title: DNA hypomethylation enables the transcriptional repressor SlSPL-CNR to control fruit flavor ester biosynthesis

city: Shenzhen

first: Yu

last: Ma

address: 1088 Xueyuan Bivd, Nanshan District

institute: Southern University of Science and Technology

summary: DNA hypomethylation is traditionally associated with gene activation. Here we show that DNA hypomethylation permits the binding of a transcriptional repressor SlSPL-CNR, leading to gene silencing in tomato. SlSPL-CNR exhibits methylation-sensitive DNA binding and preferentially occupies unmethylated GTACGG motifs. During fruit ripening, SlDML2-mediated DNA demethylation at the SlAAT1 promoter allows SlSPL-CNR binding, which represses SlAAT1 expression and modulates the biosynthesis of fruit flavor esters. Structural analysis reveals that cytosine methylation introduces a steric clash with Gln94 in the SBP domain. CRISPR knockout of SlSPL-CNR de-represses SlAAT1 and increases ester accumulation. This methylation-sensitive binding is conserved across SBP domain proteins from rice, maize, and tomato. Our findings reveal a mechanism where DNA hypomethylation facilitates repressor recruitment, linking epigenetic dynamics to metabolic control in plants.

overall_design:
DAP-seq (DNA affinity purification sequencing) was performed to profile the genome-wide binding sites of transcription factor SlSPL-CNR in red ripe tomato fruits (Solanum lycopersicum cv. Ailsa Craig, 46 days post-anthesis). Genomic DNA was extracted and used for DAP-seq library construction while preserving DNA methylation. Sequencing was performed on an Illumina NextSeq 550 platform to identify SlSPL-CNR binding regions and its methylation-sensitive DNA binding properties.

Please note that the raw data from the previous samples (GSM5250645-GSM5250647 GSM5250660-GSM5250662 in GSE172260) has been re-analyzed using the same analysis pipeline for our current study, which will be incorporated into a new research context.

*data processing step:
Custom bioinformatics pipeline (fastp + bowtie2 + MACS2)
Raw reads were trimmed for adapter and low-quality sequences using fastp (v0.12.4)
Trimmed reads were mapped to the tomato SL4.0 genome using bowtie2 (v2.3.4.1)
PCR duplicates were removed using GATK MarkDuplicates
Peak calling was performed using MACS2
genome build/assembly: SL4.0
processed data files format and content: bigWig files for read coverage

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

last: Lang

first: Jiamu

last: Du


title: Glycine Receptor α2 Mediates Endothelium-dependent Vasodilation via Activation of eNOS Signaling

status: Public on Jun 18 2026

city: Nanjing

first: Bai

last: xueya

address: No. 101 Longmian Avenue, Jiangning District, Nanjing, Jiangsu, China

country: China

institute: Nanjing Medical University

type: Expression profiling by high throughput sequencing

summary: Background: Endothelium-derived nitric oxide (NO) is an important vasodilator essential for maintaining vascular homeostasis. However, how endothelial NO synthase (eNOS) is regulated in hypertension conditions is not yet fully understood. In this study, we describe a critical role of the α2 subunit of the glycine receptor (GLRA2) in modulating eNOS signaling and blood pressure regulation. Methods: Endothelial-specific Glra2 deficient mice and the adeno-associated viral transfected mice were generated to assess the role of GLRA2 in hypertension models. Endothelium-dependent relaxation response and whole-cell patch clamp recording were determined. Results: We first demonstrated selective expression of GLRA2 in arterial endothelial cells. Activation of GLRA2 by its ligand, glycine, effectively counteracts hypertension in a GLRA2-dependent manner. Our patient study indicated a negative correlation between plasma levels of glycine and blood pressure. Furthermore, we showed that endothelial GLRA2 regulates vasodilation by promoting NO production, rather than functioning solely as a chloride channel. Mechanistically, GLRA2 facilitates the phosphorylation of glycogen synthase kinase-3β at Ser9, which activates the AKT/eNOS signaling pathway in the endothelium, leading to increased NO release. Conclusions: This study discovers a novel endothelial GLRA2 pathway holds significant potential for developing new strategies to control hypertension.

overall_design: RNA-seq reveals the effects of intraperitoneal saline or glycine administration after angiotensin II-induced modeling on aortic endothelial cell function in wild-type and  Glra2 global knockout mice.

first: Xueya

last: Bai

first: Xudong

last: Zhu

first: Qi

last: Chen


title: Single-Cell RNA Sequencing Maps Heterogeneity and Devel-opmental Dynamic of Goose Satellite Cells During Embryo-genesis

city: shanghai

first: zuoyin

last: zhu

address: number 1239 siping road

institute: tongji university

summary: Skeletal muscle satellite cells (SMSCs) are central to embryonic myogenesis and post-natal muscle regeneration; however, their heterogeneity and transcriptional dynamic during avian embryogenesis remain largely unexplored. Here, we employed single cell RNA sequencing (scRNA seq) on 42,886 SMSCs isolated from goose leg muscles at four embryonic stages (E13, E15, E18, and E23). Unbiased clustering identified 22 distinct clusters, classified into six main cell types: satellite cells (PAX7+MYF5+NRXN1+), myo-cytes (MYOD1+MYOG+ACTC+), fibro adipogenic progenitors (FAPs, DCN+CDH115+COL6A3+), endothelial cells (CDH5+KDR+PECAM1+), immune cells (CD82+PTPRC5+FCER1G+), and Schwann cells (GPX3+SNCA+SKAP1+). Satellite cells rep-resented the predominant population and were further subdivided into quiescent (PAX7+), activated (PAX7+MYF5+), and proliferative/differentiating (MYF5+MYOD1+) states. Differential expression analysis revealed 2,603 genes dynamically regulated in satellite cells across developmental stages, including core regulators of stemness (PAX7), commitment (MYOD1), and differentiation (MYOG), as well as genes implicated in sarcomeric and cytoskeletal remodeling. Additionally, 517 genes were universally ex-pressed across all satellite cell states, emcompassing ACTA2, TPM1, CDK1, CCND3, FGF2, MET, MYF5 and RUNX2. Pseudotime trajectory analysis delineated a linear pro-gression from quiescent to activated and subsequently to proliferative/differentiating states, characterized by dynamic activity in Wnt, TGF β, BMP, Notch, PI3K/AKT, and MAPK pathways. Cell cell communication analysis demonstrated robust intercellular signaling networks in quiescent cells, which diminished with activation and differenti-ation, involving FGFR, Ephrin, Collagen, and CADM signaling families. Together, this work establishes a comprehensive single cell atlas of goose SMSC development, re-vealing subpopulation heterogeneity, state specific molecular signatures, and key sig-naling pathways underlying myogenic progression. Our findings advance the under-standing of avian skeletal muscle development and provide valuable resources for en-hancing muscle traits in poultry.

overall_design: In this study, skeletal muscle satellite cells (SMSCs) were collected from goose leg muscles at four embryonic developmental stages (E13, E15, E18, and E23). A total of 42,886 cells were subjected to single-cell RNA sequencing (scRNA-seq). Unbiased clustering analysis identified 22 distinct clusters, which were further classified into six major cell types. Satellite cells represented the predominant population and were subdivided into three states (quiescent, activated, and proliferative/differentiating) based on marker gene expression. Subsequently, differential expression analysis, pseudotime trajectory analysis, and cell-cell communication analysis were performed to systematically characterize the transcriptional dynamics, state transition trajectories, and signaling pathway alterations of satellite cells during embryonic development.

first: Wang

last: Cui

first: Daqian

last: He


title: Alpha Protein Kinase 3 Gene Therapy Restores Heart Function in Mouse and Human Models of Cardiomyopathy

city: Melbourne

first: Enzo

last: Porrello

state: Victoria

address: c/o Royal Children’s Hospital

department: Cell Biology

country: Australia

institute: Murdoch Children's Research Institute

summary: Here, we generated single-nucleus RNA sequencing (snRNA-seq) data from hiPSC-derived cardiac monolayers carrying TTN heterozygous (TTNhet) and TTN homozygous (TTNhom) truncating variant, alongside their PB10.5 wild-type (WT) isogenic control. Differential gene expression provided insight into the impact of TTN variants on sarcomeric gene expression.

overall_design: Expression profiling by high throughput sequencing - Single nucleus RNA sequencing (snRNA-seq) profiles of hiPSC-derived cardiac monolayers: TTN homozygous (TTNhom), TTN heterozygous (TTNhet), and PB10.5 wild-type (WT)

first: Neda

last: Rahmani Mehdiabadi

first: James

last: McNamara


title: Effects of VPS4 inhibition by VPS4A E228Q on gene expression in KMR19 and KMR46 mouse rhabdomyosarcoma cells

city: Hershey

first: Yoshinori

last: Takahashi

state: PA

address: 500 University DR., Rm C7814B

department: Pediatrics

country: USA

institute: Penn State College of Medicine

summary: The AAA+ ATPase VPS4 drives the ESCRT machinery in diverse intracellular membrane remodeling events, including endocytic receptor sorting, membrane repair, and autophagosome closure. Tumor cells often lose one VPS4 paralog (VPS4A or VPS4B), making them dependent on the remaining enzyme and creating a potential therapeutic vulnerability. Here, we report that VPS4 inhibition triggered upregulation of cytokine and innate immune signaling, along with canonical NF-κB, stress response, and cell death pathways in KMR19 and KMR46 murine rhabdomyosarcoma cells (samples J and L [KMR19]; P and R [KMR46]). In a separate set of samples (A–F, KMR46), we show that the STING–IRF3 axis is responsible for cytokine upregulation following VPS4 inhibition.

overall_design: RNA-seq profiling of (1) KMR19 and KMR46 cells transduced with a doxycycline (Dox)-inducible, GFP-tagged dominant-negative VPS4A (VPS4A E228Q; DN-VPS4A) or a GFP-only control, followed by treatment with 1 µg/mL Dox for 10 h (samples J, L, P, and R); and (2) wild-type, STING knockout, and IRF3 knockout KMR46 cells transduced with inducible DN-VPS4A and treated with 1 µg/mL Dox for 10 h (samples A–F).

first: Ray

last: Zhang

first: Hong-Gang

last: Wang


title: Choroid plexus inflammation in bipolar disorder

city: Boston

first: Maria

last: Lehtinen

state: MA

address: 300 Longwood Ave, Mailcode Bch3400

institute: Boston Children's Hospital

summary: Postmortem human choroid plexus tissue from individuals with bipolar disorder and matched controls was analyzed using cytokine protein arrays and bulk RNA sequencing to characterize immune and barrier-related alterations. The study identifies increased pro-inflammatory signaling and reduced trophic/supportive pathways, implicating the choroid plexus as a neuroimmune interface in bipolar disorder.

overall_design: Case-control study Postmortem human choroid plexus tissue Bipolar disorder vs unaffected controls Bulk RNA-seq + cytokine array validation

first: Dario

last: Figueroa Velez

first: Reza

last: Rahimian

first: Christine

last: Hehnly

first: Gustavo

last: Turecki

first: Naguib

last: Mechawar

first: Maria K.


title: A novel autopolysialylation activity of the ganglioside sialyltransferase ST8Sia5 regulates its secretion and enzyme activity

city: Nagoya-city

first: Fumiya

last: Sakamoto

address: Furo-cho, Chikusa-ku

country: Japan

institute: Nagoya University

summary: This study showed that ST8Sia5L is a novel self-polysialylating enzyme that modifies itself rather than NCAM. We found that this autopolysialylation regulates both the secretion of ST8Sia5L from cells and its conventional ganglioside-sialylation activity. These results suggest that polysialylation of ST8Sia5L plays an important role in controlling its function and extracellular behavior.

overall_design: A stable mouse melanoma B16 cell line expressing an empty vector was established, and total RNA was isolated using the NucleoSpin RNA kit for RNA-seq analysis.

first: Rina

last: Hatanaka

first: Masaya

last: Hane

first: Di

last: Wu

first: Ken

last: Kitajima

first: Chihiro

last: Sato


title: Status Epilepticus Alters the Function of Brain-Derived Extracellular Vesicles [BV2-RNA-seq]

city: Atlanta

first: Samantha

middle: Reed

last: Lynn

state: GA

address: 615 Michael St

department: Department of Human Genetics

institute: Emory University

overall_design: BV2 microglia cells were treated with brain-derived extracellular vesicles

middle: L

last: Reed

first: Yilin

first: Yangping

last: Li

first: Guoku

last: Hu

first: Jingjing

last: Yang

first: Bing

last: Yao

first: Andrew

last: Escayg


title: Status Epilepticus Alters the Function of Brain-Derived Extracellular Vesicles [N2A-RNA-Seq]

summary: Epilepsy is a neurological disorder characterised by recurrent spontaneous seizures. Approximately 30% of patients are unable to achieve adequate seizure control with available medications, highlighting the need to better understand disease mechanisms and develop improved treatments. Mesial temporal lobe epilepsy (MTLE) is a common subtype of treatment-resistant epilepsy. Patients with MTLE often have experienced a prior neurological insult, such as a traumatic brain injury, or status epilepticus (SE), that is believed to contribute to epileptogenic changes that lead to MTLE. However, the molecular mechanisms underlying epileptogenesis remain incompletely understood. Extracellular vesicles (EVs) are small membrane-bound particles released by cells that are important for intercellular communication. Recent studies identified altered microRNA (miRNA) content in brain-derived EVs (BDEVs) in models of MTLE, but whether BDEV function is altered has not been explored. Using the pilocarpine mouse model of MTLE, we examined the effects of SE on the function and miRNA cargo of hippocampal BDEVs during the epileptogenic period. BDEVs were isolated from hippocampi of control and pilocarpine-treated mice 24 h after SE. To assess functional changes, we compared gene expression in N2a neuronal-like cells and BV2 microglial-like cells exposed to control BDEVs (CON-BDEVs) or BDEVs collected after SE (SE-BDEVs). SE-BDEVs induced distinct transcriptional changes in N2a cells including alterations in the expression of genes related to TGF-β signalling, amino acid regulation of mTORC1 and neurotransmitter signalling. In BV2 cells, SE-BDEVs increased the expression of genes associated with inflammatory cytokine release. Analysis of BDEV miRNA content revealed multiple differentially expressed miRNAs between SE- and CON-BDEVs, with predicted targets overlapping with genes uniquely altered by SE-BDEVs. Notably, SE-induced miRNA changes were still observed 10 days post-SE, indicating sustained modulation of BDEV cargo. These findings identify SE-induced alterations in both the function and miRNA composition of hippocampal BDEVs, suggesting that BDEVs may contribute to epileptogenesis in MTLE.

overall_design: N2a neuroblastoma cells were treated with brain-derived extracellular vesicles

last: Wang


title: Status Epilepticus Alters the Function of Brain-Derived Extracellular Vesicles [miRNA-24hr]

type: Non-coding RNA profiling by high throughput sequencing

overall_design: miRNA-sequencing profiling of extracellular vesicles (EVs) isolated from the brain tissue of mice that had experienced status-epilepticus (SE-BDEVs) or matched control mice (CON-BDEVs)


title: IL15 — Driven Crosstalk Between Liver Sinusoidal Endothelial Cells and CD8⁺ Tissue-Resident Memory T Cells Promotes Inflammation in Alcohol-Associated Hepatitis

city: Rochester

first: Vijay

middle: H

last: Shah

state: MN

address: 200 First Street SW, Guggenheim Building 10th Floor

institute: Mayo Clinic

summary: Background: Alcohol-associated hepatitis (AH) is a severe inflammatory liver condition driven by dysregulated immune responses. CD8 T cells accumulate in the liver during AH, yet their functional role remains poorly defined. Approach & Results: Single-cell RNA sequencing (scRNA-seq) in a murine AH model revealed a distinct population of CD8 tissue-resident memory T cells (TRM) with heightened activation and proinflammatory cytokine production. Analysis of human AH liver scRNA-seq data, along with immunohistochemistry validation, supported CD8 TRM enrichment in diseased tissue. IL15 emerged as a prominent pathway linked to TRM activation, and IL15 blockade reduced TRM abundance and attenuated EtOH/LPS-induced liver injury. Mechanistically, liver sinusoidal endothelial cells (LSECs) not only provided a structural niche for TRM retention but also amplified IL15 signaling. In vitro, co-culture experiments demonstrated that LSECs intensified activation in pre-stimulated CD8 T cells in a stimulus-dependent manner: under IL15 stimulation, LSECs boosted effector function without inducing cell death, whereas under TCR-stimulation, LSECs drove hyperactivation and activation-induced cell death. Bulk RNA-seq and phospho-protein analysis identified the PI3K–AKT pathway as a shared pathway enhanced by LSEC co-culture in activated CD8 T cells. These findings define a context-dependent mechanism in which LSECs promote IL15-driven signaling through AKT pathway amplification, promoting TRM persistence and inflammatory activity in AH. Conclusion: IL‑15–associated signaling within the hepatic microenvironment, shaped by LSEC–CD8 T cell interactions, promotes activation and persistence of CD8 TRM cells in alcohol‑associated hepatitis. Targeting IL15–LSEC–AKT axis may disrupt pathogenic TRM niches and represents a promising therapeutic strategy for severe AH.

overall_design: scRNAseq of mouse model of inflammatory liver injury. Paired PBMC and liver resident samples per mouse.

first: Weizhe

last: Zhong

first: Sheng

last: Cao

first: Shawna

middle: A

last: Cooper

first: Mengfei

last: Liu


title: Status Epilepticus Alters the Function of Brain-Derived Extracellular Vesicles [miRNA_10Day]


title: RNA-seq analysis of human iPSC-derived oligodendrocytes cultured on nanofibers

city: Kyoto

first: Haruhisa

last: Inoue

state: Kyoto

address: 53 Kawahara-cho, Shogoin, Sakyo-ku

institute: Kyoto University

summary: Human iPSC-derived oligodendrocytes were cultured under conventional 2D conditions or on nanofibers to investigate transcriptomic changes associated with ensheathment. RNA sequencing was performed to compare gene expression profiles between the two conditions.

overall_design:
Human iPSC-derived oligodendrocytes were cultured under two conditions: conventional 2D culture and nanofiber culture. Each condition included three biological replicates (n=3). RNA-seq was performed to identify differentially expressed genes between the two groups.

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

last: Morita

first: Takayuki

last: Kondo


title: Effect of exosomes from exercised vs. sedentary donors on rat basal ganglia region cells

city: Newark

first: Alexander

last: Lemenze

state: New Jersey

address: 185 South Orange Ave

institute: Rutgers

summary: Determine the degree of exercising donor exosome-induced neuroprotective adaptations in the brains of sedentary model rats.

overall_design: Exosomes from exercised (treadmill) vs. sedentary rats were infused through intracerebroventricular canula daily for one week into the brains of sedentary rat recipients (11 months old). Basal ganglia regions were dissected and intact nuclei were isolated. Cell type specific gene expression changes induced by the different types of exosomes were characterized by scRNA-seq.

first: Bruce

last: Citron

first: Vedad

last: Delic


title: Astrocyte molecular changes during basolateral amygdala-related emotional behaviors [set8]

city: Los Angeles

first: Riki

last: Kawaguchi

state: CA

address: 760 Westwood Plaza, Room 37-420

department: Department of Psychiatry and Neurology Department of Psychiatry

institute: University of California, Los Angeles

summary: Astrocytes tile the central nervous system (CNS) and have fundamental roles in physiology and disease, yet there remain open questions about their contributions to physiological and pathological processes in the CNS. The basolateral amygdala (BLA) integrates rewarding and aversive stimuli and is integral to mood regulation and emotional behaviors. As many past studies have focused on neurons in the BLA, the contribution of BLA astrocytes to emotional behaviors is largely unknown. A major bottleneck has been the paucity of reliable tools to explore astrocyte functions and molecular mechanisms in vivo. This shortfall has been addressed by recent developments in the field reporting approaches to systematically explore the role of astrocytes with improved tools. Here, we used several such tools to elucidate BLA astrocytic changes during emotional behavioral responses. Applying several mouse models of stress (negative emotional triggers) and astrocyte-specific adenoassociated viruses (AAVs), [Ca2+] imaging, RNA sequencing, and proteomics, we explored the role of astrocytes at the molecular and cellular level in the BLA. We analyzed the data to evaluate how astrocytes might be exploited in vivo to improve behavioral outcomes in emotion-related disorders such as anxiety and depression.

overall_design: Tissue from basolateral amygdala was dissected from Aldh1l1-CreERT2 x Arl13b f/f mice used to perform RNAseq.

first: Sara

middle: G

last: Pelaz

first: Katsu

last: Mitsui

first: Fuying

last: Gao

first: Bal

last: Khakh


title: Fibrotic Remodeling in the NOD/ShiLtJ Mouse Model of Sjögren’s Disease: Insights from Single-Cell Transcriptomics and AI-Driven Quantification

status: Public on Jun 19 2026

city: Albany

first: Melinda

last: Larsen

state: NY

address: 1400 Washington Ave

institute: University at Albany

summary: Sjögren’s Disease (SjD) is a systemic autoimmune disorder characterized by salivary gland hypofunction and lymphocytic infiltration, yet the contribution of fibrosis to glandular dysfunction remains unclear. The NOD/ShiltJ mouse is a well-established model for SjD. In this study, we evaluated the presence of and impact of fibrosis in the salivary glands of the NOD/ShiLtJ mouse. Using scRNASeq, we investigated differential gene expression in the fibroblasts of NOD mouse vs control mice. Fibroblast populations in the salivary glands of the NOD mouse exhibited increased levels of extracellular matrix mRNAs, including Col1a1, Col1a2, and Col3a1, relative to the control strain. From histological staining with Picrosirius red and AI-driven fibrosis quantification, we identified significant fibrotic remodeling in the submandibular glands of non-obese diabetic NOD/ShiLtJ mice relative to controls, which correlated with the diabetic phenotype in this mouse strain. We assessed the therapeutic potential of Nintedanib to alleviate this fibrotic phenotype. Nintedanib is an FDA-approved antifibrotic agent for chromic fibrosing interstitial lung disease. While Nintedanib did not significantly reduce immune infiltration or restore salivary function, it modestly decreased multiple fibrosis scores in long-term treatment cohorts. These findings demonstrate that the NOD/ShiLtJ strain models the fibrotic response that occurs in SjD patients and supports further investigation into antifibrotic therapies for salivary gland dysfunction.

overall_design: Submandibular salivary glands were dissociated into single cells followed by two rounds of magnetic activated cell sorting (MACs) to deplete for epithelial cells expressing EpCAM and red blood cells expressing Ter119. The samples then went through one round of dead cell removal using Miltenyi dead cell removal kit.

first: Jennifer

last: Morrissey

first: Deirdre

last: Nelson

first: Li

last: Chen

first: Nathan

last: Aist

first: Mathieu

last: Petitjean

first: Joey

last: Tavarez

first: Amber

last: Altrieth

first: Nicholas

last: Moskwa

first: Renae

last: Williams-Atkinson

first: Ben

last: Fowler

first: Nikhita

last: Kumar


title: Astrocyte molecular changes during basolateral amygdala-related emotional behaviors [set6]

first: Riki

last: Kawaguchi

overall_design: Tissue from basolateral amygdala was dissected from Ift88 f/f mice and MACS was used to isolate astrocytes to perform RNAseq.


title: Astrocyte molecular changes during basolateral amygdala-related emotional behaviors [set5]

overall_design: Tissue from basolateral amygdala was dissected from Ift88 f/f mice.

first: Sara

last: Pelaz


title: Identification of Biomarkers in Myocardial Hypertrophy and Fibrosis via Integrated Transcriptomic and Phosphoproteomic Profiling

city: Kunming

first: Kang

last: Luo

state: Yunnan

address: No. 1168, Chunrong West Road, Yuhua Street, Chenggong District, Kunming,

institute: Kunming Medical University

summary: Myocardial hypertrophy and fibrosis (MHF) are key structural changes in adverse cardiac remodeling. They are commonly observed in hypertension, metabolic disorders, and cardiomyopathies. These processes contribute to heart failure and sudden death, yet their molecular mechanisms remain unclear. We established in vivo and in vitro models of MHF and performed transcriptomic and label-free phosphoproteomic sequencing. These data were integrated with public single-cell RNA sequencing datasets. This multi-tier strategy enabled us to move beyond bulk-tissue signals and prioritize candidates based on cross-omics concordance and cell-type-specific expression. We identified five candidate biomarkers, CLIP2, PLA2G4A, PRRX1, SLAIN2, and XPO1. These candidates showed coordinated upregulation or downregulation at both the transcriptomic and phosphoproteomic levels. They were also specifically enriched in disease-relevant cardiac cell populations, including cardiomyocytes and fibroblasts. PRRX1 and PLA2G4A were enriched in fibrogenic fibroblast subsets and increased along activation trajectories. XPO1 and SLAIN2 were downregulated in cardiomyocytes and fibroblasts, suggesting impaired nuclear export and cytoskeletal regulation. Molecular docking revealed flurandrenolide and selinexor as potential modulators of PLA2G4A and XPO1 respectively. However, their cardiovascular safety and efficiency remain uncertain. Notably, the therapeutic implications of XPO1 modulation appear context-dependent, warranting careful evaluation of its functional role in specific MHF etiologies. Overall, these findings highlight novel targets and provide mechanistic insights into MHF progression.

overall_design: To investigate the molecular mechanisms underlying MHF, we established in vivo and in vitro models. Eight-week-old male Sprague–Dawley rats (250-300 g; SPF Biotechnology Co., Ltd., Beijing, China) were randomly assigned to a control group or an MHF group (n = 3 per group). The MHF model was induced by subcutaneous injection of ISO (1.5 mg/kg/day) for 7 consecutive days. Control rats received an equal volume of saline18. At the endpoint, rats were euthanized by inhalation of an overdose of isoflurane and hearts were excised. Heart tissues were used for morphological assessment and histological validation by hematoxylin-eosin (H&E) staining. They were also used for molecular analyses, including quantitative polymerase chain reaction (qPCR) of ANP and BNP expression and transcriptomic sequencing. All animal procedures complied with institutional ethical guidelines and were approved by the Ethics Committee of Yan'an Hospital, Kunming City (Approval No. 2022035).  Total RNA was extracted from rat myocardium. RNA quality was assessed using a NanoPhotometer (IMPLEN) and an Agilent 2100 Bioanalyzer. Libraries were sequenced on an Illumina NovaSeq platform to generate 150 bp paired-end reads. Clean reads were aligned to the Rattus norvegicus reference genome using HISAT2. Gene expression was quantified as fragments per kilobase of transcript per million mapped reads (FPKM) using featureCounts. Differentially expressed genes (DEGs) were identified using DESeq2, with thresholds of |log₂(fold change)| > 0.5 and p < 0.05. Principal component analysis (PCA) confirmed clear separation between MHF and control groups

first: Yangguang

last: Ma

first: Yayong

last: Zhang

first: Yunfeng

last: Zi

first: Guangyuan

last: Guo

first: Xingyuan

first: Wenjuan

last: Feng

first: Qifan

last: Jing

first: Lin

last: Li

first: Shen

last: Han

first: Bingrong

last: Zheng


title: Astrocyte molecular changes during basolateral amygdala-related emotional behaviors [set7]

overall_design: Tissue from basolateral amygdala was dissected from Arl13b f/f mice and MACS was used to isolate astrocytes to perform RNAseq.

first: Katsu

last: Mitsui

first: Fuying

last: Gao

first: Bal

last: Khakh


title: Timing-dependent neuroprotection of dexamethasone in neonatal hypoxic-ischemic brain injury mouse model : Transcriptomic insights into synaptic signaling and calcium homeostasis

city: Seoul

first: Joohee

last: Lim

address: Yonseiro 50-1

country: South Korea

institute: Yonsei University

summary: Background: Neonatal hypoxic–ischemic (HI) brain injury is a leading cause of neurodevelopmental disabilities. While dexamethasone has shown potential neuroprotective effects, its molecular mechanisms and the optimal timing of administration remain incompletely understood. Main body: In this study, we investigated the neuroprotective effects of dexamethasone pretreatment in a neonatal hypoxic–ischemic brain injury model and explored the underlying molecular mechanisms using next-generation sequencing (NGS). Neuropathological analysis demonstrated that dexamethasone pretreatment attenuated brain injury. Differentially expressed genes (DEGs) were identified based on an adjusted p-value (FDR) < 0.05 using the Benjamini–Hochberg correction. A total of 962 DEGs were identified, including 407 upregulated and 555 downregulated genes. Functional enrichment analysis revealed that upregulated genes were primarily associated with central nervous system development, synaptic signaling, and ionic homeostasis, whereas downregulated genes were mainly involved in cellular metabolic processes. Protein–protein interaction network analysis further demonstrated that DLG4, CALM1, and GRIN1 were highly interconnected within the enriched signaling pathways. Conclusion: Our findings demonstrate that dexamethasone provides time-dependent neuroprotection by stabilizing synaptic networks and modulating metabolic demand. These results highlight the critical importance of early intervention and provide a molecular framework for developing pharmacological strategies against neonatal HI injury

overall_design: The ICR mouse pups were randomly assigned to three experimental groups: (1) control (n = 6), (2) dexamethasone pretreatment (n = 8), and (3) dexamethasone post-treatment (n = 7). Hypoxic–ischemic (HI) brain injury was induced on postnatal day 7. In the dexamethasone-pretreated group, a 0.5 mg/kg dose of dexamethasone was administered intraperitoneally 6 h prior to HI induction, whereas in the dexamethasone post-treatment group, the same dose was administered 6 h after HI injury. Control animals received an equal volume of phosphate-buffered saline (PBS). Brain injury was assessed by neuropathological analysis, and the ipsilateral hemisphere was selectively dissected for RNA extraction to identify differentially expressed genes (DEGs).

first: Jungho

first: Jeung Eun

last: Shin

first: Kwang Soo

last: Jung

first: Il-sun

last: Kim

first: Younhee

last: Ko

first: Kook In

last: Park


title: CBP/p300 deficiency induces the loss of functional pancreatic α cell mass

city: Shanghai

first: Shushu

last: Wang

address: 197 Ruijin Road Ⅱ

institute: Ruijin Hospital, Shanghai Jiao Tong University School of Medicine

summary: Pancreatic α cell senses amino acid availability to adjust secretion function and proliferation, yet the underlying molecular mechanisms remain unclear. Here, α cell-specific deletion of CBP/p300 in mice leads to hypoglucagonemia and hyperaminoacidemia, along with decreased functional pancreatic α cell mass due to impaired cell proliferation, dedifferentiation, and cell loss. The knockout of CBP/p300 blocks glucagon receptor antibody-stimulated α cell proliferation and mTORC1 signaling in mice.  These findings uncover a critical role for CBP/p300 in the maintenance of α cell identity and function.

overall_design: To investigate the effect of CBP and p300 knockout in alpha cells on the transcriptome pancreatic islet cells, islets from 4-week-old control and CBP/p300αDKO mice were isolated, dissociated, and subjected to single-cell RNA sequencing.


title: Depletion of Macrophages during Early Postnatal Development Leads to Disrupted Tooth Root Development and Altered Gli1⁺ MSC Trajectory

city: suzhou

first: Yan

last: Lei

address: No. 199, Ren'ai Road

institute: soochow university

summary: Mammalian tooth development proceeds through two principal stages—crown formation and root development—driven by intricate interactions between the oral epithelium and neural crest–derived mesenchyme. After crown formation, root development is guided by Hertwig’s epithelial root sheath (HERS), during which Gli1⁺ mesenchymal stem cells (MSCs) give rise to dental pulp, dentin, cementum, and the periodontal ligament (PDL). The root anchors the tooth to alveolar bone via PDL fibers, forming a dynamic occlusal buffer that mediates mechanosensation and nutrient supply. While previous work has shown that macrophages are abundant in the dental pulp and follicle, the functional importance of macrophages in tooth development has not been well characterized. Here, we examined the dynamically changing macrophage populations, labelled by CD68, F4/80, CD206 and other markers, in molars and surrounding tissues during root development in early postnatal mice. We also tracked the dynamic distribution of osteoclasts during tooth development. Importantly, selective depletion of macrophages using clodronate liposomes led to shortened tooth root, impaired PDL elongation and retarded alveolar bone shooting surrounding the root. Gli1⁺ MSCs exhibited increased proliferation but delayed differentiation upon macrophage depletion. Single-cell RNA sequencing and in vitro co-culture experiments support a model in which macrophage-derived TGF-β acts on mesenchymal TGF-β receptors to direct MSC fate and thereby regulate root morphogenesis. Collectively, these findings establish macrophages as critical niche components that orchestrate tooth root development through immune–mesenchymal crosstalk.

overall_design: Neonatal C57BL/6J mice received intraperitoneal injections of clodronate liposomes (40 μg/g body weight) beginning at postnatal day 3.5 (P3.5) and subsequently every three days (P6.5, P9.5, and P12.5) until sacrifice at P15.5. Control mice were administered an equivalent volume of vehicle liposomes following the same schedule. Dental tissues were harvested at P15.5 and subjected to single-cell RNA sequencing for transcriptomic profiling.

first: Peishan

first: Wen

first: Shiqing


title: Cardiovascular exercise drives neuroprotection in Spinocerebellar Ataxia 1 via rescue of abherrant splicing

first: J

middle: Andrew

last: Berglund

address: 1400 Washington Avenue

department: Biology

institute: University at Albany, State University of New York

summary: Objective: Spinocerebellar Ataxia 1 (SCA1) is a fatal hereditary neurodegenerative disorder with no approved therapies, and gene-targeting strategies have thus far failed in clinical trials. Exercise remains the only intervention shown to provide clinical benefit in patients with spinocerebellar ataxias, yet the underlying mechanisms remain poorly understood.  Results: Unrestricted exercise rescued motor ataxia in SCA1 mice but not degeneration in this model at the ages in this study. Transcriptional profiling of cerebellar tissue did separate WT sedentary and exercise mice by differential gene expression, but in SCA1 mice the most pronounced changes occurred at the level of RNA splicing, particularly in ion channel modules. Exercise led to a significant rescue of splicing events in SCA1 mice, with minimal impact on gene expression changes. Further, both exercised SCA1 and wild-type mice exhibited splicing patterns more similar to each other than their sedentary counterparts. Interpretation: Together with emerging evidence in other SCAs, our findings confirm aberrant splicing as a central driver of spinocerebellar ataxia (SCA) pathophysiology and identify splicing-regulated networks as actionable therapeutic targets. The observed benefits in SCA1 mice suggest that pharmacologic activation of ion channels may be a viable strategy to mimic exercise for disease modification across SCAs and related neurodegenerative disorders.

overall_design: Methods: Using the Atxn1154Q/2Q knock-in mouse model, we implemented a prolonged voluntary wheel-running paradigm from 4 to 16 weeks of age. Mice were then phenotyped using motor and cognitive behavioral assays. Following euthanasia, cerebellar tissue was harvested for histological analysis and unbiased transcriptomics.

first: Isabel

last: Soto

first: Michale

last: Bonomo

first: Brianna

last: Nelthrope

first: Emma

last: Palmer

first: Mariana

last: Sierra

first: Ilkim

last: Erturk

first: David

last: Peppercorn

first: Eleanor

last: Cox

first: Tiare

last: Vasconcellos

first: Henry

last: Paulson

first: Hannah

last: Shorrock

first: Sharan

last: Srinivasan


title: Type I Interferon Reprograms Intestinal Epithelial Cells for Sustained HIV-1 Latency in CD4+ T Cells of People with HIV-1 Receiving Antiretroviral Therapy

city: Montréal

first: Jean-Philippe

last: Goulet

state: Québec

address: C.P. 6128, succursale Centre-ville

country: Canada

institute: Université de Montréal

summary: The intestinal environment sustains a state of HIV latency via yet unclear mechanisms. We recently demonstrated that specific cytokines act on intestinal epithelial cells (IEC) to promote viral reservoir (VR) latency or reactivation, with TNF-activated IEC limiting HIV outgrowth in CD4+ T cells of people with HIV (PWH) on antiretroviral therapy (ART). The pro-latency effect of TNF coincided with the induction of IL-32, a pro-inflammatory cytokine overexpressed in ART-treated PWH. Since type I IFNs are strong modulators of IL-32, we investigated IFN-β ability to modulate the crosstalk between IEC and CD4+ T cells via IL-32-dependent mechanisms.

overall_design: HT-29 intestinal epithelial cells; 2 CRISPR conditions (CTL, IL-32 KO) x 4 stimulations (Medium, TNF-a, IFN-b, TNF-a+IFN-b) x 2 biological replicates; 16 samples total.

first: Julie

last: Moreaux

first: Etiene

last: Moreira Gabriel

first: Jonathan

last: Dias

first: Jean-Francois

last: Schmouth

first: Soumia

last: Khalfi

first: Tomas Raul

last: Wiche Salinas

first: Chernkhwan

last: Kaofai

first: Kimiya

last: Majidi Ivari

first: Jean-Pierre

last: Routy

first: Madeleine

last: Durand

first: Cécile

last: Tremblay

first: Mohamed

last: El-Far

first: Petronela

last: Ancuta


title: Therapeutic TG2 Inhibition Reverses Systemic Multiomic Dysregulation in Celiac Disease

city: Tampere

first: Keijo

last: Viiri

address: Arvo Ylpön katu 34

country: Finland

institute: Tampere University

summary: Background and Aims: Celiac disease (CeD) is an autoimmune disease triggered by dietary gluten in genetically predisposed individuals. Deamidation of gluten peptides by the CeD autoantigen and enzyme transglutaminase 2 (TG2) is central to the pathogenesis of CeD. Inhibition of TG2 with the specific inhibitor ZED1227 effectively prevents gluten-induced histological damage in CeD patients. Here we aimed to explore the blood DNA methylomic changes in ZED1227-treated CeD patients undergoing a gluten challenge. Results: Drug treatment revealed consistent patterns suggesting normalization of the DNA methylome indicating that ZED1227 attenuated the systemic responses to gluten challenge. Conclusions: These findings provide evidence that ZED1227 can significantly prevent the gluten-induced CeD-associated systemic changes. Clinical trial: EudraCT 2017-002241-30

overall_design: Individuals with CeD on a long-term gluten-free diet (GFD) underwent a 6-week gluten challenge combined with daily 100mg ZED1227 drug (PGCd) or placebo (PGCp). Samples were collected at baseline (GFD) and post-gluten challenge (PGC). Blood genome-wide DNA methylation analysis was performed with EPIC2 arrays for 72 samples, one of which was removed after QC from the processed data.


title: The VgrG2 effector of Acinetobacter baumannii mediates immune evasion by repressing Csu pilus assembly and triggering phagocyte methuosis [scRNA-seq]

city: Hangzhou

first: xu

last: wenzeng

address: Department of Respiratory Medicine, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310016, China.

institute: Zhejiang University

summary: Acinetobacter baumannii is a formidable nosocomial pathogen whose multidrug resistance and immune evasion capabilities present a major therapeutic challenge. This study identifies the type VI secretion system (T6SS) effector VgrG2 as a critical virulence regulator in A. baumannii. VgrG2 employs a two-pronged strategy to undermine host innate immunity. First, it transcriptionally represses the major adhesin Csu pilus, reducing bacterial recognition, phagocytic uptake, and neutrophils recruitment. Second, VgrG2 directly targets and hyperactivates the small GTPase Rac1 within phagocytes. This leads to actin cytoskeletal disarray, which drives excessive macropinocytosis, resulting in compromised phagocytosis and methuosis—a non apoptotic, vacuole dependent death specific to phagocytes. Thus, VgrG2 selectively eliminates key immune sentinels and alters pulmonary inflammation, promoting bacterial persistence and dissemination. These findings extend the role of T6SS effectors beyond interbacterial competition to include sophisticated eukaryotic directed attacks, and highlight the VgrG2 Rac1 axis as a promising therapeutic target.

overall_design: mice infected with PBS, AB5075 WT, ΔvgrG2（AV）

first: Wenzeng

last: Xu

first: Hua

last: Zhou


title: Early differential impact of MeCP2 mutations on functional networks in Rett syndrome patient-derived human cortical organoids [WES]

city: Cambridge

first: Tatsuya

last: Osaki

address: 43 Vassar street, 46-6227

department: Picower Institute for Learning and Memory

institute: Massachusetts Institute of Technology

type: Genome variation profiling by high throughput sequencing

summary: Human cerebral organoids derived from induced pluripotent stem cells can recapture early developmental processes  and reveal changes involving neurodevelopmental disorders. Mutations in the X-linked methyl-CpG binding protein 2 (MECP2) gene are associated with Rett syndrome, and disease severity varies depending on the location and type of mutation. Here, we focused on neuronal activity in Rett syndrome patient-derived organoids, analyzing two types of MECP2 mutations—a missense mutation (R306C) and a truncating mutation (V247X)—using calcium imaging with three-photon microscopy. Compared to isogenic controls, we found abnormal neuronal activity in Rett organoids and altered network function based on graph theoretic analyses, with V247X mutations impacting functional responses and connectivity more severely than R306C mutations. These changes paralleled EEG data obtained from patients with comparable mutations. Labeling DLX promoter-driven inhibitory neurons demonstrated differences in activity and functional connectivity of inhibitory and excitatory neurons in the two types of mutations. Transcriptomic analyses revealed HDAC2-associated impairment in R306C organoids and decreased GABAA receptor expression in excitatory neurons in V247X organoids. These findings demonstrate mutation-specific mechanisms of vulnerability in Rett syndrome and suggest targeted strategies for their treatment.

overall_design: Genomic DNA was isolated from the cells from 2D culture using DNeasy Kit (Qiagen) following manufacture protocol. Whole exome sequencing was performed (Germline Whole Exome Sequencing (WES) v6.0., 2 x 150 bp reads, Broad Institute).SNVs and indels were characterized by mapping on the reference genome (GRCh37/hg19).

first: Chloe

last: Delepine

first: Yuma

last: Osako

first: Devorah

last: Kranz

first: April

last: Levin

first: Charles

last: Nelson

first: Michela

last: Fagiolini

first: Mriganka

last: Sur


title: Programming effects of removing maternal heat abatement on offspring growth, immunity, thermotolerance, and liver transcriptomics during backgrounding

city: Auburn

first: Wellison

middle: J. S.

last: Diniz

state: Alabama

address: CASIC Building 559 Devall Drive Auburn University, 205

department: Animal Sciences

institute: Auburn University

summary: This study used transcriptomic profiling to investigate hepatic gene expression differences in Angus-cross calves for a 112-day background period during the summer. Calves were born from cows given (S) or not given access (N) to shade during gestation. Liver biopsies were performed on d 56 on calves randomly selected, which were subjected to RNA-Seq analysis, yielding 02 differentially expressed genes (DEGs) (FDR < 0.1) due to the main effect of treatment (No shade  vs. Shade; N vs. S). Within sex, we identified nine genes differentialy expressed in females. No DEGs were observed in males due to the treatment. Likewse, no interaction between sex and treatment was identified.

overall_design: Fifty-six Angus-cross calves [225 ± 5.3 kg body weight (BW), 9 ± 1.5 months of age] were enrolled in the study at weaning for a 112-day background period during the summer. Calves were born from cows given (n = 28; steers = 16 and heifers = 12) or not given access to shade (n = 28; steers = 16 and heifers = 12) during gestation. Liver biopsies were performed on d 56 on calves randomly selected on day 0 [10 calves per treatment (5 male and 5 females)] for transcriptomics analysis. After collecting, liver samples were stored in cryogenic tubes, snap-frozen in liquid nitrogen, and stored at −80 °C until RNA extraction.

first: Matheus

last: Ferreira

first: Wellison J. S.


title: Early differential impact of MeCP2 mutations on functional networks in Rett syndrome patient-derived human cortical organoids [RNA-Seq]

overall_design: Total RNA was isolated from the cells from 2D culture using RNAeasy Mini Kit (Qiagen) following manufacture protocol. RNA-sequencing was performed by the Broad Institute Sequencing Platform. 50M paired-end configuration and read-data were mapped to human reference genome GRCh37/hg19.


title: Single-cell multiomic approaches define a gradual, spatially-regulated epigenetic and transcriptional transition from embryonic to adult neural stem cells [Xenium]

city: Vancouver

first: Freda

last: Miller

state: BC

address: 2185 East Mall

department: Michael Smith Laboratories

institute: University of British Columbia

summary: Here, we ask how adult neural stem cells (NSCs) arise developmentally, focusing on murine cortical precursors that generate excitatory neurons embryonically and interneurons and glial cells postnatally. Using complementary single-cell spatial, transcriptomic, and epigenomic approaches, we show that postnatal NSC state acquisition involves a gradual transcriptional and epigenetic shift in the entire embryonic cortical precursor cell population and identify a distinct transition precursor state at E17/18 when both embryonic and the first postnatal progeny are being generated. Non-proliferative adult NSCs are also first seen at this transition timepoint, but they arise in a spatial domain distinct from that of the first postnatal progeny, indicating that NSC state acquisition is not a necessary prelude to the switch in cell genesis. These findings support a gradual epigenetically-continuous model for the transition from developing cortical precursors to NSCs and show that this is spatially separable from the transition to generating postnatal cell types.

overall_design: Xenium multiplexed in situ hybridization was performed on coronal sections across perinatal timepoints (E15, E18, P2) in order to study the dorsal ventricular-subventricular zone.

first: Beatrix

middle: S

last: Wang

first: Konstantina

last: Karamboulas

first: Nareh

last: Tahmasian

first: Daniel

middle: J

last: Dennis

first: David

middle: R

last: Kaplan

middle: D


title: Effect of PPARγ2 acetylation in at lysine 382 in mouse beige adipocyte differentiation

city: Kumamoto

first: Tomonori

last: Tsuyama

state: Kumamoto

address: 1-1-1, Honjo Chuo-ku

department: Faculty of Life Sciences

institute: Kumamoto university

summary: PPARr is a master regulator of adipogenesis which undergo different post translational modification during adipogenesis. This post translational modification of PPARγ control unique subset of genes rather full PPARr target genes. Recently we reported that SIRT7 deacetylate PPARr2 at lysine 382 residue and regulate lipogenesis in C3H10T1/2 cells. Here, we investigate this SIRT7-mediated PPARγ2 lysine deacetylation in mouse beige adipocyte differentiation of subcutaneous white AT (scWAT) stromal vascular fraction (SVF) cell line. At first we prepared PPARr2 K382 acetylation (KQ) and deacetylation (KR) mimicking mutant expressing mouse scWAT SVF cell line. After beige adipocyte differentiation, we isolated total RNA at day 2 and performed RNA-seq analysis.

overall_design: RNA-seq profiling of PPARr2 K382R or PPARr2 K382Q overexpressing mouse scWAT SVF cell line after 2 days beige adipocyte differentiation.

first: Avizit

last: Das

first: Kazuya

last: Yamagata

first: Tatsuya

last: Yoshizawa


title: Targeting the Mesenchymal Lineage of Pancreatic Ductal Adenocarcinoma via PP2A Inhibition

city: Göttingen

first: Nignjun

last: Duan

address: Robert-Koch-Straße 40

country: Germany

institute: Universitätsmedizin Göttingen

summary: Pancreatic ductal adenocarcinoma (PDAC) remains a therapeutic challenge, with the aggressive basal-like/mesenchymal subtype demonstrating pronounced resistance to current standard-of-care chemotherapy. Novel, targeted therapeutic strategies are urgently needed to improve outcomes for these patients. Leveraging CRISPR-Cas9 screens, we identified PP2A’s catalytic subunit, PPP2CA, as a relevant PDAC target. Pharmacological PP2A inhibition (PP2Ai) selectively impaired mesenchymal PDAC growth. To delineate the molecular mechanisms underlying PP2Ai sensitivity, we employed a dual-pronged strategy. Functional characterization of mesenchymal PDAC cells revealed metabolic reprogramming, marked by suppressed oxidative phosphorylation and heightened autophagy, coupled with endoplasmic reticulum stress and subsequent apoptosis induction upon blockade of PP2A. Genome-wide CRISPR screens identified key genetic modifiers of PP2Ai sensitivity, revealing critical roles for transcriptional regulators, mRNA processing, translation, and metabolic pathways. Guided by human expression data implicating PP2A in splicing and transcriptional regulation, we prioritized these interconnected processes for orthogonal validation. Mesenchymal PDAC cells exhibited significantly enhanced splicing following PP2Ai treatment, with skipped exons (SE) representing the most prominently altered splicing event. Notably, we identified enhanced transcriptional elongation upon PP2A inhibition, particularly of short genes, driven by CDK9. Our findings establish a reciprocal regulatory relationship between PP2A and CDK9 that controls the activation of ER stress response factors, particularly the key transcriptional regulator ATF4. Our findings establish PP2A as a promising therapeutic target in mesenchymal PDAC and reveal its critical role in regulating transcriptional elongation. These insights enable both the precise application of PP2A inhibitors and the development of rational combination therapies.

overall_design: RNA profiling of MIAPaCa-2 cells, which were genetically modified by Cas13-based RNA-targeting of PPP2R1A. The control cell line expresses the CasRx enzyme without a guide RNA.


title: Single-cell multiomic approaches define a gradual, spatially-regulated epigenetic and transcriptional transition from embryonic to adult neural stem cells [Multiomic]

type: Genome binding/occupancy profiling by high throughput sequencing

overall_design: Multiomic (paired single-nucleus RNA sequencing and single-nucleus ATAC sequencing) data generated from the ventricular-subventricular zone (V-SVZ) across perinatal timepoints (E14, E17, P2).


title: Single-cell multiomic approaches define a gradual, spatially-regulated epigenetic and transcriptional transition from embryonic to adult neural stem cells [scRNA-seq]

overall_design: Single-cell RNA sequencing (scRNA-seq) was performed on the cortex, including the dorsal ventricular-subventricular zone (V-SVZ), at E18, as well as the dorsal and lateral V-SVZ at P2. P2 samples were generated from Emx1-Cre;R26-Eyfp mice, where cortically derived cells are labeled by Eyfp. Together, and in combination with previously published scRNA-seq from our lab, these samples seek to characterize the dorsal V-SVZ across the perinatal period.


title: scRNAseq data of WT mouse liver portal mesenchymal cells

city: Paris

first: Wenrui

last: Gao

address: 27 rue Chaligny

country: France

institute: Centre de Recherche Saint Antoine

summary: We employed single cell sequencing approach using 10× Genomics scRNAseq to study fibroblasts in mouse liver portal area. We isolated portal mesenchymal cells from WT mouse liver tissue to identify and characterize portal fibroblasts.

overall_design: The process began by extracting the bilio-vascular tree and enzymatically digesting it to obtain a single-cell suspension. We then enriched for mesenchymal cells by excluding those expressing lineage markers which are EpCAM, CD31, CD45, and CD11b.

first: Thierry

last: Jaffredo

first: Axelle

last: Cadoret

first: Nicolas

last: Chignard

first: Chantal

last: Housset


title: Analyzing the effects of growth factors and extracellular matrix on gene expression in three-dimensional cultured bovine uterine gland fragments

city: Okayama

first: Yosuke

last: Sugino

address: 1-1-1, Tsushimanaka, Kita-Ku

institute: Okayama University

summary: In the endometrium, growth factors and the extracellular matrix (ECM) contribute to gene expression profiles of cells and tissues, as well as to associated morphological changes and their maintenance. Here, we report the effects of growth factors and ECM on the gene expression profiles of three-dimensionally (3D) cultured bovine uterine gland fragments. Bovine uterine gland fragments cultured in Matrigel (M) in the presence of epidermal growth factor (EGF) exhibited altered expression of genes associated with cell proliferation and ECM ligand–receptor interactions compared with those cultured in the absence of EGF. In contrast, under EGF-supplemented conditions, bovine uterine gland fragments cultured in Matrigel mixed with type I collagen showed minimal changes in gene expression compared with those cultured without type I collagen. Collectively, these data show that growth factors and ECM differentially influence gene expression profiles in 3D-cultured bovine uterine gland fragments, with growth factors exerting a more pronounced effect than ECM.

overall_design: RNA-seq profiling of 3D-cultured bovine uterine gland fragments cultured for 5 days in the presence or absence of EGF and with or without type I collagen.

first: Rei

last: Ichikawa

first: Shuichi

last: Matsuyama

first: Yuki

last: Yamamoto

first: Kohei

last: Kawano

first: Koji

last: Kimura


title: Investigate changes in gene expression and enriched pathways in endothelial cells following Liver endothelial Heg1 knockout.

city: Tianjin

first: Min

last: Zheng

state: Tianjin

address: Xinxing Street

department: School of Basic Medical Sciences

institute: Tianjin Medical University

summary: Knockout of Heart-of-glass (Heg) in liver endothelial cells alters the metabolic patterns of hepatocytes. To further investigate whether endothelial cells regulate hepatocyte function and gene expression patterns by secreting certain proteins or factors mediated by Heg1, we collected mice at postnatal days 3 (P3) and 42 (P42), isolated liver endothelial cells, and performed RNA-seq analysis to explore the interaction patterns between endothelial cells and hepatocytes.

overall_design: Endothelial cells were isolated from the liver of P3/P42 mice by enzymatic digestion combined with magnetic-activated cell sorting (MACS) for RNA sequencing (RNA-seq).

first: Xiyun

last: Rao

first: Shichao

last: Zhu


title: RNA-seq technique to identify key differentially expressed genes in hepatocytes of HFD-treated Lyve1-Cre;Heg1fl/fl mice.

summary: Heart-of-glass (Heg) is a type I transmembrane protein. Previous studies have demonstrated that knockout of the Heg1 gene in mouse liver endothelial cells disrupts hepatic metabolic zonation by downregulating Wnt ligands in endothelial cells. To further investigate the metabolic changes in hepatocytes, alterations in Wnt receptor genes, and other potential genetic changes following endothelial-specific Heg1 knockout in mice with hepatic steatosis, this study was conducted.


title: Mouse retina CUT&Tag for ATF4 and BACH1 proteins.

city: Bethesda

first: Matthew

last: Brooks

state: MD

address: 6 Center Dr Bldg 6, Rm 303

department: NEI

institute: NIH

summary: ATF4 and BACH1 binding sites determinied from mouse rod photoreceptors.

overall_design: NRL-GFP mice of age 1.8-months old were used to obtain flow-sorted rod photoreceptors for input into CUT&Tag using antibodies against ATF4 and BACH1. Three biological replicates were used per each antibody.

first: Kiam

last: Preston Jr

first: Madhuri

last: Arya

first: Anjani

last: Kumari

first: Jacob

last: Nellissery

first: Zachary

last: Batz

first: Xulong

last: Liang

first: Gianluca

last: Tosini

first: Anand

last: Swaroop


title: Exceeding Conventional Maximum Carbon Yields via Heterotrophic CO2 Fixation

city: Incheon

first: Hyungyu

last: Lim

address: Inha ro 100

institute: Inha University

summary: Maximizing carbon yields is crucial in the microbial production of diverse biochemicals. However, microorganisms, particularly heterotrophs, release carbon dioxide (CO2) during the oxidation of organic compounds for energy and building blocks. This metabolism limits the theoretical maximum carbon yield and constrains the development of efficient microbial cell factories. Specifically, metabolite production from tricarboxylic acid (TCA)-cycle intermediates involves major CO2 emission steps, leading to unavoidable carbon loss. In the present study, the metabolic pathway in Escherichia coli, a model heterotroph, was synthetically rewired to facilitate CO2 fixation and maximize carbon yields. Specifically, we blocked multiple routes to prevent pyruvate oxidation to acetyl-CoA, which was identified as a major CO2 emission step, and promoted CO2 incorporation into TCA cycle intermediates by reengineering endogenous pathways. This strategy was applied to produce itaconate, a promising bioplastic precursor, achieving a notable itaconate yield of 0.86 C mol/C substrate mol, exceeding the conventional maximum carbon yield of 0.83 C mol/C mol. This heterotrophic CO2 fixation strategy can be used to produce TCA-derived chemicals and enhance the economic viability of microbial production.

overall_design: Total RNA samples were extracted by cell pellets harvested at 24 h and stabilized by using RNAprotect Reagents from Qiagen (Hilden, Germany).

first: Hyun Gyu

first: Gyoo Yeol

last: Jung


title: Mouse retina scRNA in Atf4 and Bach1 knock-down

summary: Gene expression of single cells from mouse retina in knockdown using shRNA of Atf4 and Bach1.

overall_design: Newborn CD-1 mice were subretianlly injected with cocktails of Nrlp-EGFP plasmid and shRNA directed against Atf4 or Bach1. Injected plasmid of Nrlp-EGFP and uninjected retina were used for controls. Mouse retinas aged post-natal day 21 were used to generate scRNA profiles. Dissociated GFP-positive retina punches were used as input into 10x Genomics Single Cell 3' v3.1.


title: Temporal Transcriptomic Profiling Identifies Core Regulators in Cytokine-Induced Gut Barrier Disruption in Differentiated Caco-2 Cells

city: Newton

first: Matt

last: Kanke

state: MA - Massachusetts

address: 112 Harding Street

institute: Amgen

summary: The intestinal epithelial barrier is a primary governor for gut homeostasis, and its disruption is a critical factor in the pathogenesis of many inflammatory diseases including Inflammatory Bowel Diseases (IBD). Although strategies to restore and enhance barrier function have been proposed as promising therapeutic approaches for treating inflammation-associated intestinal disorders, most therapies in development act on immune-cell response dampening rather than directly reinforcing epithelial function.

overall_design: Comparison of transcriptomics across time line with or without stimulation of inflammatory response.

first: Cheng-Yuan

last: Kao

first: Hyo Shin

last: Yoon

first: Chi-Ming

last: Li

first: Shining

last: Ma

first: Xin

last: Lou


title: Gene expression of Cupriavidus necator H16 in response to itaconic acid, methylsuccinic acid, and mesaconic acid

city: Kaunas

first: Naglis

last: Malys

address: Radvilenu st. 19

country: Lithuania

institute: Kaunas University of Technology

summary: The genome of Cupriavidus necator H16 encodes multiple homologous enzymes predicted to be involved in itaconic acid metabolism. Here, we performed RNA-seq analysis to identify genes and gene clusters that are differentially expressed in response to itaconic acid, as well as the metabolically related compounds methylsuccinic acid and mesaconic acid.

overall_design: RNA-seq profiling of exponentially growing wild-type H16 cells cultivated in gluconate minimal medium, six hours after supplementation with itaconate, methylsuccinate, and mesaconate.

first: Erik

last: Hanko


title: Induced osteogenic transdifferentiation reprograms malignant phenotypes in pancreatic ductal adenocarcinoma

city: Heidelberg

first: Gong

last: Chen

state: Baden-Württemberg

address: Im Neuenheimer Feld 420

department: Department of General, Visceral & Transplant Surgery

institute: University of Heidelberg

summary: This study characterizes transcriptional changes associated with osteogenic induction in pancreatic ductal adenocarcinoma (PDAC) cell lines. Capan-2 and PANC-1 cells were cultured under control conditions or osteogenic induction and collected at day 0, day 7, and day 14. Bulk RNA sequencing was performed to identify gene expression dynamics during osteogenic reprogramming. Analyses revealed activation of osteogenic markers and related pathways, along with suppression of cell-cycle programs. These datasets provide a transcriptomic framework for understanding osteogenic plasticity in PDAC cells.

overall_design: Bulk RNA-seq was performed on Capan-2 and PANC-1 cells under control or osteogenic induction at three time points (0, 7, and 14 days), with three biological replicates per condition. Libraries were prepared using poly-A selection and sequenced on an Illumina platform. Differential expression and pathway analyses were conducted to evaluate transcriptional changes during osteogenic induction.


title: Transcriptomic Profiling Identifies the Cyclin D–CDK4/6 Axis as a Druggable Mediator of Cisplatin Resistance in Bladder Cancer [RNA-seq]

city: Taipei

first: Tsung-Han

last: Hsieh

address: XinYi dist.,WuXing Street, No.250.

country: Taiwan

institute: Taipei Medical University

summary: Purpose Cisplatin resistance remains a critical challenge in bladder cancer (BC). This study aimed to define molecular drivers of cisplatin resistance and to assess potential therapeutic targets that may help restore treatment responsiveness. Methods Integrative transcriptomic analyses were performed using The Cancer Genome Atlas (TCGA) cohort to compare cisplatin non-responders with responders, alongside a cisplatin-resistant BC cell model to identify dysregulated pathways. Functional studies, including siRNA-mediated knockdown, SRB viability assays, flow cytometry, western blotting, and microarray-based transcriptomics, were used to characterize the dysregulated pathways. Results Both TCGA data and resistant BC cells exhibited upregulation of CCND1 and enrichment of E2F target genes. Silencing of Cyclin D1 restored cisplatin sensitivity in resistant cells. Abemaciclib selectively inhibited proliferation of cisplatin-resistant BC cells, reduced RB phosphorylation, induced sub-G1 accumulation, and suppressed expression of key regulators of cell-cycle progression and homologous recombination repair. Combined treatment with abemaciclib and cisplatin synergistically suppressed the proliferation of cisplatin-resistant BC cells in vitro and resulted in significantly greater tumor growth inhibition in an RT112 xenograft model in vivo. Conclusion Activation of the Cyclin D1/CDK4/6–E2F axis is a key driver of cisplatin resistance and demonstrate that CDK4/6 inhibition reduces proliferative capacity and DNA repair competency while enhancing cisplatin responsiveness. Targeting this pathway represents a rational therapeutic strategy for advanced or refractory BC.

overall_design: NTUB1 (a high-grade urothelial carcinoma cell line) and its corresponding cisplatin-resistant subline N/P(14) were used as representative models for cisplatin-sensitive and resistant BC cell lines, respectively. To analyze the possible mechanism underlying cisplatin-resistance in BC cells, DSGs between N/P(14) and NTUB1 cells were analyzed by RNA-seq and bioinformatics analysis.

first: Chun-Han


title: Transcriptomic Profiling Identifies the Cyclin D–CDK4/6 Axis as a Druggable Mediator of Cisplatin Resistance in Bladder Cancer [array]

summary: Purpose  Cisplatin resistance remains a critical challenge in bladder cancer (BC). This study aimed to define molecular drivers of cisplatin resistance and to assess potential therapeutic targets that may help restore treatment responsiveness.  Methods  Integrative transcriptomic analyses were performed using The Cancer Genome Atlas (TCGA) cohort to compare cisplatin non-responders with responders, alongside a cisplatin-resistant BC cell model to identify dysregulated pathways. Functional studies, including siRNA-mediated knockdown, SRB viability assays, flow cytometry, western blotting, and microarray-based transcriptomics, were used to characterize the dysregulated pathways.   Results  Both TCGA data and resistant BC cells exhibited upregulation of CCND1 and enrichment of E2F target genes. Silencing of Cyclin D1 restored cisplatin sensitivity in resistant cells. Abemaciclib selectively inhibited proliferation of cisplatin-resistant BC cells, reduced RB phosphorylation, induced sub-G1 accumulation, and suppressed expression of key regulators of cell-cycle progression and homologous recombination repair. Combined treatment with abemaciclib and cisplatin synergistically suppressed the proliferation of cisplatin-resistant BC cells in vitro and resulted in significantly greater tumor growth inhibition in an RT112 xenograft model in vivo.  Conclusion  Activation of the Cyclin D1/CDK4/6–E2F axis is a key driver of cisplatin resistance and demonstrate that CDK4/6 inhibition reduces proliferative capacity and DNA repair competency while enhancing cisplatin responsiveness. Targeting this pathway represents a rational therapeutic strategy for advanced or refractory BC.

overall_design: N/P(14) cells were treated with Abemaciclib (0.625 M) for 24 h, and total RNA was isolated for microarray analysis.


title: High-throughput sequencing of chemosensitive small cell lung cancer cell lines H82 and DMS114, and their corresponding chemoresistant counterparts

city: Guangzhou

first: Qiong

last: Lyu

state: Guang Dong

address: 253 GongYe Road

department: Oncology

institute: Zhujiang Hospital, Southern Medical University

summary: Small cell lung cancer (SCLC) is the most aggressive subtype of lung cancer. Although most patients are initially sensitive to first-line chemotherapy with combined cisplatin and etoposide, chemotherapy drug resistance easily develops and quickly leads to tumor progression. Therefore, understanding the mechanisms of chemotherapy drug resistance and how to reverse it is key to improving the prognosis of patients with SCLC. The parental SCLC cell lines H82 and DMS114, along with their corresponding cisplatin-induced resistant counterparts (H82DDP and DMS114DDP), were used to explore the mechanisms of chemoresistance in SCLC.

overall_design: Total RNA was isolated from SCLC cell lines H82, H82DDP, DMS114, and DMS114DDP to construct libraries for sequencing. Subsequently, differential expression analysis was conducted to identify genes related to chemoresistance.

first: Haoxuan

last: Ying

first: Huiying

last: Liu


title: Multiomic analysis of equine aging-related osteoarthritis highlights gut microbiome and metabolomic alternations

city: Fort Collins

first: Steven

last: Dow

state: CO

address: 300 W Drake Rd

department: Clinical Sciences

institute: Colorado State University

summary: Aging-related osteoarthritis (OA) is a leading cause of lameness and reduced performance in horses. Mounting evidence in humans and laboratory species indicates both systemic and local inflammation play a role in OA pathogenesis, with increasing recognition that the gut microbiome contributes to a pro-inflammatory state. However, the role of the gut-joint-axis has not been fully explored in etiopathogenesis of equine OA. Therefore, the aim was to investigate fecal and leukocyte microbiome profiles and host gene expression patterns in horses with naturally occurring aging-related OA compared to controls.

overall_design: We analyzed samples from a total of 90 horses (31 OA, 59 controls). Fecal (31 OA, 35 controls) and peripheral blood mononuclear cell (PBMC) samples (20 OA, 32 controls) were collected for 16S rRNA sequencing. PBMC were collected for mRNA sequencing (20 OA, 39 controls). Metabolomics were performed on paired feces and serum samples (10 OA, 10 controls). Microbial community differences were analyzed using alpha/beta diversity metrics and differential taxonomic abundance. Differential gene expression and pathway enrichment were assessed via RNAseq using PBMCs. Targeted metabolomics were performed using rapid LC-MS analysis. Aged OA horses displayed alterations in fecal and PBMC microbiomes

first: Lyndah

last: Chow

first: Lynn

last: Pezzanite


title: CQMUH-011 mitigated LPS-induced acute lung injury in neonatal rabbits

first: Yaling

last: Xu

address: Jinsui Road 9

institute: Guangzhou Women and Children's Medical center

summary: Background: Neonatal sepsis-associated acute lung injury (ALI) is a therapeutic challenge. This study evaluated the efficacy of CQMUH-011, a novel small-molecule compound, against lipopolysaccharide (LPS)-induced ALI in neonatal rabbits. Methods: Neonatal rabbits at postnatal age 5-7 days were intraperitoneally injected with LPS (50 mg/kg) to induce ALI, and subsequently treated with CQMUH-011 at  675 μg/kg at 0.5 hour. Outcomes within 10-hour of observation were assessed through survival analysis, neurobehavioral assessment, blood gas, histopathological scoring, alveolar phospholipid quantification in bronchoalveolar lavage fluid, RT-PCR for inflammatory mediators and surfactant proteins, and gene expression profiles through transcriptomic analysis. Results: LPS administration induced severe ALI characterized by metabolic acidosis, hypoxemia, lung inflammatory injury, neuromotor dysfunction, and mortality. CQMUH-011 improved neurological deficits, restored blood gas balance, enriched phospholipid pool, reduced lung injury scores, diminished leukocyte infiltration and improved alveolar expansion. RT-PCR results showed significantly mitigated mRNA expressions of proinflammatory cytokines and enhanced surfactant proteins and phospholipid synthesis-associated enzymes.  Transcriptomic analysis revealed the dual mechanism of CQMUH-011 by downregulating multiple inflammatory pathways, including cytokine-cytokine receptor interaction, T-helper 17 cell differentiation, interleukin-17 and nuclear transcription factor-kappa B, tumor necrosis factor-α, concurrent with activation of phosphatidylinositol 3-kinase/protein kinase B-dependent cytoprotection, cytoskeletal remodeling, and intercellular junction reinforcement. Conclusions: CQMUH-011 exerts potent anti-inflammatory and lung-protective effects in neonatal ALI by modulating critical inflammatory and repair pathways, making it a promising therapeutic candidate for sepsis-associated ALI.

overall_design: Neonatal rabbits were randomly selected to receive saline, LPS (50 mg/kg), or LPS with CQMUH-011 (675 ug/kg) treatment via intraperitoneal injections. Right lung samples from animals in the Saline, LPS and LPS-011-675 groups (3-4 samples in each group) were randomly chosen for transcriptomic analysis.

first: Xiaojing

last: Guo

first: Xiao

last: Han

first: Xiangnan

last: Hu

first: Bin

last: Gao

first: Bo

last: Sun

first: Huayan

last: Zhang


title: Rewiring Oncogenic Transcriptional Complexes with Domain-ALTeration Chimeras (DALTACs) in Prostate Cancer [RNA-seq]

city: Ann Arbor

first: Arul

last: Chinnaiyan

state: MI

address: 1500 East Medical Center Dr

department: MCTP

institute: University of Michigan

summary: Transcriptional addiction to the androgen receptor (AR) underlies metastatic castration-resistant prostate cancer (mCRPC), where AR maintains oncogenic enhancer programs through dynamic, domain-specific interactions with the lysine acetyltransferase p300 and associated cofactors. Here, we describe a mechanistically distinct therapeutic modality, Domain-ALTeration Chimeras (DALTACs), designed to rewire endogenous protein complexes by enforcing non-native domain–domain interactions rather than degrading or inhibiting individual components. Our first-in-class molecule, AR–p300 DALTAC-1, induces a synthetic proximity between the AR ligand-binding domain and the p300 bromodomain, thereby misconfiguring the native AR–p300 interface and locking the complex into a non-productive, transcriptionally inert state. DALTAC-1 triggers a profound “super-inhibitory” effect, suppressing AR-driven transcription and proliferation more potently than combined AR and p300 inhibition. Mechanistically, DALTAC-1 reprograms the substrate specificity of p300, extinguishing the enhancer-associated histone mark H2B N-terminal acetylation (H2BNTac) while inducing neomorphic acetylation of AR and SRC2/3, culminating in collapse of the AR neo-enhanceosome. Chromatin profiling revealed widespread redistribution of AR and p300 toward canonical palindromic AREs, coupled with attenuation of ERG/BRD4 recruitment and a near-complete loss of histone H2BNTac acetylation and RNA polymerase II loading at oncogenic AR/ERG neo-enhancers. Strikingly, DALTAC-1 exhibits exquisite lineage selectivity, displaying potent activity in AR-positive prostate cancer cells and patient-derived organoids while sparing AR-negative or non-prostate lineages. In multiple in vivo models, including castration-resistant and patient-derived xenograft tumors, DALTAC-1 induces deep and durable tumor regressions with favorable tolerability. Together, these findings establish DALTACs as a universally applicable strategy to rewire disease-defining protein complexes by altering their domain topology, expanding the conceptual and therapeutic landscape of induced proximity agents. The precision and lineage-selective action of DALTAC-1 highlight its strong translational potential for treating AR-driven prostate cancer.

overall_design: VCaP cells were treated with DMSO, 100nM DALTAC-1 or combo of p300 inhibitor and AR inhibitor for 4, 12 and 24 hours then RNA-seq were performed.

first: Jie

last: Luo

first: Jocelyn

last: Cai

first: Kenneth

last: Gu

first: Eleanor

last: Young


title: Transcriptomic profiling of young, replicative senescent, and premature senescent HUVECs

city: Kyoto

first: Tomoya

last: Kitani

address: 465 Kajii-cho Kawaramachi-Hirokoji Kamigyo-ku

institute: Kyoto Prefectural University of Medicine

summary: This study compares global gene expression profiles of human umbilical vein endothelial cells (HUVECs) under three conditions: young, replicative senescent, and premature senescent states. RNA sequencing was performed to identify transcriptional changes associated with endothelial aging. The dataset provides gene-level counts and processed expression matrices for downstream analysis.

overall_design: Bulk RNA sequencing of HUVECs under three conditions: young (passage 4-5), replicative senescent (passage 17-20), and premature senescent induced by TRF2 dominant-negative overexpression. Three biological replicates were analyzed for each condition (total n = 9).

first: Koji

last: Ikeda


title: Single-cell RNA sequencing of stem cell–like memory T (Tscm) cells from rheumatoid arthritis patients and healthy controls

city: Seoul

first: Eun Bong

last: Lee

address: 101 Daehak-ro, Jongno-gu

institute: Seoul National University Hospital

summary: Stem cell–like memory T (Tscm) cells are a subset of T cells with self-renewal capacity and multipotent differentiation potential upon antigen stimulation. Tscm cells have been implicated in the pathogenesis of autoimmune diseases. In this study, we performed single-cell RNA sequencing using the 10x Genomics platform on Tscm cells enriched by fluorescence-activated cell sorting (FACS). Our objective was to characterize the transcriptomic signatures of Tscm cells in patients with rheumatoid arthritis (RA) and to identify disease-specific features that may contribute to RA pathogenesis and progression.

overall_design: Following peripheral blood mononuclear cells (PBMCs) isolation from healthy control and rheumatoid arthritis (RA) patients, CD3+CCR7+CD45RA+CD27+CD95high Tscm cells were sorted by fluorescence-activated cell sorting (FACS) and analyzed using scRNA-seq.

first: Seojin

last: Yang


title: Single-cell transcriptomic profiling of Hulunbuir short-tailed sheep and Hu sheep embryos at E16 and E19 reveals T gene mutation-mediated regulatory mechanisms underlying tail length phenotype

city: Inner Mongolia

first: Hong

last: Su

state: Inner Mongolia

address: No. 306, Zhaowuda Road, Saihan District, Hohhot, Inner Mongolia Autonomous Region

institute: Inner MongoliaAgricultural University

summary: This study presents a comprehensive single-cell RNA sequencing (scRNA-seq) atlas of embryonic development in two distinct Chinese sheep breeds: the cold-adapted Hulunbuir short-tailed sheep (HSTS) and the heat-tolerant Hu sheep (HS). We profiled embryos at two critical developmental timepoints—16 and 19 days post-insemination—to investigate the cellular heterogeneity and molecular mechanisms underlying tail length dimorphism. Our analysis identified 12–15 distinct cell types across samples and revealed MDK_ITGA6+ITGB1 as a central ligand-receptor pair in intercellular communication. We observed that HSTS embryos exhibit premature degeneration of the apical ectodermal ridge (AER), driven by a loss-of-function mutation in the T gene (c.G334T), which dysregulates BMP and FGF signaling pathways. Functional validation in a T mutant mouse model confirmed the role of this mutation in tail shortening. These findings provide insight into the genetic and cellular basis of adaptive tail morphology and offer potential targets for livestock breeding.

overall_design: Organism: Ovis aries (sheep)  Sample types: Whole embryos at E16 and E19 days post-insemination  Breeds: Hulunbuir short-tailed sheep (HSTS) and Hu sheep (HS)  Sample breakdown:  1  E19 of HSTS embryo  3  E16 of HS embryos  1  E19 of HS embryo  HSTS E16 of HSTS scRNA-seq data were obtained from GEO (publicly available) Single-cell processing: Embryos were dissociated using collagenase II/IV, filtered through 70μm and 40μm strainers, and counted using Countstar. Approximately 17,000 cells were loaded per sample on the 10x Chromium Controller (v3.1 chemistry).  Library preparation: Libraries were constructed using the Single-Cell 3′ Reagent Kit v3.1 and sequenced on Illumina NovaSeq 6000 with 150 bp paired-end reads.  Data processing: Raw sequencing data were aligned to the Ovis_aries_genome_v1.0 using Cell Ranger v6.1.2. Downstream analysis was performed in R with Seurat v4.1.1, including normalization, clustering, UMAP projection, and differential expression analysis.  Additional analyses: Cell-cell communication (CellChat), pseudotime trajectory (Monocle), and transcription factor regulatory networks (SCENIC) were applied to investigate developmental dynamics and T gene regulatory mechanisms.  Validation: Genotyping and RT-qPCR were performed on sheep and mouse embryos to confirm T gene mutation and expression patterns of key genes (T, WNT5B, FGF8, etc.).

first: Guifang

last: Cao


title: Bulk RNA-seq of EO771 tumor sample Gq_DREADD vs. Ctr

city: Cold Spring Harbor

first: Yue

last: Wu

address: One Bungtown Rd, Demerec RM 120

department: Cancer and Neuroscience

institute: Cold Spring Harbor Laboratory

summary: Bulk RNA-seq was performed to compare mRNA expression in EO771 murine breast tumors between tumors expressing a Gq-DREADD driven CRH-neuron activation paradigm (DCZ injection at in-phase ZT10.5) and matched controls receiving PBS. The goal is to identify transcriptional programs in the tumor that are altered downstream of CRH-neuron activation (acute transcriptional responses, immune/tumor cell signaling, and pathway changes) and generate data suitable for differential expression, pathway enrichment, and hypothesis generation for follow-up functional work.

overall_design: RNA-seq profiling of two experimental groups: (1) Gq_DREADD + DCZ (in-phase ZT10.5) — animals bearing EO771 tumors with DREADD activation (DCZ injection given at zeitgeber time 10.5). (2) Control (PBS) — matched EO771 tumor animals receiving PBS at the same circadian time. Biological replicates: n = 4 independent tumor samples per group. Randomization: allocate animals to groups randomly and process samples in interleaved order to avoid batch confounding. Blinding: perform RNA extraction and library prep with the operator blinded to group where possible.

first: Elena

last: Ghiban

first: Adrian

last: Gomez

first: Jeremy

last: Borniger


title: Endothelial AGO1 Deficiency Reduces Breast Cancer Burden in Mice

city: Duarte

first: Zhen

last: Chen

address: 1500 E Duarte Rd

department: DMRI

institute: City of Hope

summary: Endothelial cells are crucial in cancer development and progression, in part through tumor angiogenesis and immune modulation. As a key component of RNA-induced silencing complex, Argonaute 1 (AGO1) protein has been shown to regulate tumor biology. However, its role in ECs within the tumor microenvironment remains undefined. In this study, we investigated the effects of EC-conditional AGO1 knockout (EC-AGO1-KO) on tumor vascularization and immune regulation in a mouse xenograft breast cancer model. EC-AGO1-KO developed significantly reduced tumor burden when compared to their wild-type littermates. The tumor suppression was accompanied by lower tumor vascularization and stronger immune infiltration. Histological and single cell RNA sequencing analysis revealed that tumors in the EC-AGO1-KO mice exhibited increased CD8⁺ T cells and macrophages, reflecting a pro-immunostimulatory microenvironment. In vitro experiments show that EC-AGO1-knockdown (AGO1-KD) conditioned media suppresses breast cancer cell migration, attendant with the downregulation of C-X-C chemokine receptor type 4 (CXCR4) and upregulation of RUNX1 Partner Transcriptional Co-Repressor 1 (RUNX1T1). These findings suggest that EC-AGO1 plays a crucial role in regulating tumor angiogenesis and immune cell infiltration, thereby influencing tumor progression. Targeting EC AGO1 may offer a novel therapeutic strategy for disrupting tumor vascularization while enhancing anti-tumor immunity.

overall_design: WT and KO littermates were injected with E0771 breast cancer cells into the fourth mammary fat pad of 16 week old female mice. After 21 days, tumors were removed and single-cell susensions were prepared via enzymatic suspension and analyzed using scRNAs-seq.

last: Bouman Chen

first: Xuejing

last: Liu

first: Alonso

last: Tapia

first: Yingjun


title: Bulk RNA-seq of CRH neuron_Ctr vs Tumor

summary: Bulk RNA sequencing was performed on fluorescence-activated cell sorting (FACS)-isolated CRH-expressing neurons from the hypothalamus of control and EO771 tumor-bearing mice. The objective was to determine how breast tumor development influences transcriptional programs in CRH neurons, including acute stress-related signaling, immune-neuroendocrine communication, and downstream pathway alterations. These datasets are intended for differential gene expression analysis, pathway enrichment, and hypothesis generation for future functional validation.

overall_design: RNA-seq profiling of two experimental groups: (1) Control: FACS-isolated CRH neurons from no tumor mice. (2) Tumor-bearing: FACS-isolated CRH neurons from mice with EO771 tumors. Biological replicates: n = 2 independent samples per group. Randomization: allocate animals to groups randomly and process samples in interleaved order to avoid batch confounding. Blinding: perform RNA extraction and library prep with the operator blinded to group where possible.


title: P4HA3 drives cervical cancer lymphatic metastasis by facilitating ACLY-mediated ferroptosis resistance [HeLa, SiHa]

first: Li

last: Yuan

address: 58, Zhongshan 2nd road

institute: sun yat-sen university

summary: The lymph node is the most common site of distant metastasis of cervical cancer (CCa), which elicits dismal prognosis and limited efficiency for treatment. Identification of the factors contributing to CCa lymphatic metastasis is needed to develop effective prevention and treatment strategies. Here, we found upregulation of prolyl 4-hydroxylase subunit alpha 3 (P4HA3), an α-subunit of prolyl hydroxylase, in lymphatic metastatic lesions of cervical cancer, which is strongly associated with poor prognosis. In vitro and in vivo experiments showed that P4HA3 promoted CCa lymphatic metastasis by conferring ATP-citrate lyase (ACLY)-mediated ferroptosis resistance. Mechanistically, P4HA3 stabilizes ACLY protein by competitively inhibiting its interaction with the E3 ubiquitin ligase UBR4, which prevents UBR4-mediated proteasomal degradation of ACLY. ACLY-derived acetyl-CoA enhances H3K27 acetylation (H3K27Ac) modification level in the promoter of SLC7A11 gene, ultimately enhancing SLC7A11 transcription and ferroptosis resistance. Collectively, our study provides a mechanistic understanding of the interplay between ferroptosis resistance and lymph node metastasis, providing a possibility to combat lymph node metastasis in cervical cancer.

overall_design: RNA-seq profiling of highly lymph node metastatic cervical cancer cell lines (HeLa LNM2 and SiHa LNM2) and their parental conteraparts (HeLa PR and SiHa PR)

first: Hongye

last: Jiang

first: Meng

last: Xia

first: Junxiu

first: Shuzhong

last: Yao

first: Chunyu

last: Zhang


title: NDUFS6 promotes neuroblastoma progression and represents a potential therapeutic target

city: Shanghai

first: rui

last: Dong

address: 399 Wan Yuan Road

institute: Department of Pediatric Surgery, Children’s Hospital of Fudan University, and Shanghai Key Laboratory of Birth Defect

summary: Active oxidative phosphorylation is increasingly recognized as a defining metabolic feature of high-risk neuroblastoma (NB). NDUFS6, an essential subunit of mitochondrial respiratory chain complex I, plays a critical role in sustaining oxidative phosphorylation. Nevertheless, its precise contribution to NB pathogenesis and progression remains largely undefined. We found NDUFS6 expression was significantly upregulated in high-risk NB and was positively associated with disease progression and poor prognosis. Functional assays revealed that NDUFS6 knockdown suppressed proliferation, invasion, and migration of NB cells, whereas its overexpression promoted these malignant behaviors. Transcriptomic analysis revealed that high NDUFS6 expression activated pathways related to energy metabolism and ATP synthesis, while concurrently suppressing neuronal differentiation and immune activation. Structure-based virtual screening identified several candidate inhibitors of NDUFS6, including guanosine 5′-triphosphate, 1,4-β-D-xylopentaose, and deferoxamine. Subsequent drug sensitivity assays demonstrated that guanosine 5′-triphosphate exerted potent inhibitory effects in both MYCN-amplified and non-amplified NB cell lines. These findings underscore the oncogenic role of NDUFS6 and highlight its potential as a therapeutic target for precision treatment in high-risk NB.

overall_design: SK-N-BE(2) and SH-SY5Y cell lines with NDUFS6 overexpression or knockdown were generated to conduct functional assays. Transcriptomic alterations induced by NDUFS6 modulation were profiled by RNA sequencing.

first: Enqing

last: Zhou

first: Xiaoran

last: Du

first: Deqian

first: Shuyang

last: Dai

first: Yong

last: Zhan

first: Yi

last: Li

first: Yifei

last: Lu

first: Lian

first: Kuiran

first: Ran

first: Rui


title: Transcriptome analysis of CMK cells with DLK1 knockout

city: Wilmington

first: Anilkumar

last: Gopalakrishnapillai

state: DE

address: 200 Powder Mill road

institute: Nemours Children's Health

summary: We recently identified DLK1 as a new target in Down syndrome associated myeloid leukemia. We generated CMK cells with CRISPR/Cas9 mediated knockout of DLK1 and performed transcriptome analysis to understand the changes in gene expression profiles following loss of DLK1.

overall_design: Transcriptome profiles in DLK1-KO cells in comparison with parental CMK cells.

first: Sonali

middle: P

last: Barwe

first: Joshua

last: Faust


title: Single-cell RNA sequencing of orthotopic pancreasic cancer reveals characterization of tumor microenvironment by treatment of anti-VSIG4 antibodies in KPC cell transplantation mouse model

city: Chengdu

first: Guoling

last: Huang

address: No. 4, Section 2, North Jianshe Road

institute: University of Electronic Science and Technoloogy of China

summary: Immune checkpoint blockade (ICB) therapies, such as PD-1/PD-L1 inhibitors, have revolutionized cancer treatment by reactivating exhausted T cells. However, their efficacy varies substantially among tumor types and is particularly limited in immunologically “cold” malignancies such as pancreatic ductal adenocarcinoma. These tumors exhibit minimal T-cell infiltration and a profoundly immunosuppressive tumor microenvironment (TME), leading to poor responses to ICB. VSIG4 is a B7-related transmembrane protein highly expressed by tissue-resident macrophages. Previous studies have shown that VSIG4 suppresses proinflammatory macrophage polarization by modulating pyruvate metabolism and enhances M2-like states via lactate-STAT3 signaling and fatty acid oxidation. VSIG4 also inhibits T-cell activation and proliferation, making it a candidate immune checkpoint molecule. Recent work has linked VSIG4⁺ tumor-associated macrophages to T-cell suppression and therapeutic resistance in multiple cancers, although the identity of the T-cell receptor for VSIG4 remains unknown. So we demonstrate that VSIG4 binds SLC3A2 to suppress Gln uptake and disrupt ion homeostasis, thereby impairing T-cell activation. Antibody-mediated VSIG4 blockade restores T-cell function and induces robust antitumor responses, especially in pancreatic cancer models. These findings define a novel VSIG4–SLC3A2 axis that integrates metabolic and ionic control to suppress immunity, offering a promising strategy to overcome resistance in “cold” tumors.

overall_design: All six C57BL/6J mice with orthotopic KPC tumors were randomly divided into two groups and treated with either IgG or #44-anti-mVSIG4 antibody. At 11 days post-inoculation, the tumor tissues were collected and sent to Shanghai Majorbio Co., Ltd., for scRNA-seq. Library construction was performed via the DNBelab C TaiM4 V3.0 platform, and sequencing was conducted via the MGI DNBSEQ-T7 system. Bioinformatics analysis was carried out via the proprietary platform of Shanghai Majorbio Co., Ltd.

first: Chenhui

last: Wang


title: P4HA3 drives cervical cancer lymphatic metastasis by facilitating ACLY-mediated ferroptosis resistance

first: Li

last: Yuan

overall_design: RNA-seq profiling of SiHa PR cells and their P4HA3 ovexpression derivatives


title: Dysregulated differentiation kinetics underlie essential role of DNA damage repair in cloned placentas

first: Shanshan

last: Yi

state: Shanghai

address: 1239 Siping Road, Yangpu District

department: College of Life Science and Technology

institute: Tongji University

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

overall_design: Refer to individual Series


title: mRNA Therapeutics Encoding Multiple Reparative Factors using Polyplex Nanomicelle Attenuating Myocardial Infarction

city: Osaka

first: Kazuma

last: Handa

state: Not required for this country

address: Yamada-Oka 2-2, Suita

department: Department of Cardiovascular Surgery

institute: The University of Osaka

summary: Background: Gene therapy for heart failure has been explored using single factors such as angiogenic agents; however, clinical success remains limited. In this study, we investigated an alternative approach by directly administering mRNA encoding multiple genes that are transiently upregulated during cardiac recovery. Using a model in which heart function is restored through the administration of extracellular vesicles secreted by human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CM-derived EVs), we aimed to evaluate the potential of multi-gene mRNA therapy for heart failure, being delivered using polyplex nanomicelles, which serve as an effective delivery system with superior mRNA stabilization and target tissue penetration properties. This study aimed to evaluate the therapeutic efficacy of mRNA encoding multiple cardiac-reparative factors on cardiac dysfunction in heart failure mouse model using nanomicelles. Methods: Multiple cardiac-reparative factors involved in cardiac functional recovery were identified through comprehensive RNA sequencing data of myocardial infarction (MI) model animals treated with hiPSC-CM-derived EVs. MI model mice were created by left coronary artery ligation, followed by injection of mRNA encoding those factors (1 µg/each factor), an equal amount of Luciferase (Luc) -mRNA as a control, or PBS into the border zone. Cardiac function was evaluated at two and four weeks later by echocardiography and subsequent histological analysis. Results: Comprehensive RNA sequencing of myocardial tissue treated with hiPSC-CM-derived EVs showed that five genes (Hgf, Igf1, Pdgfb, Cxcl12, Tgfb1) were notably upregulated on day 3 post-treatment may be involved in the therapeutic effect. To evaluate their potential, an mRNA cocktail encoding these factors was administered to the border zone of mouse heart with impaired cardiac function due to MI. The five-factor mRNA group exhibited significantly mitigated cardiac dilation and improved contractility at two weeks post-treatment compared with the other groups, with this trend persisting at four weeks. Subsequent histological analysis was performed four weeks after treatment. Sirius red staining revealed a significant reduction in fibrosis in the five-factor mRNA group compared with the other groups. Additionally, CD31 staining of capillary endothelial cells was conducted to assess angiogenesis in the border zone, revealing a significant increase in capillary density in the five-factor mRNA group. Conclusion: Five cardiac-reparative factors (Hgf, Igf1, Pdgfb, Cxcl12, Tgfb1) were identified from RNA sequencing data of MI myocardial tissue treated with hPSC-CM-derived EVs. Administration of mRNA cocktails encoding these factors to the MI heart achieved an increase in angiogenesis and an inhibition of fibrosis, resulting in improvement of cardiac function.

overall_design: RNA sequencing analysis of left ventricular myocardium in mice that underwent MI surgery (including control group and 5-factor mRNA group).

first: Yasunobu

last: Mano

first: Lisa

last: Fujimura

first: Akima

last: Harada

first: Kenji

last: Miki

first: Hideyuki

last: Nakanishi

first: Kosuke

last: Torigata

first: Takuji

last: Kawamura

first: Keiji

last: Itaka

first: Shigeru

last: Miyagawa


title: Translation efficiency (TE) changes between shNC and shGm26917 FGSCs were quantified by ribosome profiling  (Ribo-seq) and RNA-seq integration [Ribo-Seq]

first: Ji

last: Wu

address: No.800, Dongchuan Road

institute: Shanghai Jiao Tong University

summary: Integrated analysis of Ribo-seq and RNA-seq data was performed to identify translation efficiency altered upon Gm26917 knockdown, To assess changes in translational efficiency and validate Gm26917 function.

overall_design: FGSCs were infected with lentivirus to knockdown Gm26917 and detected TE by Ribo-seq


title: Dysregulated differentiation kinetics underlie essential role of DNA damage repair in cloned placentas [ChIP-Seq]

summary: To investigate the mechanisms underlying cloned placenta hyperplasia, we employed single-cell RNA and ATAC-seq multi-omics at the critical window of placental overgrowth. Our work offers the first comprehensive and novel single-cell–level dissection of developmental barriers in SCNT placentas, demonstrating that genomic instability constitutes the principal determinant of SCNT placental dysfunction, and outlines a feasible approach to improve reproductive cloning outcomes.

overall_design: Extraembryonic ectoderm (ExE) tissues derived from somatic cell nuclear transfer (SCNT) and in vitro fertilization (IVF) were collected at embryonic day 7.5 (E7.5) for ultra-low-input native chromatin immunoprecipitation sequencing (ULI-NChIP-seq) to profile the genome-wide distribution of repressive histone mark H3K27me3.

first: Mingzhu