<0.05). Subsequently, we isolated and identified exosomes derived from skeletal muscle (SKM-Exos). Co-culture experiments with myoblasts demonstrated that SKM-Exos can promote both myoblast proliferation and differentiation. Furthermore, sequencing analysis confirmed that miRNAs present in SKM-Exos are selectively coated miRNAs. It is noteworthy that the expression of miR-4331-3p was notably higher in SKM-Exos compared to its derived skeletal muscles. It was significantly elevated in the SKM-Exos of HC-L when compared to those of HC-P, and have interactions with the differentially expressed genes between HC-L and HC-P. Interestingly enough, miR-4331-3p has been shown to enhance myoblast proliferation while inhibiting the differentiation process. By investigating the interaction between SKM-Exos, their derived miRNAs, and myoblasts, this study elucidated the molecular mechanism underlying the regulation of muscle fiber differentiation by SKM-Exos and provided valuable insights into the intricate molecular processes involved in meat formation.

overall_design: Analyze the expression of oxidative and glycolytic muscle tissue mRNA and the expression of miRNA between these tissues and their derived exosomes.

first: Daiyu

last: Zhang

first: Zhenhao

last: Wen

first: Qiang

last: Pu

first: Taorun

first: Xiaoqian

last: Wu

first: Jie

last: Chai

first: Li

last: Chen

first: Changfeng

last: Yang

first: Yongfu

last: Huang


title: Knockouts of sulfur metabolism genes induce chronic inflammation and immune dysregulation in Drosophila melanogaster

city: Moscow

first: Alexander

middle: Pertovich

last: Rezvykh

state: Moscow

address: Vavilova, 32

department: Russian Academy of Sciences

country: Russia

institute: Engelhardt Molecular Biology Institute

summary: In this study, we examined a unique collection of Drosophila melanogaster strains with knockouts of three key genes involved in H₂S synthesis and metabolism, with the aim of elucidating the role of this adaptive system in immunity. Genetic disruptions in sulfur metabolism—specifically, combined deletions of the cbs, cse, and tst1 genes—lead to reduced H₂S levels and hyperhomocysteinemia in flies. These metabolic changes induce oxidative stress and trigger chronic inflammatory responses. Transcriptomic analysis and q-PCR revealed significant activation of major immune pathways, including IMD, Toll, and Jac-Stat. A septic injection of Bacillus subtilis induces increased expression of antimicrobial peptides (AMPs) and pattern recognition receptors in knockout flies. Notably, double- and triple-knockout strains exhibit prolonged immune activation. The triple knockout exhibits the worst survival rate following septic injury induced by Bacillus subtilis. These results highlight the critical role of H₂S in modulating innate immunity and suggest that sulfur metabolism is an important regulator of inflammatory homeostasis in Drosophila.

overall_design: mRNA sequencing of intact and Bacillus subtilis-inoculated adult females of Drosophila melanogaster

last: Zatsepina

last: Shilova

last: Evgen’ev

last: Garbuz


title: OsELP3/ELP4, rice Elongator factor complex subunits, epigenetically regulates rice blast resistance

first: Zhensheng

last: Qiao

address: School of Life Sciences, Hubei University, Wuhan, China

institute: Hubei University

summary: Rice blast, caused by Magnaporthe oryzae (M.oryzae), is one of the three most devastating rice diseases, significantly reducing both yield and grain quality. The Elongator complex, first characterized in Arabidopsis thaliana, regulates growth, development, and innate immunity by tightly associating with hyperphosphorylated RNA polymerase II. However, its immunological role in rice remains unexplored. Here, we demonstrate that Elongator plays an essential role in rice blast resistance. The OsELP3 subunit mutant exhibited susceptibility to M.oryzae, while its overexpression increased resistance. OsELP3 interacts with its homologous subunit OsELP4 in the nucleus, and that OsELP4 also positively regulates rice blast resistance. RNA-seq and histone acetylation analyses demonstrated that OsELP3/ELP4 enhances transcriptional activation of key rice blast resistance genes by modulating histone acetylation levels in both the jasmonic acid (JA) signaling pathway (OsAOS1, OsLOX6, OsPROPEP3) and lignin biosynthesis pathway (OsMYB30, OsMYB55, OsMYB110), thereby strengthening plant defense mechanisms against M. oryzae. These findings reveal that OsELP3/ELP4 regulates histone acetylation-mediated defense responses against M.oryzae, providing both theoretical foundations and genetic resources for developing blast-resistant rice cultivars.

overall_design: Three genotypes of rice (Oryza sativa cv. Nipponbare), including wild type (WT), OE-ELP3 and OE-ELP4 overexpression lines, were used in this study. Rice seedlings were subjected to mock treatment and Magnaporthe oryzae (rice blast fungus) inoculation. Leaf tissues were collected at 3d post inoculation. Each group contained three independent biological replicates. Transcriptome profiling was performed using RNA-seq to explore the molecular response to rice blast infection.

first: Yanfei

first: Zhenshneg

first: Yuquan

last: Fu

first: Zixiang

last: Li

first: Zhichao

last: Wang

first: Xuezhu

last: Du

first: Feng

last: Sheng


title: SETDB1 regulates gene expression in mouse brown adipose tissue and primary brown adipocytes

city: hangzhou city

first: qiang

last: chen

address: No. 1369, Wenyi West Road, Yuhang District

institute: Liangzhu Laboratory

summary: SETDB1 is a histone methyltransferase that catalyzes H3K9me3 and plays critical roles in transcriptional repression. To investigate its function in brown adipose tissue (BAT), we performed RNA-seq across three complementary models: (1) BAT tissue from BAT-specific Setdb1 knockout mice (Setdb1 AKO) vs control mice under thermoneutral conditions; (2) primary brown adipocytes from Setdb1 flox/flox; Rosa26Cre-ERT2 mice treated with 4-hydroxytamoxifen (4-OHT) vs vehicle (ETOH); and (3) primary brown adipocytes transfected with siRNA targeting Setdb1 (siSetdb1) vs non-targeting control siRNA (siNC).

overall_design:
Three independent RNA-seq experiments:
1. BAT tissue: Control (Setdb1 fl/fl; Adipoq-Cre-) vs Setdb1 AKO (Setdb1 fl/fl; Adipoq-Cre+) mice.
2. Primary brown adipocytes (4-OHT induction): Setdb1 flox/flox; Rosa26Cre-ERT2 cells treated with 4-OHT (1 μM) vs ETOH vehicle.
3. Primary brown adipocytes (siRNA knockdown): Cells transfected with siSetdb1 vs siNC.
All libraries were prepared using NEBNext Ultra II RNA Library Prep Kit and sequenced on Illumina NovaSeq 6000 (paired-end, 150 bp).


title: Transcriptomic profiling of C2C12 myotubes treated with D-galactose and red ginseng-derived interventions

first: Byeong-Don

last: Min

state: Daejeon

address: 99 Daehak-ro, Yuseong-gu

institute: Chungnam National University

summary: This study investigated transcriptomic alterations in differentiated C2C12 myotubes following treatment with D-galactose and red ginseng-derived interventions. Fully differentiated C2C12 myotubes were treated with Korean Red Ginseng water extract (RGW), saponin fraction (SFr), non-saponin fraction (NSFr), or ginsenoside Rb2 either alone or in combination with D-galactose. Bulk RNA sequencing was performed to characterize the transcriptional effects of each intervention under basal conditions and to evaluate their modulatory effects on D-galactose-induced cellular aging-associated transcriptomic changes.

overall_design: Differentiated C2C12 myotubes were assigned to control, D-galactose-treated, red ginseng-derived intervention-treated, and red ginseng-derived intervention plus D-galactose-treated groups. The intervention-treated groups included Korean Red Ginseng water extract (RGW, 100 μg/mL), saponin fraction (SFr, 100 μg/mL), non-saponin fraction (NSFr, 100 μg/mL), and ginsenoside Rb2 (20 μM). For combination treatment groups, cells were pretreated with each intervention for 12 h and subsequently exposed to D-galactose (20 mg/mL) for 24 h. Bulk RNA-seq was performed using biological replicates for each condition, and paired-end sequencing was conducted on the MGISeq platform.

first: Aeyung

last: Kim

first: Seokwon

first: No soo

first: Sang-Min

last: Park


title: RNA-sequencing results of the human thyroid papillary carcinoma cell TPC-1 with overexpression of the PTCSC3-AS1 gene

city: taiyuan

first: Yutong

last: Zhang

state: Shanxi

address: NO.56 Xinjian South Road

institute: Shanxi Medical University

summary: Here we report gene expression profiles of TPC-1 cells treated with PTCSC3-AS1 overexpressed vector (OE) or empty vector (EV). PTCSC3-AS1 gene was cloned from expressed sequence tag (AA632637). And the sequence of PTCSC3-AS1 is included in EST AA632637. A number of dysregulated genes of PTCSC3-AS1 were discovered. This study reveals the role of PTCSC3-AS1 in downstream gene regulation and its function in the tumorigenesis of thyroid cancer.

overall_design: Profiling of 5 pairs TPC-1 cells transfected with PTCSC3-AS1 overexpressed vector (OE) or empty vector (EV) were performed using RNA-seq. Total RNA was isolated using TRIzol reagent according to the manufacturer's protocol. RNA libraries were prepared for sequencing using standard Illumina protocols. Sequencing was performed in paired end reads using NovaSeq 6000 platform (Illumina).

first: Yanqiang


title: Bulk RNA sequencing of murine mesenchymal stromal cells (MSCs) under cardiac stress induced by transverse aortic constriction.

city: Chiba

first: Ichiro

last: Manabe

address: 1-8-1 Inohana, Chuo

institute: Chiba University

summary: We performed bulk RNA-seq to investigate how cardiac stress influences the transcriptional profiles of murine MSCs. MSCs were isolated from bone marrow of control (sham-operated) and mice subjected to transverse aortic constriction (TAC) for four weeks. Comparative analysis of transcriptomes was conducted to identify stress-induced alterations in MSC states.

overall_design: Eight-week-old male mice underwent TAC under anesthesia to induce cardiac stress. The aorta was constricted between the innominate and left common carotid arteries using a 7-0 nylon suture tied against a blunted 27-gauge needle. Sham-operated mice underwent identical procedures without constriction. Four weeks after surgery, bone marrow MSCs were isolated by fluorescence-activated cell sorting (FACS) and subjected to bulk RNA-seq.

first: Manabe

last: Ichiro

first: Nakayama

last: Yukiteru

first: Goto

last: Kohsaku


title: Single-cell RNA sequencing (scRNA-seq) of murine mesenchymal stromal cells (MSCs) under cardiac stress induced by transverse aortic constriction.

summary: We performed scRNA-seq using the 10x Genomics platform to investigate how cardiac stress influences the transcriptional profiles of female murine MSCs. MSCs were isolated from bone marrow of control (sham-operated) and mice subjected to transverse aortic constriction (TAC) for four weeks. Comparative analysis of single-cell transcriptomes was conducted to identify stress-induced alterations in MSC states.

overall_design: Eleven-week-old female mice underwent TAC under anesthesia to induce cardiac stress. The aorta was constricted between the innominate and left common carotid arteries using a 7-0 nylon suture tied against a blunted 27-gauge needle. Sham-operated mice underwent identical procedures without constriction. Four weeks after surgery, bone marrow MSCs were isolated by fluorescence-activated cell sorting (FACS) and subjected to scRNA-seq.


title: Common mycelial network modulates neighbour-primed plant defences against foliar pathogens by co-opting distinct inter-plant metabolic and biotic stress responses.

city: Riga

first: Ayman

last: Osman

address: Riga

country: Latvia

institute: University of Latvia

summary: Inter-plant communication is key for the successful thriving of plant communities in nature with yet untapped potential for agroecosystem engineering towards more resilient crops and plant defences against pathogens. Arbuscular mycorrhizal fungi (AMF) are ubiquitous root symbionts, well-known to constitute underground common mycelial networks (CMNs) linking multiple plant hosts underground. The wired connection among plants via CMNs are hypothesized to play a key role for information exchange between plants for the neighbour-primed inter-plant defences. However, the key transcriptomic and metabolome responses in receiver plant associated with inter-plant CMN connections remain yet to be elucidated. Moreover, no studies to date have clearly resolved the confounding effects of hyphal damage from the inter-plant network disconnection. To uncover the contribution of CMN integrity to neighbour-primed plant defences, we used model AMF Rhizophagus irregularis to inter-connect two Medicago truncatula plants and explored the effect of sender wounding and flg22 elicitation on receiver plants’ leaf responses and pathogen tolerance. For the first time, we demonstrate that changes in receiver plants’ biotic stress and defence signalling pathways rely on inter-plant signals via the CMN, not on mycelial network damage itself. This response was associated with distinct leaf isoprenoid production, including volatile monoterpenes and triterpene saponins. Furthermore, CMN-mediated signals from stressed senders enhanced receiver resistance to Fusarium sporotrichoides whilst simultaneously increasing susceptibility to Botrytis cinerea. Our findings highlight the critical role of CMNs in inter-plant signalling for pathogen-specific susceptibility and resistance which can be a key for understanding plant community-level defence in nature and agroecosystems.

overall_design: 4 treatments: H20_CONNECTED H2O_CUT WF_CONNECTED WF_CUT

first: Zigmunds

last: Orlovskis

first: Ilva

last: Nakurte

first: Ēriks

last: Voroņins

first: Annija

last: Kotova

first: Daniels

last: Pugačevskis

first: Dawood

last: Shah

last: Andersone

first: Kārlis

last: Blūms

first: Ivars

last: Silamiķelis

first: Soon-Jae

last: Lee


title: Single-cell RNA sequencing (scRNA-seq) of murine hematopoietic stem and progenitor cells (HSPCs) and mesenchymal stromal cells (MSCs) under cardiac stress induced by transverse aortic constriction.

summary: We performed scRNA-seq using the 10x Genomics platform to investigate how cardiac stress influences the transcriptional profiles of murine HSPCs and MSCs. HSPCs and MSCs were isolated from bone marrow of control (sham-operated) and mice subjected to transverse aortic constriction (TAC) for four weeks. Comparative analysis of single-cell transcriptomes was conducted to identify stress-induced alterations in hematopoietic differentiation and MSC states. Integrated analysis of HSPCs and MSCs enabled the characterization of cell–cell communication networks and niche remodeling associated with cardiac stress.

overall_design: Eight-week-old male mice underwent TAC under anesthesia to induce cardiac stress. The aorta was constricted between the innominate and left common carotid arteries using a 7-0 nylon suture tied against a blunted 26-gauge needle. Sham-operated mice underwent identical procedures without constriction. Four weeks after surgery, bone marrow HSPCs and MSCs were correspondingly isolated by fluorescence-activated cell sorting (FACS) and subjected to scRNA-seq.


title: Nynrin Sustains Leukemia Stem Cell Viability via TXNIP Destabilization to Maintain Redox Homeostasis and Confer Venetoclax Resistance [KG-1a RNA-Seq]

city: Chongqing

first: Jianming

last: Wang

state: Chongqing

address: 1 Yixueyuan Road, Yuzhong District

institute: Chongqing medical university

summary: Acute myeloid leukemia (AML) is driven by chemotherapy-resistant leukemia stem cells (LSCs), which rely on precise regulation of reactive oxygen species (ROS) for survival. We identify NYNRIN as a novel post-transcriptional regulator of LSC redox homeostasis. NYNRIN is selectively overexpressed in ROS-low LSCs and correlates with poor clinical outcomes in AML patients. Genetic targeting of Nynrin in murine models impairs LSC self-renewal, reduces leukemic burden, and prolongs survival, while sparing normal hematopoietic stem and progenitor cells. Mechanistically, NYNRIN binds to TXNIP mRNA, promoting its degradation and maintaining redox balance. Loss of NYNRIN leads to TXNIP stabilization, oxidative stress, mitochondrial dysfunction, and LSC apoptosis, which can be rescued by TXNIP knockdown or ROS scavenging. Notably, Nynrin ablation synergizes with venetoclax to overcome resistance, enhancing LSC cytotoxicity in vitro and in vivo. These findings highlight the NYNRIN-TXNIP-ROS axis as crucial for LSC maintenance and suggest NYNRIN inhibition as a potential therapeutic strategy for relapsed AML.

overall_design: KG-1a cells transfected with Control (shCTL) and NYNRIN-knockdown (shNYNRIN) shRNA were sorted, followd by RNA-seq


title: Nynrin Sustains Leukemia Stem Cell Viability via TXNIP Destabilization to Maintain Redox Homeostasis and Confer Venetoclax Resistance

overall_design: LSCs (GFP+c-Kit+Gr-1-) from HOXA9/MEIS1-driven Nynrin+/+ (Wild-type) and Nynrin-/- (Nynrin-KO) AML mice were sorted, followd by RNA-seq


title: DDIT4 overexpression reshapes the histone modification landscape in human coronary artery smooth muscle cells: an H3K9ac and H3K27ac CUT&Tag study

city: Guangzhou

first: Fengfeng

last: Li

address: 253 Gongye Dadao Zhong, Haizhu District

department: Department of Cardiovascular Medicine

institute: ZhuJiang Hospital, Southern Medical University

summary: This study investigates the epigenetic mechanisms by which DDIT4 promotes vascular smooth muscle cell (VSMC) dedifferentiation. We performed CUT&Tag sequencing for the active histone marks H3K9ac and H3K27ac in HCASMCs following DDIT4 overexpression. Our findings reveal that DDIT4, by inhibiting the pyruvate dehydrogenase complex, reduces acetyl-CoA levels and globally decreases histone acetylation. Specifically, we observe loss of H3K9ac and H3K27ac at the promoters of key contractile genes, providing an epigenetic explanation for the DDIT4-mediated suppression of the contractile phenotype and acceleration of atherosclerosis.

overall_design: Primary human coronary artery smooth muscle cells (HCASMCs) were transduced with an adenovirus overexpressing DDIT4 or an empty vector control. After 48 hours, cells were harvested for CUT&Tag sequencing targeting two active histone marks: H3K9ac and H3K27ac. The experiment included 3 biological replicates per condition (DDIT4-OE and control) for each histone mark.

first: Bixuan

last: Yue

first: Luoxing

last: Xia

first: Yunxiang

last: Long

first: Chenjie

last: Zhao

first: Miaoyun

last: Qiu

first: Zhi

last: Zeng


title: Transcriptome analysis of human coronary artery smooth muscle cells under pro-differentiation and pro-dedifferentiation treatments

summary: This study explores the transcriptomic landscape of human coronary artery smooth muscle cells (HCASMCs) in response to stimuli that promote differentiation (Repsox) or dedifferentiation (PDGF-BB, IL-1b). Our RNA sequencing analysis identifies DNA damage-inducible transcript 4 (DDIT4) as a key regulator of vascular smooth muscle cell (VSMC) phenotypic switching, showing its significant upregulation in synthetic phenotypes and downregulation in contractile phenotypes. This dataset provides a resource for understanding the transcriptional programs governing VSMC plasticity in the context of vascular remodeling and atherosclerotic disease.

overall_design: Primary human coronary artery smooth muscle cells (HCASMCs) were treated in vitro with one of three conditions: 1) 20 ng/mL PDGF-BB for 48 hours to induce a synthetic phenotype, 2) 10 ng/mL IL-1b for 48 hours to induce inflammatory dedifferentiation, or 3) 25 μM Repsox for 48 hours to promote a contractile phenotype. Control cells were incubated with vehicle (0.5% BSA) for 48 hours. Each condition included three biological replicates. RNA was extracted and subjected to strand-specific RNA sequencing.


title: In vivo safety assessment of METTL3 inhibitors STM2457 in neuroblastoma therapy

city: Fuzhou

first: Tian

last: Lin

address: No. 20, Chazhong Road

institute: The First Affiliated Hospital of Fujian Medical University

summary: Neuroblastoma (NB) is one of the most common malignant tumors in children, characterized by high heterogeneity and poor prognosis, posing notable therapeutic challenges. The present study investigated the therapeutic potential and safety profile of two N6-adenosine-methyltransferase 70 kDa subunit (METTL3) inhibitors, UZH1a and STM2457, in NB. A toxicity test of zebrafish showed that the maximum tolerated concentration of UZH1a and STM2457 was 20 μg/ml, and there were some toxic reactions including delayed yolk sac absorption but without notable mortality. Furthermore, through a series of in vitro and in vivo experiments, both UZH1a and STM2457 markedly inhibited SK-N-SH cells viability, migration and invasion, while potently promoting apoptosis, and effectively inhibiting the growth and migration of zebrafish xenograft tumors. Mechanistically, molecular analysis revealed that UZH1a and STM2457 downregulated the gene expression levels of pro-tumorigenic factors (basic helix-loop-helix family member e41, SREBF chaperone, IL-6, and IL-1β) and upregulated the expression of antitumor cytokine (TNF-α). Transcriptomic sequencing results further indicated that the neuroactive ligand-receptor interaction is a key pathway through which STM2457 affected NB development. In conclusion, UZH1a and STM2457 exhibited potent anti-NB activity both in vitro and in vivo by inhibiting viability, migration, invasion, and promoting apoptosis. These findings provide a notable theoretical basis for potential use of METTL3 inhibitors as therapeutic agents against NB.

overall_design: RNA-seg profiling of SK-N-SH cells and SK-N-SH cells treatment with STM2457 after 24 h.

first: Xinghe

last: Chen

first: He

last: Huang

first: Jianxing

last: Zhang

first: Yali

last: Xu

first: Junshan


title: Gain- and loss-of-function RNA-seq analysis reveals DDIT4-driven transcriptional programs in human coronary artery smooth muscle cells

summary: This dataset profiles the transcriptomic changes resulting from DDIT4 manipulation in human coronary artery smooth muscle cells (HCASMCs). We performed RNA sequencing on HCASMCs following adenovirus-mediated DDIT4 overexpression or shRNA-mediated DDIT4 knockdown. Our analysis reveals that DDIT4 is both necessary and sufficient to drive a transcriptional program characteristic of VSMC dedifferentiation, establishing its critical role in phenotypic switching. These findings provide mechanistic insight into how this stress-responsive gene promotes proliferative arterial disease.

overall_design: Primary human coronary artery smooth muscle cells (HCASMCs) were transduced with adenoviruses for either DDIT4 overexpression, DDIT4 knockdown, or their respective controls (empty vector and non-targeting shRNA). Cells were harvested for RNA extraction after 48 hours. Each condition included two biological replicates. Strand-specific RNA sequencing was performed on the resulting libraries.