title: Spatiotemporal Transcriptomic Immune Responses to a Recombinant Hemagglutinin Protein Vaccine

city: Gold Coast

first: Laurelle

last: Jackson

state: Queensland

address: 1 Parklands Dr, Southport

department: Pharmacy and Medical Sciences

institute: Griffith University

summary: Vaccination triggers coordinated immune responses that begin at the injection site and propagate to draining lymph nodes, yet spatially resolved maps linking these events remain limited. Here, we applied high-plex spatial transcriptomics to profile early responses to an adjuvanted recombinant haemagglutinin (rHA) protein vaccine. In mice, early innate activation was observed in non-follicular lymph node regions at Day 1, transitioning to adaptive, germinal centre–associated responses within follicles by Day 7. At the injection site, stromal and muscle cells exhibited strong chemokine and interferon responses, spatially localised to fibroblast-rich regions. These tissue-level dynamics were accompanied by transient systemic cytokine responses and increased antigen-specific IgG. Together, this study links spatially organised local inflammation with lymph node architecture to define early vaccine-induced immune responses.

overall_design: Groups of three female BALB/c mice per treatment were immunised intramuscularly (quadriceps) with either AF03-adjuvanted recombinant haemagglutinin (rHA) protein or PBS on Days 0 and 21. Blood samples were collected longitudinally (Days 0, 14, and 35) for serum isolation and immunogenicity assessment. For spatial analyses, injection site muscle and draining lymph nodes were harvested at Days 1 and 7 post-vaccination, formalin-fixed, paraffin-embedded, and sectioned for downstream GeoMx™ DSP and CosMx™ SMI profiling with the Whole Ttanscriptome Atlas probe set and the 1000-plex mouse probe set respectively. Matched H&E-stained sections were used for histological evaluation.

first: Sarah

last: Williams

first: James

last: Sinclair

first: Ana

last: Kume

first: Azadeh

last: Bahadoran

first: Ingeborg

last: Langohr

first: Hillary

last: Danz

first: Bin

last: Lu

first: Dinesh

last: Bangari

first: Amanda

middle: J

last: Cox

first: Laurence

last: Macia

first: Sudha

last: Chivukula

first: Nicholas

last: West


title: Aberrant laminin signaling drives melanocyte dedifferentiation and unveils a tractable therapeutic target in vitiligo

status: Public on Apr 16 2026

city: Osaka

first: fei

last: yang

state: Osaka

address: Abeno Medix 212, 1-2-7, Asahimachi, Abeno-ku

country: Japan

institute: Department of Pigmentation Research and Therapeutics, Graduate School of Medicine, Osaka Metropolitan University

summary: Vitiligo is characterized by progressive loss of melanocytes, but the underlying mechanisms governing melanocyte dysfunction remain incompletely understood. In this study, we aimed to investigate the role of the extracellular matrix microenvironment in regulating melanocyte identity and function.  We performed spatial transcriptomics using the 10x Genomics Visium platform on human skin samples from healthy controls and vitiligo patients. This approach enabled spatially resolved analysis of gene expression changes associated with melanocyte dedifferentiation.  Our analysis revealed that aberrant laminin signaling, particularly involving Laminin-332, is associated with transcriptional reprogramming of melanocytes toward a dedifferentiated state. Spatially resolved gene expression patterns indicated alterations in pathways related to cell adhesion, cytoskeletal organization, and stress responses in vitiligo lesions.  These findings provide insight into how extracellular matrix remodeling contributes to melanocyte dysfunction and identify potential therapeutic targets for restoring melanocyte differentiation in vitiligo.

overall_design: This study includes spatial transcriptomics data generated from human skin samples obtained from vitiligo patients and healthy controls. The experimental design consists of two groups: vitiligo perilesional skin and normal skin.  Each sample represents an independent biological replicate derived from a different individual. The primary variable under investigation is disease state (vitiligo versus healthy control).  Spatial transcriptomic profiling was performed to compare gene expression patterns between these groups and to identify spatially resolved transcriptional changes associated with melanocyte dedifferentiation in vitiligo.

first: Ichiro

last: Katayama

first: Lingli

last: Yang

first: Fei


title: BMP signaling regulates dorsal skeletal growth in the sea urchin embryo

city: Pittsburgh

first: William

middle: Brent

last: Douglas

state: PENNSYLVANIA

address: 6336 Aurelia St., 1

department: Biological Sciences

country: USA

institute: Carnegie Mellon University

type: Expression profiling by high throughput sequencing

summary: The development of the elaborate, calcified endoskeleton of sea urchin embryos is a model for understanding the dynamic nature of developmental gene regulatory networks and the control of biomineralization. While several signaling pathways have been shown to regulate  gene expression and biomineral formation by sea urchin skeletogenic cells, important gaps in our understanding remain. Here, we focused on signals regulate skeletogenesis along the dorsal/ventral axis of the late-stage embryo. We used specific inhibitor of Type I BMP receptors, K02288, to show that BMP signaling regulates skeletal growth selectively in the dorsal region. K02288 treatment led to dorsal skeletal defects and inhibited the expression of genes typically expressed specifically in the dorsal skeletogenic cells, including biomineralization genes. Using RNA-seq, we identified genes that were uniquely downstream of either the BMP or a ventral signaling pathway (the VEGF pathway) at late developmental stages and genes downstream of both pathways. Our findings establish BMP signaling as a key pathway regulating dorsal skeleton formation and show that BMP signaling functions in concert with VEGF signaling to define the dorsal/ventral axis of the skeleton.

overall_design: To understand the separate contributions of VEGF signaling and BMP signaling to late-stage sea urchin embryonic skeletogenesis, Lytechinus variegatus embryos were cultured until after the formation of the tri-radiate spicule rudiments (~18-20hpf @ 21oC) at which point embryos were incubated in various treatment conditions (DMSO in ASW, 75 nM axitinib in ASW, or 1 μM K02288 in ASW). Embryos were then cultured until the late pluteus stage (2dpf @ 21oC). Embryos were lysed and total RNA was extracted using a Pure Link™ RNA Mini Kit (Invitrogen) following the manufacturer's protocol. Samples were then treated with Turbo DNase™ (Invitrogen) and LiCl precipitated to remove genomic DNA. RNA samples were then shipped to Novogene Corporation Inc. for sequencing. mRNA was purified by Novogene using poly-A enrichment purification, strand-specific cDNA synthesis was performed, and sequenced by synthesis using the Illumina sequencing platform.

middle: B

first: Charles

middle: A

last: Ettensohn


title: Effect of SREBP1 cDNA overexpression on gene expression in LN229 cells

city: New York

first: Thomas

last: O'Loughlin

state: NY

address: Hess CSM Building, 1470 Madison Avenue

department: Neuroscience

institute: Mount Sinai

summary: Aberrant activation of the PI3K/AKT/mTOR signaling pathway is a common feature of cancer but, while mTOR kinase represents an attractive drug target, mTOR inhibitors have not seen broad success as single agents. To identify strategies to enhance the utility of mTOR inhibitors we performed forward genetic screens with new bi-steric mTORC1 inhibitors. These screens show that mTORC1 inhibitor-mediated cytostasis leaves cells exquisitely dependent on the lipid peroxide scavenging enzyme GPX4. Mechanistically, using unbiased gene activation screens and RNA-seq, we demonstrate that mTORC1-dependent control of ferroptosis occurs, in part, through regulation of SREBP1 and donwstream impact on SCARB1 expression.

overall_design: RNA-seq profiling of LN229 cells overexpressing GFP or SREBP1 cDNA performed in duplicate

first: Abolfazl

last: Arab

first: Luke

last: Gilbert


title: F-box control of Multiple Organellar RNA Editing Factor 2 coordinates seed germination and plastid signaling

city: Athens

first: Zhihua

last: Hua

state: Ohio

address: 22 Richland Ave

department: Department of Environmental and Plant Biology

institute: Ohio University

summary: Plastids communicate with the nucleus through retrograde signaling pathways that coordinate nuclear and plastid gene expression to support plant development and environmental adaptation. However, how plastid regulatory factors are dynamically controlled to modulate these signals remains largely unknown. Here we identify a proteostasis mechanism that regulates plastid retrograde signaling through the ubiquitin–26S proteasome system. We show that the nuclear-encoded plastid RNA-editing factor MULTIPLE ORGANELLAR RNA EDITING FACTOR 2 (MORF2) is targeted for degradation by a Skp1–Cullin1–F-box (SCF) ubiquitin ligase assembled with the MORF2-INTERACTING F-BOX (MIF) protein. MIF physically associates with MORF2 and promotes its ubiquitylation and proteasome-dependent turnover. Genetic and physiological analyses reveal that this pathway balances early plant development. MIF overexpression suppresses seedling growth and disrupts chloroplast structure and function, whereas mif null mutants or MORF2 overaccumulation retard seed germination and reduce photosynthetic efficiency. Transcriptomic profiling and RNA-editing analyses further demonstrate that MIF-dependent MORF2 turnover modulates plastid RNA editing and retrograde signaling pathways. Together, our results uncover a previously unrecognized cytoplasmic regulatory layer that links ubiquitin-mediated proteostasis to plastid RNA editing and retrograde signaling. This mechanism enables plants to coordinate seed germination and chloroplast development during early seedling establishment.

overall_design: RNA-seq was performed on 7-day-old Arabidopsis thaliana seedlings grown on half-strength Murashige-Skoog (1/2 MS) medium plus 1% (w/v) sucrose supplemented with 10 μM dexamethasone. Whole seedlings were harvested for total RNA extraction and mRNA sequencing. Differential transcriptome analyses were used to examine transcriptional perturbations associated with MIF expression and MORF2 regulation.

first: Hua

last: Zhihua

first: Yu

last: Peifeng


title: Transcriptomic profiling of skeletal muscle in CT26 tumor-bearing mice with or without aerobic exercise

city: Chengdu

first: jia hao

last: lv

state: Sichuan

address: No. 1942, Huanhu North Road, Jianyang City, Chengdu, Sichuan Province

department: Institute of Sports Medicine and Health

country: China

institute: Chengdu Sport University

summary: This study investigates the effects of aerobic exercise on skeletal muscle atrophy in CT26 tumor-bearing mice through transcriptomic and weighted gene co-expression network analyses.

overall_design: RNA-seq analysis of skeletal muscle samples from four groups of mice: control, exercise, CT26 tumor-bearing, and CT26 tumor-bearing plus exercise, with four biological replicates per group.

first: Jiahao

last: Lu

first: Shuling

last: Zhang


title: Effect of RM-006 treatment on gene expression in LN229 cells

summary: Aberrant activation of the PI3K/AKT/mTOR signaling pathway is a common feature of cancer but, while mTOR kinase represents an attractive drug target, mTOR inhibitors have not seen broad success as single agents. To identify strategies to enhance the utility of mTOR inhibitors we performed forward genetic screens with new bi-steric mTORC1 inhibitors. These screens show that mTORC1 inhibitor-mediated cytostasis leaves cells exquisitely dependent on the lipid peroxide scavenging enzyme GPX4. Mechanistically, using unbiased gene activation screens and RNA-seq, we demonstrate that mTORC1-dependent control of ferroptosis occurs, in part, through regulation of SCARB1 expression.

overall_design: RNA-seq profiling of LN229 cells after treatment with vehicle (DMSO) or 0.098, 0.39, 1.56 nM RM-006 for 72 hours


title: CRISPRi/a screens to identify modifiers of response to the bi-steric mTORC1 inhibitor RM-006

summary: Aberrant activation of the PI3K/AKT/mTOR signaling pathway is a common feature of cancer but, while mTOR kinase represents an attractive drug target, mTOR inhibitors have not seen broad success as single agents. To identify strategies to enhance the utility of mTOR inhibitors we performed forward genetic screens with new bi-steric mTORC1 inhibitors. These screens show that mTORC1 inhibitor-mediated cytostasis leaves cells exquisitely dependent on the lipid peroxide scavenging enzyme GPX4. Mechanistically, using unbiased gene activation screens, we demonstrate that mTORC1-dependent control of ferroptosis occurs, in part, through regulation of SCARB1 expression. Together, our work reaffirms combining mTORC1 with GPX4 inhibition as one of the most promising combinatorial approaches for mTOR-targeted cancer therapies and defines an HDL-dependent ferroptosis suppression system that is regulated by mTORC1 activity.

overall_design: CRISPRi screens in LN229 dCas9-KRAB cells treated with DMSO, 1.56 nM RM-006 or 0.098 nM RM-006 and CRISPRa screens in LN229 dCas9-Suntag cells treated with DMSO, RM-006, RSL3 and RM-006+RSL3 in combination.


title: On-demand GLUT3 expression augments CAR-T cell metabolic fitness and antitumor efficacy whereas preventing toxicity in glioblastoma

city: Tokyo

first: Hiroyoshi

last: Nishikawa

state: Tokyo

address: 5-1-1 Tsukiji, Chuo-ku

department: 3Division of Cancer Immunology, Research Institute/Exploratory Oncology Research & Clinical Trial Center (EPOC)

institute: National Cancer Center Japan

summary: We show that the dysfunction of CAR-T cells in GBM is attributed to glucose deficiency in the tumor microenvironment (TME) and that on-demand, but not continuous, metabolic replenishment significantly improves the antitumor efficacy of CAR-T cells. The massive consumption of glucose by cancer cells reduces the glucose level in the TME of GBM, consequently impairing CAR-T cells. Adding stable expression of glucose transporter 3 (GLUT3), a high-affinity glucose transporter, to CAR-T cells  restored their cytokine production and killing activity. However, whereas CAR-T cells with stable GLUT3 expression induced tumor reduction in a GBM model, their overactivation led to adverse events and mouse death. On-demand GLUT3-expressing CAR-T cells, in which GLUT3 transcription is driven by the nuclear translocation of nuclear factor of activated T cells (NFAT) by target antigen stimulation, exhibited enhanced metabolic fitness and increased antitumor efficacy, leading to long-lasting tumor control in intracranial human GBM cell xenograft models whereas it prevented adverse events.

overall_design: Sample 1-4: RNA-seq profiling of conventional EGFRvIII-targeting CAR-T cells after 24 hours of culture in 0.5 mM or 10 mM glucose conditions. Sample 5-16: RNA-seq reads were processed using the Genomon RNA-seq pipeline. Adapter sequences and low-quality bases were trimmed prior to alignment. Reads were aligned to the human reference genome (hg38), and gene-level read counts were generated for downstream analysis.

first: Junya

last: Yamaguchi

first: Keisuke

last: Watanabe

first: Akihiro

last: Nakamura


title: A scalable Tn5-based method for genome-wide DNA methylation profiling in development and disease

city: Geneva

first: Nahuel

last: Simonet

address: 9 chemin des Mines

country: Switzerland

institute: EPFL

summary: DNA methylation is a critical epigenetic modification involved in various diseases, including cancer, and serves as a biomarker for early disease detection. Traditional detection methods, such as bisulfite sequencing, offer base-pair resolution but are costly and require high sequencing depths. We developed CmeCUT&Tag, a novel approach using methylation-binding domain fusion proteins coupled to hyperactive Tn5 transposase that selectively targets methylated DNA regions in both chromatinized and isolated DNA. These fusion proteins insert sequencing adapters into methylated regions, allowing low-depth sequencing for quantitative methylation assessment or bisulfite treatment for base pair resolution. Our approach enables comprehensive genome-wide DNA methylation profiling with minimal sequencing coverage. We demonstrated its efficacy in detecting DNA methylation in human stem cells and organoid systems. The system exhibits a high correlation with traditional bisulfite sequencing. It efficiently identifies CpG islands and DNA methylation dynamics during brain organoid development, highlighting its potential for biomedical applications in disease monitoring and aging research.

sample_organism:
Danio rerio
Homo sapiens

platform_organism:
Danio rerio
Homo sapiens

overall_design: CmeCUT&Tag, a method enabling selective targeting of methylated DNA regions in both chromatinized samples and isolated genomic DNA. Libraries were generated from the genomic DNA of  human induced pluripotent stem cells (iPSCs, CAU) and brain tumor biopsies. Raw FASTQs avaliable upon request.

first: Hanrong

last: Hu

first: Nahuel Jonas

first: Fides

last: Zenk


title: HIV-1 Nef programs long-lasting innate immune memory in hematopoietic stem and progenitor cells in a mouse model

city: Melbourne

first: Andrew

last: Fleetwood

address: 75 Commercial Road

country: Australia

institute: Baker Heart and Diabetes Institute

type: Genome binding/occupancy profiling by high throughput sequencing

summary: The HIV infection is accompanied by chronic inflammation and inflammation-related co-morbidities, even when viral replication is effectively supressed by therapy. It is often assumed that a complete cure would resolve this inflammation; however its origin and mechanisms may be more complex and not entirely dependent on the continuous presence of the virus. To investigate whether inflammatory programming can be imprinted in hematopoietic cells, we treated mice with extracellular vesicles containing the HIV protein Nef (exNef), a major viral pathogenic and inflammatory factor. Using a multi-omics approach, we found that haematopoietic cells exposed to exNef displayed epigenetic modifications and reprogramming of energy and lipid metabolism pathways characteristic of trained innate immunity (TRIM).

overall_design: Wild-type (C57BL/6) mice were administered either exNef or control exGFP exosomes over 2 weeks. Total bone marrow cells were collected from mice and stained with a mixture of antibodies to isolate LSKs, cKit+ and monocytes by FACS-sorting. Multiome-seq: Single nuclei were extracted from LSK, cKit+ and monocytes and joint snRNA- and scATAC libraries were prepared using 10x Genomics platform.

first: Nigora

last: Mukhamedova

first: Dragana

last: Dragoljevic

first: Man K

middle: S

last: Lee

first: Yangsong

last: Xu

first: Malathi S

middle: I

last: Dona

first: Ian

last: Hsu

first: Camila

last: Bertuzzo Veiga

first: Fumihiko

last: Takeuchi

first: Alex

last: Pinto

first: Michael

last: Bukrinsky

last: Murphy

first: Dmitri

last: Sviridov


title: Steroid hormone antagonism affords vascular protection in a mouse model of Vascular Ehlers-Danlos Syndrome

city: Baltimore

first: Leda

last: Restrepo

state: MD

address: 733 N Broadway, Miller Research Building

department: Human Genetics

institute: Johns Hopkins

summary: Aortic dissection is a significant cause of mortality in vascular Ehlers-Danlos syndrome (VEDS), a disorder caused by mutations in the COL3A1 gene. Col3a1G938D/+ mice recapitulate features of VEDS, including high risk of aortic rupture, and aortic risk in this model accelerates at the onset of puberty, especially in males. We identify developmentally regulated gene programs associated with this vulnerability and targeted by treatments that mitigate it, including androgen receptor (AR) and mineralocorticoid receptor (MR) antagonism. We provide ATAC-seq data from aortic nuclei collected at postnatal day 60 from Col3a1G938D/+ (vEDS model) and Col3a1+/+ (WT) mice. For each genotype, aortic tissue from two age- and sex-matched animals was pooled prior to nuclei isolation. Downstream sequence and motif analyses (gkm-SVM/gkmPWM/mapTF) were performed to characterize sequence features and transcription factor binding site enrichment differences between genotypes.

overall_design: ATAC-seq was performed on mouse aortic tissue at 60 days of age to compare chromatin accessibility between Col3a1+/+ (WT) and Col3a1G938D/+ (VEDS model) mice. Each library represents pooled aortic tissue from two age- and sex-matched animals per genotype. Libraries were prepared using the 10x Genomics Chromium Single Cell ATAC workflow, sequenced paired-end and analyzed in aggregate per library.

first: Emily

middle: E

last: Juzwiak

first: Rhiannon

last: Edwards

first: Dustin

middle: T

last: Shigaki

first: Micheal

last: Beer

first: Harry

middle: C

last: Dietz

first: Elena

last: Gallo MacFarlane


title: The mechanism of reproductive toxicity induced by Triptolide was revealed by epitranscriptomics

city: Fuzhou City

first: xinru

last: liu

state: Fujian Province

address: No. 1, Xuefu North Road, Shangjie Town, Minhou County

department: School of Basic Medical Sciences

institute: Fujian Medical University

summary: Triptolide is the core active component of the traditional Chinese herbal medicine Tripterygium wilfordii Hook F, which has multiple pharmacological effects such as anti-inflammation, neuroprotection, immunosuppression and anti-tumor, but the mechanism of its significant reproductive toxicity has not been clarified. This study aims to investigate the relationship between triptolide-induced reproductive toxicity and m6A methylation modifications.

overall_design: To investigate whether m6A modification is involved in reproductive toxicity following triptolide treatment, we performed MeRIP-seq and experimental verification on control HTR-8/SVneo cells and HTR-8/SVneo cells treated with triptolide.

first: Xinru

last: Liu


title: S100A10-ANXA2 TETRAMER INHIBITION HAMPERS HEPATIC STELLATE CELL ACTIVATION IN MASLD MODELING HUMAN LIVER ORGANOIDS

first: Miranda

last: Türkal

address: 24 rue du Général-Dufour

institute: University of Geneva

summary: Metabolic dysfunction-associated steatotic liver disease (MASLD), which begins with the pathological lipid accumulation within hepatocytes, can progress to metabolic dysfunction-associated steatohepatitis (MASH), characterized by inflammation and fibrosis. Fibrosis is the strongest predictor of liver-related mortality, yet effective antifibrotic therapies remain limited, underscoring the need for new molecular targets. Our previous work identified S100A10 as a MASLD promoter, suggesting that its association with Annexin A2 (ANXA2) within the S100A10-ANXA2 heterotetramer (A2t) might promote hepatic fibrosis. Here, we inhibited A2t using its specific inhibitor, A2ti-1, in human hepatic stellate cells (LX-2) and in human multilineage liver organoids (HLOs) modeling MASLD. A2ti-1 reduced α-SMA protein levels and decreased expression of profibrotic genes in LX-2 cells by directly suppression of stellate cell activation. In HLOs, A2ti-1 significantly attenuated fibrosis by reducing α-SMA expression, collagen deposition, and profibrotic genes, without altering steatosis. Mechanistically, A2ti-1 inhibited LX-2 activation through reducing STAT3 phosphorylation independently of SMAD signaling. These findings identify A2t as a previously unrecognized regulator of hepatic fibrosis and establish its pharmacological inhibition as a promising antifibrotic therapeutic strategy in MASH.

overall_design: Human ESCs (HS420) were differentiated into human liver organoids (HLOs) using a stepwise medium-switch protocol. Cells were dissociated at 70-80% confluency and seeded (~100 cells/well) into air-liquid interface microwells (Airliwells). Differentiation involved sequential media containing Activin A and BMP4, followed by RPMI with graded KSR, then Advanced DMEM/F12 with B27, N2, FGF4, and CHIR99021. Retinoic acid and Matrigel (20%) were added on day 7, and cultures were later transitioned to HCM medium supplemented with HGF, dexamethasone, Oncostatin M, and Matrigel (20%). Organoids were removed from Airliwells on day 17 and maintained in suspension culture with 10% Matrigel until day 21. Day-21 HLOs were collected for scRNA-seq.

first: Pierre

last: Maecher

first: Etienne

last: Delangre


title: small RNA-seq of Extraceullular Vesicles derived from human immortalized podocytes treated with glucose and RabGTPase silenced

city: Valencia

first: Ana

last: Ortega

state: VALENCIA

address: Av. Menendez Pelayo 4

country: Spain

institute: Incliva Health Research Institute

type: Non-coding RNA profiling by high throughput sequencing

summary: Diabetic nephropathy (DN) is a major cause of end-stage renal disease and is characterized by early podocyte injury, leading to progressive glomerular dysfunction. Increasing evidence highlights extracellular vesicles (EVs) as crucial mediators of intercellular communication in the diabetic kidney, transferring bioactive molecules such as non-coding RNAs (ncRNAs) that modulate cellular responses and contribute to disease progression. The molecular mechanisms governing the selective packaging of ncRNAs into podocyte-derived EVs under hyperglycaemic stress, as well as the role of vesicle trafficking regulators such as RAB GTPases, remain poorly understood. In this study, conditionally immortalized human podocytes were exposed to high glucose conditions to model the diabetic environment. To investigate the contribution of vesicular trafficking to EV release, the small GTPases RAB27A and RAB3A were silenced using siRNA. EVs were isolated and their small RNA content was profiled by next-generation sequencing followed by RT-qPCR validation. The results demonstrated that both hyperglycaemia and RAB GTPase knockdown significantly modified the ncRNA composition of podocyte-derived EVs, indicating that glucose stress and vesicular trafficking pathways jointly shape the extracellular RNA landscape. These findings provide new insights into how RAB GTPase–dependent mechanisms regulate EV-mediated communication in podocytes during diabetic injury, potentially influencing key signaling pathways involved in disease progression.

overall_design: small RNA-seq of Extraceullular Vesicles from human immortalized podocyte cell line subjected to silencing and/or glucose treatment. Groups: silenced Rab (siRab), scramble (scr), NG (normal glucose) and HG (high glucose)

first: Olga

last: Martinez-Arroyo

last: Flores-Chova

first: Lesley

last: Escriva

first: Marta

last: Mendez-Debaets

first: Maria

last: Forner

first: Josep

last: Redon

first: Raquel

last: Cortes


title: Cystine import and oxidative catabolism fuel nutrient-responsive histone acetylation to unlock chromatin at endothelial cell loci and ensure vascular growth and repair [HUVEC_Ribo_ext553]

city: Mannheim

first: Fredy

middle: Andres

last: Delgado Lagos

address: Ludolf-Krehl- Straße 13-17

department: Vascular Dysfunction

country: Germany

institute: UMM, Heidelberg University

summary: Endothelial metabolic reprogramming is essential for vascular growth and critical for organ (re)generation, health and life span. Here, we identify a nuclear oxidative catabolic pathway that links cystine metabolism to endothelial gene regulation and angiogenesis. Endothelial cells preparing to proliferate, increase the translation of the transporter (SLC)7A11 to import cystine, which is further oxidatively catabolized by cystathionine gamma lyase (CSE) within the nuclear compartment. This process, preserved in young but not aged tissues, generates acetyl moieties in a pyruvate dehydrogenase dependent manner and initiates specific histone H3 lysine acetylation, leading to chromatin reorganization. Such changes solidify endothelial cell transcriptional programmes and maintain cell proliferation. Combined deletion of the SLC7A11 and CSE causes embryonic lethality and abrogates vascular growth. While SLC7A11 deficiency triggers compensatory de novo cysteine synthesis from methionine, partially preserving angiogenesis; CSE deletion disrupts nuclear cystine oxidative catabolism, endothelial transcription, and vessel formation. Therapeutically, oral cystine supplementation in models of retinopathy of prematurity, acute myocardial infraction and vascular injury in aging promotes vascular growth and repair. Together, our study highlights the role of cyst(e)ine nuclear oxidative catabolism in robust control of endothelial gene transcription, vessel growth and repair.

overall_design: Bulk RNA-sequencing from ribosomal RNA or input RNA from human umbilical vein endothelial cells infected with an Rpl22 (RiboTag) lentivirus and maintained in contact inhibition for 10 days (0 hours, G0) or seeded after 10 days in low density. Following 2 hours of cell adhesion, cells were harvested after 2, 6 hours (G0 exit), 12 hours (Prior to G2/M entry), or 24 hours (G2/M cycling).

first: Sofia-Iris

last: Bibli


title: Cystine import and oxidative catabolism fuel nutrient-responsive histone acetylation to unlock chromatin at endothelial cell loci and ensure vascular growth and repair [MLEC_WT_ACT]

overall_design: Antibody-guided chromatin tagmentagtion sequencing (ACT-seq) for H2AK5ac, H3K9ac, H3K14ac, H3K18ac, H3K23ac, H3K27ac, H3K4me3, and H4K8ac in isolated mouse lung endothelial cells from WT mice.


title: Cystine import and oxidative catabolism fuel nutrient-responsive histone acetylation to unlock chromatin at endothelial cell loci and ensure vascular growth and repair [MLEC_WT_CSE-KO_ATAC_ext251]

overall_design: ATAC-sequencing from isolated mouse lung endothelial cells from WT and CSE-KO mice.


title: Transcriptomic profiling of the intra-amygdala kainate mouse model across the stages of epileptogenesis

city: Seoul

first: Sangwoo

last: Kim

state: State...

address: 50-1 Yonsei-ro, Seodaemun-gu

department: Dept. of Biomedical Systems Informatics

country: South Korea

institute: Yonsei University College of Medicine

summary: Mesial temporal lobe epilepsy (MTLE) is a prevalent form of drug-resistant epilepsy often associated with hippocampal sclerosis (HS). While various rodent models exist to study this condition, their molecular fidelity to human MTLE requires detailed evaluation. As part of a larger cross-species transcriptomic meta-analysis, we generated this dataset to characterize the intra-amygdala kainate mouse model, which provides a unique framework for studying status epilepticus-induced epileptogenesis. We performed bulk RNA-sequencing on hippocampal tissues to capture the evolving molecular landscape during the acute, intermediate, and chronic phases following seizure induction. This dataset allows for the investigation of key epileptogenic processes, including neuroinflammation, neuronal death, and reactive gliosis, and serves as a critical component in comparing chemical induction models against human MTLE pathophysiology.

overall_design: Adult male C57BL/6 mice (8–10 weeks old) were used to induce a model of temporal lobe epilepsy. Status epilepticus was triggered via a unilateral stereotaxic microinjection of kainic acid into the basolateral amygdala. Control animals received an equivalent volume of vehicle (PBS). To ensure survival and standardize seizure duration, diazepam was administered intraperitoneally 40 minutes after the injection. Ipsilateral hippocampal tissues were harvested at three distinct time points post-injection: 3 days (Acute), 7 days (Intermediate), and 14 days (Chronic). Total RNA was extracted (RIN values 8.0–9.5) and libraries were prepared using the TruSeq Stranded mRNA Sample Preparation Kit. High-throughput sequencing was performed on the Illumina NovaSeq X Plus platform, generating 100 bp paired-end reads.

first: Joonho

first: Bora

first: Won-Joo


title: SRSF1 modulates the pH microenvironment of the dark nucleolar caps to restorenucleolar integrity and function

city: Xiamen

first: Suibin

last: ma

state: Fujian

address: Xiang'an Campus of Xiamen University, Xiamen City, Fujian Province

department: School of Life Sciences

institute: Xiamen university

summary: Nucleolus is a multiphase biomolecular assembly containing three distinct subcompartments. Evidence is just emerging that nucleolar proteins with characteristic electrochemical properties condense to generate a pH gradient, which serves as a key driving force for organizing the nucleolar sub-phases. Given the indispensable functionality of the nucleolus in most, if not all, cellular activities, it is vital for a cell to sense potential fluctuations in the nucleolar pH and subsequently maintain pH homeostasis. The mechanisms by which a cell achieves this task remain poorly decoded. Here, we show that splicing factor SRSF1 is shuttled from nuclear speckle (NS) to the nucleolus during times of stress, which interrogates the nucleolar pH. SRSF1 nucleolar localization is reliant on an acidic patch. Loss of SRSF1 impedes pH homeostasis in the dark nucleolar cap and subsequently obstructs the restoration of the nucleolar multiphase and function. The RS (arginine/serine rich) domain of SRSF1, due to its high isoelectric point (pI), directly alkalizes the nucleolar microenvironment. Interestingly, synthetic arginine-rich dipeptide derivatives of SRSF1 RS domain safeguard the nucleolus from pH and functional disturbance. Our findings uncover unprecedented mechanistic insights into nucleolar pH-sensing and regulation.

overall_design: RNA-seq profiling was performed on SiCtrl and Si-SFPQ-transfected U-2OS cells subjected to actinomycin D-induced transcriptional stress.

last: Ma

first: Jierui

last: Guo

first: Xiang

last: Zhan

first: Shuo

last: Yang

first: Fan

last: Wu

first: Chaoqun

last: Huang

first: Bo

last: Wang


title: Cystine import and oxidative catabolism fuel nutrient-responsive histone acetylation to unlock chromatin at endothelial cell loci and ensure vascular growth and repair [MLEC_WT_CSE-KO_RNA_ext248]

overall_design: Bulk RNA-sequencing from isolated mouse lung endothelial cells from WT and CSE-KO mice.


title: Cystine import and oxidative catabolism fuel nutrient-responsive histone acetylation to unlock chromatin at endothelial cell loci and ensure vascular growth and repair [MLEC_WT_CSE-KO_H3K9ac_CnR_ext577]

overall_design: Cleavage Under Targets and Release Using Nuclease (CUT&RUN) sequencing for H3K9ac in isolated mouse lung endothelial cells from WT and CSE-KO mice.


title: IL-9 and Blimp-1 protects the transcriptional identity of group 2 innate lymphocytes in allergic asthma

first: Amanda

middle: Catherine

last: Poholek

state: Pennsylvania

address: 4401 Penn Ave., Rangos Research Center 8129

department: Pediatrics

institute: University of Pittsburgh

summary: Allergic asthma is driven by type 2 immune responses, including those mediated by type 2 innate lymphoid cells (ILC2s). Although ILC2s are activated by the tissue alarmins IL-33 and IL-25, these signals do not intrinsically enforce type 2 identity, and the mechanisms that maintain type 2 cytokine expression remain unclear. Here we show that allergen-induced IL-33 and IL-25 rapidly induce IL-9, which in turn upregulates the transcriptional repressor Blimp-1 in ILC2s. Blimp-1 sustains type 2 immunity by directly repressing type 1 inflammatory programs, including expression of IFNg and TNF. Deletion of Blimp-1 in ILC2s increased type 1 cytokine production and reduced IL-5 and IL-13 expression, eosinophil recruitment, and mucus production in the lung. In contrast, IL-9 expression was enhanced in the absence of Blimp-1, leading to increased mast cell recruitment. Together, these findings identify Blimp-1 as a key regulator of ILC2 transcriptional fidelity that stabilizes type 2 inflammation while constraining divergent inflammatory programs during allergic responses.

overall_design: Control or Blimp-1 knockout mice were treated with either PBS, papain or Alternaria intranasally daily for 3 days. ILC2s were flow sorted from lungs

first: Yijia

last: Chen

first: Yibo

last: Zheng

first: Shilpi

last: Giri

first: Abbe

last: Pannucci


title: Differential transcriptomic response of Atlantic salmon to fermented sunflower meal under commercial seawater farming conditions

city: Ås

first: Byron

last: Morales Lange

address: Arboretveien 6

country: Norway

institute: Norwegian University of Life Sciences

summary: The study focused on the differential transcriptome of immune organs (i.e., head kidney and spleen) from farmed Atlantic salmon (Salmo salar) fed fermented sunflower meal (FSFM) at 5% and 10% in two commercial farms (CS: coast and FD: fjord location). Data showed that both head kidney and spleen (from  fish fed FSFM5% at CS) up-regulated mRNA biogenesis (linked to lipid metabolism and mRNA surveillance) as well as glycosyltransferases (associated with vitamin B6 and lipoic acid metabolism, or pantothenate and CoA biosynthesis). Regarding FD, head kidney from FSFM10% group had up-regulated enzymes (related to lysosome, glutathione metabolism, ribosomes and fatty acid elongation) and the downregulation of transcription machinery and DNA repair/recombination proteins (involved in nucleocytoplasmic transport or spliceosome)

overall_design: RNA-seq profiling of head kidney and spleen from Atlantic salmon (Salmo salar) fed one of three diets (Diet 1: 5% sunflower meal, Diet 2: 5% fermented sunflower meal, Diet 3: 10% fermented sunflower meal) at two farming sites (CS: Coast, FD: fjord).

first: Margareth

last: Øverland


title: Cystine import and oxidative catabolism fuel nutrient-responsive histone acetylation to unlock chromatin at endothelial cell loci and ensure vascular growth and repair [MLEC_WT_CSE-KO_ACT]

first: Fredy

last: Delgado Lagos

overall_design: Antibody-guided chromatin tagmentagtion sequencing (ACT-seq) for H3K23ac, H3K27ac, and H3K4me3 in isolated mouse lung endothelial cells from WT and CSE-KO mice.

first: Sofia-Iris

last: Bibli


title: Neurotranscriptomics of mutualistic cleaning in Ladridae wrasses

city: Austin

first: Rebecca

middle: L

last: Young

state: TX

address: 2415 Speedway

department: Integrative Biology

institute: University of Texas at Austin

summary: Despite the astonishing diversity of life, evolutionary biologists have documented numerous instances where species converge in how they behave, look, and function. Given the importance of happenstance in evolution, it is often assumed that mechanisms driving independent evolution of similar phenotypes (convergence) are distinct; yet recent discoveries suggest that conserved genomic mechanisms can underlie convergent traits. Here, we generate forebrain transcriptomes from six sympatric Labridae wrasses that vary in mutualistic cleaning behavior and apply differential gene expression, co-expression, and phylogenetic comparative analyses to address three questions. First, do neurotranscriptomes vary among species with distinct cleaning behavior? Second, do species that have independently evolved facultative cleaning share neurotranscriptomic patterns? Third, are transcriptomic signatures linked to facultative cleaning also expressed in obligate cleaners? We identify shared neurotranscriptomic patterns in the repeated evolution of facultative cleaning, including 25 novel candidate genes. We then find that transcriptomic patterns associated with facultative cleaning are shared in our focal obligate cleaner species, with more genes than expected by chance with concordant expression patterns in obligate and facultative cleaners. Our results illuminate the neuromolecular basis of cooperative behavior and demonstrate the predictive potential of comparative transcriptomics to unravel the mechanistic underpinnings of the repeated evolution of complex phenotypes.

sample_organism:
Halichoeres melanurus
Thalassoma lunare
Coris batuensis
Hemigymnus melapterus
Labrichthys unilineatus

overall_design: Transcriptome profiling of a forebrain section taken from five species of Labridae wrasses (Hemigymnus melapterus, Coris batuensis, Thalassoma lunare, Halichoeres melanurus, Labrichthys unilineatus) using 3'tag-seq.

first: Hans

last: Hofmann

first: Redouan

last: Bshary

first: Chelsea

last: Weitekamp

first: Zegni

last: Triki

first: Yiheng

last: Su

first: Abigail

middle: G

last: Beman

first: Matthew

last: Petershack


title: Cystine import and oxidative catabolism fuel nutrient-responsive histone acetylation to unlock chromatin at endothelial cell loci and ensure vascular growth and repair [Human_young_old_ATAC_ext353]

overall_design: ATAC-sequencing from young and aged endothelial cells isolated from human mesenteric arteries


title: Spatial and genetic constraints govern transcription-translation coupling and mRNA degradation in bacteria

city: Urbana

first: Yan

last: Zhang

state: IL

address: 600 S Mathews Ave Roger Adams Laboratory

department: Biochemistry

institute: University of Illinois Urbana-Champaign

summary: Bacterial gene expression is thought to involve tightly coupled transcription, translation, and mRNA degradation. However, recent work has indicated that this is not always the case, leaving the generality and regulation of this coordination unclear. Here, we use genetic, kinetic, and spatial analyses in Escherichia coli to show that transcription–translation coupling requires high translational activity and that nearly half of the transcriptome exhibits signatures consistent with partial uncoupling. We find that co-transcriptional mRNA degradation is rare due to membrane localization of RNase E, except for transcripts encoding inner membrane proteins. Our results show that translation efficiency determines the level of premature transcription termination, which in turn shapes mRNA degradation patterns and kinetics. Comparative analyses in Bacillus subtilis and Caulobacter crescentus also reveal gene- and species-specific coordination strategies. This challenges the universality of co-transcriptional coupling and defines how spatial and genetic features coordinate bacterial gene expression.

sample_organism: Escherichia coli str. K-12 substr. MG1655

overall_design: Rif-seq of E. coli MG1655 wild-type cells in MOPS rich defined media at 37˚C: mRNA sequencing (mRNA-seq) and total RNA sequencing (total RNA-seq) of samples collected at time points t = 0, 0.5, 1, 2, 3, 4, 5, 6, 8, 10 min following treatment with the transcription initiation inhibitor rifampicin (Rif-seq)

first: Seunghyeon

last: Kim

first: Xiangwu

last: Ju

first: Albur

last: Hassan

first: Yu-Huan

last: Wang

first: Shixin

last: Liu

first: Sangjin


title: Effect of JAK1/2 Inhibitor treatment on beta cells from mice fed on high fat diet

city: Boston

first: Hui

last: Pan

address: 1 Joslin Place

department: Bioinformatics and Biostatistics Core

institute: Joslin Diabetes Center

summary: Cellular senescence is a stress response mechanism marked by upregulation of antiapoptotic pathways, loss of cellular function, and remodeling of the cellular secretory profile. Pancreatic beta cells undergo senescence with age and insulin resistance. Targeted removal of senescent cells in mouse models of diabetes improves glucose homeostasis, demonstrating the role beta cell senescence in diabetes progression. Especially, JAK1/2 inhibitor counteracted secondary senescence induction and restored eta cell function in high-fat diet-fed mice

overall_design: After two weeks of HFD feeding (60% v/v), the animals (8-week-old or 6-9-month-old male C57BL/6 mice) were subdivided into the following groups: Vehicle control (Chow, 0.9% NaCl), vehicle HFD (HFD, 0.9% NaCl), JAK1/2i HFD (HFD+momelotinib, 12.5 mg/kg/day). The mice were sacrificed after 4 weeks of treatment. The pancreatic islets were then isolated for RNA-seq analysis.

first: Cristina

last: Aguayo-Mazzucato


title: Transcriptome sequencing of drug-resistant oral squamous cell carcinoma cell lines

city: Taizhou

first: yin

last: yuan

state: jiangsu

address: 210 Yingchun Road, Hailing District, Taizhou City, Jiangsu Province

institute: Nanjing Medical University Affiliated Taizhou People's Hospital

summary: NOT PROVIDED; REQUESTED

overall_design: Oral squamous cell carcinoma cell lines were cultured in vitro with apatinib until the cells were resistant to apatinib. The WT cell line, the cell line treated with apatinib for 24 hours, and the resistant cell line were sent for transcriptome sequencing.

first: Yin


title: The mechanism of POSTN in psoriasis in vivo or in vitro on dorsal root ganglia(DRG) culture

city: Guangzhou

first: Caiwei

last: Zhuang

address: No. 74, Zhongshan Second Road, Nonglin Street, Yuexiu District

department: Zhongshan School of Medicine

institute: Sun Yat-Sen University

summary: DRGs  transcriptome sequencing,DRG neuron  transcriptome sequencing

overall_design: Total RNA from T10-L5 DRGs was extracted from mice after being treated with Vehicle or IMQ for 5 days. DRG neurons were cultured in medium with or without recombinant POSTN for 72 h. At the endpoint, the supernatant was removed, cells were lysed with TRIzol reagent, and total RNA was extracted for bulk RNA-seq analysis.

first: Qiulin

last: Dong


title: Neurotranscriptomics of mutualistic cleaning in Labroides dimidiatus

first: Rebecca

last: Young

overall_design: Transcriptome profiling of a forebrain section taken from the obligate cleaner Labroides dimidiatus using 3'tag-seq.

first: Hans

last: Hofmann

first: Redouan

last: Bshary

first: Chelsea

first: Zegni


title: Dual function of DOT1L suppresses tumor intrinsic immunogenicity in Hepatocellular carcinoma [ChIP-seq]

city: Shanghai

first: Siyuan

last: Xu

address: No.131, Dongan Road, Shanghai

institute: Fudan Unversity

summary: Checkpoint inhibitor therapy for Hepatocellular carcinoma (HCC) remains limited in patients’ overall response rate. Discovery and development of more effective combinatorial approaches in HCC checkpoint immunotherapy is urgent. Here, through CPlSPR/Cas9 genetic screens, we identify DOT1L as a versatile epigenetic factor that functions to suppress anti-tumor immunity through a dual mechanism. Depletion of DOT1L induces the expression of transposable elements and subsequent type-I interferon response, and meanwhile lowers ZEB1 levels to further unleash the expression of interferon simulated genes. In turn, we demonstrate that DOT1L loss or treatment with the selective DOT1L inhibitor EPZ-5676 sensitizes tumors to immune checkpoint blockade by increased immune infiltration in mouse. More importantly, EPZ-5676 treatment alone is sufficient to enhance antitumor immunity in humanized mouse model. These findings provide a rationale for targeting DOT1L to improve tumor immunogenicity and overcome immunotherapy resistance.

overall_design: Chromatin immunoprecipitation DNA-sequencing (ChlP-seq) for DOT1L, ZEB1, NPM1, H3K27ac, H3K4me3, and H3K79me2 in HuH-7 cells.

first: Xianjiang

last: Lan


title: Dual function of DOT1L suppresses tumor intrinsic immunogenicity in Hepatocellular carcinoma [RNA-seq]

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: To investigate the function of DOT1L in regulating gene expression, we established DOT1L KO cell lines and performed RNA-seq experiments.


title: chip-seq of the oral  squamous cell carcinoma cell line IRF9

summary: chip-seq of oral  squamous cell carcinoma cell line IRF9 was used to detect the promoter regions of downstream genes to which transcription factor IRF9 binds

overall_design: IRF9 was overexpressed in oral  squamous cell carcinoma cell lines, cultured to a sufficient number of cells for chip assay and sent for sequencing


title: Characterizations of G-quadruplex RNA-Protein Interactions in Living Cells

city: Riverside

first: feng

last: tang

state: CA

address: 26861 Campus Point Dr., Moreno Valley

department: chemistry

institute: University of California, riverside

summary: hnRNPA0 Clip Seq data

overall_design: After titration, 750 ng vector expressing HA-tagged HNRNPA0 was transfected into HEK293T cells in a 15 cm plate, followed by UV cross-linking and harvested the next day. CLIP-seq on HNRNPA0 was performed according to the published easyCLIP protocol28. L3 adapters had the structure /5Phos/rNrNrNrNrNBBBBBAGATCGGAAGAGCACACGTCAAAAAAAAAAAAAAAAAAAAAAAA/3AzideN/where rN is a random UMI RNA nucleotide, B is a barcode, and and/3AzideN/ is an azide group for dye conjugation and blocking 3′ ligation. L3 adapters were conjugated to DBCO-dyes before usage and L3 barcodes were used to distinguish replicates. L5 adapters were of the structure /5AzideN/TCGGCAGCGTCAGATGTGTATAAGAGACAGGTATAGrNrNrNrNrNrNrN, where/5AzideN/ is a 5′ azide group for dye conjugation and blocking ligation, B is a barcode, and rN is random RNA bases to serve as a UMI. Cells were washed once with ice-cold PBS and UVC cross-linked at 254 nm in a Stratalinker at 0.3 J/cm2. Cross-linked cells were harvested in ∼1 mL 4°C CLIP lysis buffer (50 mM Tris-HCl, pH 7.5, 200 mM NaCl and 1 mM EDTA, 10% glycerol, 0.1% NP40, 1% Triton X-100, 0.5% N-lauroylsarcosine) per plate. ~2 mg clarified lysate per replicate was combined with 22 μL anti-HA magnetic beads (ThermoFisher, #88837) for 1 h, washed, treated with 0.02 U/μL Ambion RNAse I (ThermoFisher, #AM2294) at 30°C for ∼3 min, 3′ dephosphorylated with PNK and ligated overnight to L3 adapters. Following L3 adapter ligation, replicates were pooled, 5′ phosphorylated, and ligated to L5 adapters. RNA-protein complexes were resolved by SDS-PAGE, transferred to nitrocellulose, and RNA recovered by proteinase K digestion. RNA was purified by using oligo(dT) beads to capture the poly(A) tail on L3 adapters, then reverse transcribed and amplified by PCR following previously described protocol 44. Libraries were sequenced on a NovaSeq X plus (paired-end 150 bp; ~30 M reads per sample).

first: Feng

last: Tang

first: Yinsheng


title: ov_IRF9 vs WT

summary: NOT PROVIDED; REQUESTED

overall_design: After overexpressing IRF9 in OSCC cell lines, they were sent together with WT cell lines for transcriptome sequencing


title: L1CAM generates SOX2+ metastatic progenitors through planar cell polarity signaling in lung adenocarcinoma

city: New York

first: Jin Suk

last: Park

address: 417 East 68th St

institute: MSKCC

summary: Lung adenocarcinoma (LUAD) is a leading cause of cancer-related deaths worldwide, with most fatalities attributed to metastasis. A primitive SOX2+ progenitor state, rare in primary tumors, becomes prominent in LUAD metastatic lesions and exhibits metastasis-initiating capacity. The signals that determine the emergence of SOX2+ progenitors are unknown. We report that the cell adhesion molecule L1CAM, a marker of metastasis-initiating regenerative progenitors, plays a crucial role in the emergence of LUAD SOX2+ progenitors. Mechanistically, L1CAM induces the planar cell polarity (PCP) complex to activate c-Jun, which in turn interacts with the chromodomain helicase CHD1 to drive Sox2 transcription and generate metastasis-initiating regenerative progenitors. Treatment with an L1CAM antibody drug conjugate (ADC) effectively eliminates these LUAD cells and eradicates patient-derived xenograft metastases. Our findings identify L1CAM/PCP signaling as a driver of the SOX2+ LUAD metastatic progenitor state and provide an approach to treating metastasis by targeting L1CAM+ LUAD progenitors.

overall_design: For scRNA-seq data, mouse lung cancer cells were generated from KrasG12D;TP53-/- (KP) mice and submitted for single-cell sequencing after fresh tumor dissociation (day 0) or grown as tumoroids in Matrigel before submitted for single-cell sequencing (day 7). For ChIP-seq analysis, protein bound chromatin was precipitated using anti-CHD1, anti-cJun or IgG control using H23 cells.

first: Yasemin

last: Kaygusuz

first: Carson

last: Kenum

first: Mohamed

last: Gatie

first: Lan

last: He

first: Roshan

last: Sharma

first: Ronan

last: Chaligné

first: Abdul

last: Khan

first: Mary Ann

last: Pohl

first: Thomas

last: White

first: Paul

last: Balderes

first: Ivo

last: Lorenz

first: Tuomas

last: Tammela

first: Anna-Katerina

last: Hadjantonakis

first: Karuna

last: Ganesh

first: Charles

last: Rudin

first: Joan

last: Massagué


title: Dual function of DOT1L suppresses tumor intrinsic immunogenicity in Hepatocellular carcinoma [ATAC-seq]

first: Siyuan

last: Xu

overall_design: To explore the changes of chromatin accessibility upon DOT1L KO, we performed assay for transposase accessible chromatin with high-throughput sequencing (ATAC-seq) experiments in HuH-7 cells.

first: Xianjiang

last: Lan


title: Perception of a quorum sensing signal by cell surface immune receptors increases plant disease resistance

first: Huiming

last: Zhang

address: No. 3888 Chenhua Road

institute: Shanghai Center for Plant Stress Biology, and CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences

summary: Bacterial quorum sensing (QS) during pathogenesis is an indicator of increasing danger. How sessile plants perceive QS for defense is unclear. Here, we show that Arabidopsis thaliana perceives 2'-aminoacetophenone (2’-AA), a volatile QS signal from Pseudomonas aeruginosa, through cell surface pattern recognition receptor (PRR) complexes, resulting in multistrategic defense and disease resistance. The 2’-AA-induced plant immunity requires chemical and genetic specificity. 2’-AA binds to the cytoplasmic domain of BRI1-ASSOCIATED RECEPTOR KINASE1 (BAK1) and induces the formation of PRR complexes that initiate the plant immune responses. 2’-AA stimulates plant exudation of acetic acid, a volatile compound that effectively quenches QS and inhibits P. aeruginosa virulence. Plants exposed to 2’-AA reshaped the root microbiome by suppressing the abundant Pseudomonad taxa with increased bacterial diversity. These results illustrate the ability of plants to perceive and respond to pathogen QS.

overall_design: The aim of this experiment was to study the effect of acetic acid on the gene expression of Pseudomonas aeruginosa. Acetic acid/water was added to Pseudomonas aeruginosa bacteria solution with OD=0.01, and the final concentration of acetic acid was 0.00% in the control group and 0.04% in the treatment group. Bacteria were collected after 4 hours of treatment, with 3 replicates in each group

first: Danxia

first: Yang

last: Zhou

first: Wenjia

last: Yu


title: Regulation of oxygen-sensing through oxygen-dependent degradation of transcription-coupled transducers

city: Nottingham

first: Michael

last: Holdsworth

address: University of Nottingham, University Park

country: United Kingdom

institute: University of Nottingham

summary: The sensing of molecular oxygen (O2) is an important component of growth and development in both animals and plants. Few substrates of the plant oxygen-sensing PCO N-degron pathway have been identified. Here we show that HYPOXIA TRANSDUCER (HYT)1, a nuclear-localised tail anchored-domain protein, is a substrate of this pathway through a Cys-2 dependent N-degron. Although the biochemical function of HYT1 is not known, genetic evidence shows that it is an important component in the transduction of oxygen-sensing, required for tolerance to ambient hypoxia and specific developmental processes. Expression of HYT1 is directly activated by group VII ETHYLENE RESPONSE FACTOR TRANSCRIPTION FACTORS (ERFVIIs), that are also pathway substrates. Thus HYT1 regulates hypoxia survival in an oxygen-dependent way following activation by ERFVIIs.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for prt6-1hyt1-1 mutant lines with our published datasets of Col-0, prt6-1, prt6-1erfvII lines grown for 7 days in continuous light (Zubrycka, A., Dambire, C., Dalle Carbonare, L. et al. ERFVII action and modulation through oxygen-sensing in Arabidopsis thaliana. Nat Commun 14, 4665 (2023). https://doi.org/10.1038/s41467-023-40366-y)

first: Gunjan

last: Sharma


title: Low-Strength Type I Interferon Signaling Promotes CAR T-Cell Treatment Efficacy

city: Chicago

first: Erting

last: Tang

address: 5640 S Ellis Ave

institute: the University of Chicago

summary: CD19-directed chimeric antigen receptor (CAR) T-cell therapy has significantly advanced the treatment landscape for relapsed/refractory diffuse large B-cell lymphoma (r/r DLBCL). However, up to 60% of patients do not achieve a complete response. In this study, we analyzed the infusion products of eight r/r DLBCL patients with distinct clinical responses to axicabtagene ciloleucel using single-cell transcriptomics. Compared to patients with progressive disease, infusion products of complete responders demonstrated stronger signatures of type I interferon (IFN-I) signaling and cytotoxicity. Based on these findings, we developed a novel strategy to improve CD19-directed CAR T-cell treatment efficacy by incorporating IFN-I during the ex vivo manufacturing process. While high-strength IFN-I signaling increases both CAR T-cell cytotoxicity and apoptosis, low-strength IFN-I signaling selectively enhances CAR T-cell cytotoxicity without compromising viability. Our manufacturing method leverages an existing FDA-approved pharmacophore to improve CAR T-cell efficacy without altering CAR expression or current manufacturing protocols. This study demonstrates proof-of-principle for IFN-I as a modulator to enhance CAR T-cell treatment efficacy in vivo, showcasing its translational potential for improving CAR T-cell therapy.

overall_design:
Single-cell RNA sequencing (scRNA-seq) was performed to profile cells in the infusion products (IPs) from eight relapsed/refractory diffuse large B-cell lymphoma (r/r DLBCL) patients treated with Axicabtagene Ciloleucel. Five of these patients achieved a complete response (CR), and three experienced progressive disease (PD). The raw sequencing data for the CR IPs (GSM7505070, GSM6281133, GSM6281134, GSM7505071, GSM6281135) were previously reported under accession number GSE207192 by an earlier study from our lab. In this study, we re-analyzed the raw data to generate processed data. All data pertaining to the PD IPs were newly generated for this study.

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

last: Hu

first: Jun

last: Huang


title: A multi-omic dataset of cellular and microRNA profiles in human breast milk across a spectrum of gestational ages

status: Public on Apr 15 2026

first: ling

last: ma

state: Guangdong

address: No. 9 Jinsui Road, Tianhe District, Guangzhou City, Guangdong province

institute: Guangzhou Women and Children’s Medical Center

summary: Breast milk composition dynamically adapts to factors like gestational age at birth. This multi-omics dataset integrates single‑cell RNA sequencing and exosomal miRNA profiles from the same breast milk samples, capturing cellular and molecular transformations that meet the developmental needs of preterm and term infants. It provides a unique resource for investigating maternal‑neonatal interactions, personalized nutrition, and infant development across cellular and regulatory dimensions.

overall_design: This study collected breast milk samples at one month postpartum from mothers of preterm and term infants, and simultaneously constructed an integrated single‑cell transcriptome and exosomal miRNA dataset.

first: Ling

last: Ma

first: Zhengming

last: Zhan

first: Kang

first: Xia

last: Hong

first: Yangke

last: Li

first: Yanyan

last: Huo

first: Daqian

last: Zhu

first: Lian

last: Jiang

first: Fan

last: Yang

first: Yanjun

last: Zhao

first: Wenxian

last: Wang

first: Jiaojiao

last: Song

first: Junmei

first: Jinjin

last: Chen


title: Single-cell CITE-seq profiling of human bone marrow B cells with IgD and IgM antibody-derived tags

city: Tucson

first: Bao

last: Thai

state: AZ

address: 1656 E Mabel St

institute: University of Arizona

summary: We performed single-cell RNA sequencing with cellular indexing of transcriptomes and epitopes by sequencing (CITE-seq) on human bone marrow samples to characterize B cell populations. Cells were profiled using the 10x Genomics Chromium platform with simultaneous measurement of gene expression and antibody-derived tags (ADT), including IgD and IgM surface markers. This dataset enables integrated analysis of transcriptomic and protein-level features to resolve B cell developmental and functional states within the bone marrow microenvironment.

overall_design: Human bone marrow cells were processed for single-cell CITE-seq profiling using the 10x Genomics Chromium platform. Cells were labeled with oligonucleotide-conjugated antibodies targeting IgD and IgM to quantify surface protein expression alongside transcriptomic profiling. Single-cell suspensions were loaded onto the Chromium controller for droplet-based partitioning, followed by library preparation for gene expression (GEX) and antibody-derived tag (ADT) libraries. In addition, V(D)J libraries were generated to profile B cell receptor repertoires.  Sequencing was performed on an Illumina platform to generate paired-end reads. Raw sequencing data were processed using Cell Ranger pipelines to generate gene expression and ADT count matrices. Downstream analyses integrate RNA, protein, and V(D)J information to characterize B cell populations and their functional states.


title: Ovarian transcriptomic profiling of fitness-related genes in F4 inbred mice and to validate differentially expressed genes using qRT-PCR

city: Bareilly

first: Pushpendra

last: Kumar

state: Uttar pradesh

address: Izatnagar

department: Animal Genetics

country: India

institute: ICAR-IVRI

summary:
Purpose: To investigate the differentially expressed genes in high litter size samples v/s low litter size samples of F4 inbred Swiss albino mice using RNA-Seq and to validate some identified differentially expressed genes using qRT-PCR.
Methods: Intact ovarian tissue samples were obtained from six F4 female [from two groups i.e. three from high litter size group (HLS; n=3) and three from low litter size group (LLS; n=3)] inbred mice, after assessment of estrous phase of ovarian cycle by vaginal cytology smear technique (Byers et al., 2012). After sacrifice of mice, their intact ovaries were rapidly harvested and immediately preserve in RNAlater (Invitrogen). The QC passed libraries were subjected to RNA sequencing by use of HiSeq X10 of Illumina® platform. The paired ends (2 X 150 bp) reads were sequenced and about 3GB raw data were generated for both high and low groups, separately. The provided raw data were processed with trimgalore for quality purpose and kallisto pipeline to get transcript abundances. Tximport was used to generate gene counts and DESeq2 was performed on gene count data of RNA-Seq experiment to get DEGs. DEGs in HLS v/s LLS groups in Swiss albino mice were subjected to functional enrichment using bioinformatics tools, eg: Profiler and GSEA. The interaction of important DEGs having fold change ≥ ± 1.5 and Padj ˂ 0.05 was studied using Network Analyst 3.0. A total 5 DEGs identified through RNA-Seq in high and low litter size groups were validated by quantitative real time PCR (qRT-PCR).
Results: All QC passed transcriptomic libraries were sequenced in paired end read sequencing platform and on an average 49.7 million reads of 150bp per sample were generated. All six samples produced a total of 44.7 GB of data, with an average Phred score of more than 35 per sample. All six samples yielded a total of 42.23 GB of trimmed data. The average mapping percentage was 78.5. The average GC percent and unique reads percent for clean data samples were 50 and 55.66, respectively. DESeq2 analysis yielded the 1018 genes under R environment with 5 % FDR. 347 genes were found to be up regulated, and about 671 genes were found to be down regulated out of 1018 genes. Based on functional enrichment analysis of 659 DEGs with fold change ≥ ± 1.5 and Padj ˂ 0.05, 166 significantly enriched gene ontology (GO) classes were identified. Out of 166 categories, 17, 109, 28, and 12 were significantly enriched in molecular function (MF), biological process (BP), cellular component (CC), KEGG, and REAC, respectively.
Conclusion: In the present analysis of ovarian transcriptome, cell–cell signaling and metabolic related pathways were significantly enriched in HLS as compare to LLS group of F4 inbred Swiss albino mice. In these pathways, TP63, SLC16A10, APOD, S100A8, LRRK2, GPD1, CNR1, HDAC9, WNT11, LPIN1, SLC5A7, KLB, GNAI1, IRS2, TIMP4, PRKAR2B, SLC1A3, GSTZ1, FAH, CLYBL, SYNGR1, FAT4, CIDEA, ECHDC1, FMO5, GPT and ALDH1A1genes were significantly up-regulated in HLS group of inbred mice.

overall_design: Ovarian transcriptomic profiling of estrous-phased ovary to identify DEGs related to fitness in F4 inbred mice and to validate differentially expressed genes using qRT-PCR.

first: Amit

first: B

last: Saini


title: ATRX inactivation disrupts global chromatin state and topology to dysregulate neurodevelopmental pathways in glioma cells of origin

city: Houston

first: Anand

last: Singh

address: 1901 East Road

institute: MD Anderson Cancer Center

summary: To investigate the role of cohesins in murine neuroprogenitor model (Tp53-/-, Atrx+; Tp53-/-, Atrx -/-)

overall_design: SMC1 CUT&TAG was performed on murine progenitor models

first: Prit Benny

last: Malgulwar

first: Annette

last: Machado

first: Jason

last: Huse

first: Kunal

last: Rai

middle: K

first: Ajay

last: Saw


title: The RNA-binding protein PTBP3 regulates alternative polyadenylation in naïve B cells

city: Beijing

first: Zongchang

last: Du

address: 15 Datun Road, Chaoyang District, Beijing, China

institute: IBP

summary: As an important family of RNA-binding proteins, PTB family plays crucial roles in post-transcriptional regulation of gene expression. PTBP1 and PTBP2 have been extensively characterized as important splicing factors regulating many biological processes. PTBP3 is reported to be essential for AID-targeting specificity in activated B cells. However, the physiological roles and regulatory mechanisms of PTBP3 in naive B cells are largely unknown. Here, we identified PTBP3 as a regulator of alternative polyadenylation using 2P-seq data in naive B cells. We revealed that PTBP3 promoted poly(A) signal recognition through binding to CU-rich elements in 3’ UTR and interacting with CPSF6 factor in a position- and dosage-dependent manner. Furthermore, we also demonstrated that PTBP3 could regulate mRNA stability by facilitating the usage of different poly(A) sites in mRNA. Our study will provide novel insights into the PTBP3 functions in innate immunity and immunological diseases.

overall_design: We first constructed RNA-seq libraries in naive B cells from wild type and PTBP3 knockout mice generated by CRISPR-Cas9 system, and we found that the differentially expressed genes caused by PTBP3 knockout mainly related to cell cycle and innate immunity. Given the highly enrichment of PTBP3 binding sites in intron throughthe analysis of PTBP3 CLIP-seq data, next we detected the alternative splicing events. However, few splicing changes were observed after PTBP3 depletion. Then we performed 2P-seq in naive B cells from WT and KO mice, and we identified the APA events regulated by PTBP3 and revealed that PTBP3 could promote PAS recognition through CU-rich binding sequence in a position-, and dosage-dependent manner. To clarify the mechanism of PTBP3-mediated APA events, proteomic screening and mRNA stability assay were performed and indicated that PTBP3 regulated poly(A) site usage by interacting with cleavage and polyadenylation factor CPSF6, which produced different 3’ UTR isoforms and subsequently affected mRNA abundance.

first: Lei

first: Changchang

last: Cao

first: Yuanchao

last: Xue

first: Juan


title: CAGE-seq profiling of fast and slow growing chickens in different tissues

city: Sirius

first: Ivan

last: Yevshin

address: Olympic Ave., 1

country: Russia

institute: Sirius University of Science and Technology

summary: Genetic variation in growth rate is associated with substantial metabolic differences in poultry, but its tissue-specific effects remain insufficiently characterized. Using an F2 population derived from Russian Snow White and White Cornish chickens, we profiled liver, leg muscle, breast muscle, brain, heart and kidney from fast-growing (FG) and slow-growing (SG) birds using CAGE-seq transcriptomics.

overall_design: CAGE-seq profiling of 12 fast-growing and 12 slow-growing chickens in 6 tissues

first: Vladimir

last: Kaplan

first: Mikhail

last: Kulyashov

first: Elena

last: Shagimardanova

first: Natalia

last: Volkova

first: Oleg

last: Gusev

first: Anastasia

last: Vetokh

first: Fedor

last: Kolpakov

first: Ilya

last: Akberdin


title: Decoding the Protein Composition of Whole Nucleosomes with Knic

city: beijing

first: li

middle: yi

last: xiao

address: road of xueyuan 38

institute: peking university

summary:
Histone post-translational modifications (PTMs) controls the gene expression profile via transcriptional regulation．Aberrant histone PTMs chromatin structures lead to dysregulated gene expression and cancer progression. Nicotinic acid (vitamin B3 or vitamin PP), one of the thirteen essential vitamins, has a wide range of uses, helping to function digestive system, skin and nervous system. Here we show nicotinic acid (NA) induces histone and non-histone lysine nicotinylation, and identify 17 nicotinylation sites on core histones in HeLa cells. Also, NA-derived nicotinylation of histone lysine residues is an epigenetic modification that regulates gene transcription via altering the chromatin accessibility by generating nicotinyl-CoA.
Knic inactivates oncogene PPFIA1 transcription by inhibiting its combination with transcription factors HOXB9, and PPFIA1 was found as an important role in promoting cells spreading on the extracellular matrix and is required for migration and invasion in human breast tumor cells 1,2. However, the role and the molecular mechanisms of PPFIA1 control hepatocellularcarcinoma (HCC) initiation and progression are poorly understood. Here we demonstrate PPFIA1 promotes proliferation, migration, invasion and tumorigenesis of HCC in vivo and in vitro. It is worth noting that the expression of PPFIA1 is upregulated in multiple human carcinomas, including HCC. Our study also suggests that PPFIA1 is a promising potential target of NA for the future treatment strategies of HCC. Here, we show that administration of NA inhibits liver cancer metastasis through suppressing tumor gene PPFIA1 transcription by inducing histone Knic.

overall_design: Yixiao,Li

first: Yuhan

last: Jiang

first: Haoyi

last: Yan


title: Mast cells selectively deliver extracellular vesicle-encapsulated mRNA to colorectal cancer cells

city: Bloomington

first: Heather

last: O'Hagan

state: IN

address: 1001 E 3RD ST

department: School of Medicine

institute: Indiana University

summary: Mast cells (MCs), a type of granulocytic immune cell, exert contrasting effects on tumorigenesis. The anti- or pro-tumorigenic activity of MCs depends on the cancer type, tumor microenvironment, as well as MC localization within the tumor. Consequently, their role remains controversial and poorly understood across multiple cancer types, including colorectal cancer (CRC). Most proposed mechanisms underlying MC activity in CRC have focused on MC secretion of biological factors. In this study, we demonstrated that MCs transfer extracellular vesicles containing mRNAs and proteins to CRC cells. This process occurs through a tightly regulated mechanism that requires direct cell-cell contact, calcium signaling, and integrin-mediated interactions. Such requirements resemble the aspects of an immunological synapse observed between lymphocytes and cancer cells. The novel mode of intercellular communication between MCs and cancer cells described here may help refine our understanding of MC functions in cancer biology.

overall_design: Gene expression profiling analysis of RNA-seq data for LAD2 cell-derived extracellular vesicles

first: Rosie

last: Lanzloth


title: Recognition and silencing of a new transposable element

city: Planegg

first: Luca

last: Salvi

state: Please select

address: Semmelweisstr. 3

institute: ViGeneron GmbH

summary: Genomes constantly face threats from transposable elements (TEs) and other genomic parasites. While the silencing of existing TE has been well studied, little is known about how cells recognize new invading TEs that they have not previously encountered. Here we explore this question by inserting a foreign sequences into S. pombe. Our data revealed that the newly invading TE tj1 is recognized and targeted for silencing by RNAi and heterochromatin. The efficiency of recognition, as well as the degree and stability of silencing, depends on the copy number and insertion location of the TE. We demonstrated that RNA, rather than DNA, is sensed, and that the efficiency of TE recognition correlates with levels of RNA antisense to the TE, generated from upstream transcripts. We also show that various genes of non-transposable nature can initiate silencing. Our data show that silencing may not require recognition of specific elements in the transposon by the host defense systems, and suggest that disruption of host transcription patterns can trigger recognition of TE.

overall_design: DNA sequencing to map transposition loci, ChIP sequencings to asses chromatin states, total and polyA RNA sequencing to asses transcriptional silencing, experiments in wild type cells and different S. pombe mutants

first: Yinxia

first: Mario

last: Halic


title: Evaluation of clofazimine treatment on functional gene transcription in hepatocellular carcinoma cells

city: XI'AN

first: MENGJIAO

last: SHI

state: Shaanxi Province

address: Building C, Shengyuan Square

institute: The Second Affiliated Hospital of Xi 'an Jiaotong University

summary: Clofazimine (CFZ) is an orally administered anti-mycobacterial drug that demonstrates a broad spectrum of activity against mycobacterial infections, including leprosy and tuberculosis. CFZ also possesses anti-inflammatory and anti-tumor properties by disrupting DNA replication and inhibiting the production of IL2. Currently, this compound has been utilized in research related to drug-resistant cancer treatment, and has gained increasing recognition for its potential to enhance cancer treatment in recent years. Considering the benefits of CFZ in clinical settings, it presents itself as a promising candidate for combination drug therapy aimed at hepatocellular carcinoma through the regulation of functional gene transcription. Herein, we primarily examine the role of CFZ treatment throughout the functional gene transcription process in hepatocellular carcinoma cells.

overall_design: To assess the function of CFZ treatment in hepatocellular carcinoma cells, MHCC97-H cells were treated with CFZ (30 μM)  for 16 hours. Then, both CFZ-treated and untreated MHCC97-H cells were gathered for RNA sequencing analysis.

first: Pengfei

last: Liu

first: Mengjiao

last: Shi

first: Liangwen

first: Jiayi

last: Xu

first: Xinyan

last: Li

first: Kailing

last: Hu


title: Gene expression profiling of GLP1R-IL17A axis in obesity driven PTPN11-mutant leukemia

city: Indianapolis

first: Santhosh Kumar

last: Pasupuleti

state: Indiana

institute: Indiana University School of Medicine

summary: Obesity-associated metabolic inflammation contributes to the progression of PTPN11-mutant myeloid leukemia through activation of the IL-17A–mediated inflammatory axis and suppression of GLP-1R signaling. In this study, mRNA-seq was performed on hematopoietic and immune cell populations from a murine transplantation model of Shp2E76K/+ leukemia under obese conditions, with or without treatment using an anti-IL-17A antibody and a GLP-1R agonist. Transcriptomic analysis reveals that obesity promotes leukemogenesis by enhancing myeloid expansion, lipid metabolic reprogramming, and immunosuppressive remodeling characterized by M2-like tumor-associated macrophage accumulation, T cell exhaustion, and impaired antigen presentation. Therapeutic targeting of the GLP-1R–IL-17A axis restores immune function, including Ciita-dependent antigen presentation and IFNγ signaling, and reduces leukemic burden. These data provide insight into the molecular mechanisms linking obesity-driven inflammation to leukemia progression and identify potential therapeutic targets.

overall_design: CD45.2⁺ donor bone marrow (BM) cells from Shp2E76K/+;LysM-Cre⁺ mice were competitively transplanted with age-matched Boy/J CD45.1⁺ BM cells at a 1:1 ratio into lethally irradiated recipient mice (Ob/Ob and wild-type; 700 cGy + 400 cGy) via intravenous tail vein injection. Eight weeks post-transplantation, obese (Ob/Ob) recipients were randomized to receive one of the following treatments for 30 days: vehicle control, the GLP-1R agonist Beinaglutide (3 mg/kg, subcutaneous), anti–IL-17A antibody (200 μg/mouse, intraperitoneal, three times per week), or combination therapy. At the end of treatment, total RNA was isolated from bone marrow cells and adipose tissue macrophages (ATMs). RNA-seq was performed on samples from three independent biological replicates per group (n = 3 mice per treatment group), including vehicle and wild-type (WT) controls.

first: Reuben

last: Kapur


title: Epigenetic control of microglial mitochondrial immunity by KAT7 drives Alzheimer’s disease pathogenesis [RNA-Seq]

city: Baltimore

first: Yongqing

state: MARYLAND

address: 725 N Wolfe Street, WBSB 216

department: Physiology

institute: Johns Hopkins University

summary: Mitochondrial DNA (mtDNA)-driven innate immune signaling sustains chronic neuroinflammation in neurological diseases such as Alzheimer’s disease (AD), yet how this pathway is regulated in microglia remains poorly understood. Here, we identify the histone acetyltransferase KAT7 (HBO1) as a central epigenetic regulator that links chromatin remodeling to mitochondrial immune activation. KAT7 and its histone mark H3K14ac are elevated in microglia from 5×FAD mice and human AD brains. Integrative transcriptomic and epigenomic analyses reveal that KAT7 activates transcription of Cmpk2, a mitochondrial kinase essential for mtDNA synthesis. Loss of KAT7 reduces Cmpk2 expression, impairs mtDNA replication and release, and consequently suppresses cGAS-STING and NLRP3 signaling. Importantly, both microglia-specific deletion and pharmacological inhibition of KAT7 mitigate cytosolic mtDNA-induced neuroinflammation, decrease amyloid-β burden, restore synaptic plasticity, and improve cognitive function in 5×FAD mice. Together, these findings uncover an epigenetic-mitochondrial axis sustaining microglial pathogenicity and establish KAT7 as a promising therapeutic target for AD.

overall_design: Three biological replicates were sequenced per group. For each sample, RNA was extracted from BV2 cells with TRIzol reagents (Invitrogen). High-throughput RNA sequencing (RNA-seq) was performed by Illumina NovaSeq 6000 at Novogene (CA, USA).


title: Targeting UBE2F induces a resilience program enhancing CD8 T cell immunity [Bulk RNA-seq]

first: Xiaonan

last: Ma

address: NO.30 Shuangqing Road

institute: Tsinghua University

summary: CD8 memory T cells (TMEM) and exhausted T cells (TEX) are essential for host defense against infection and cancer, yet their therapeutic potential is often limited by insufficient persistence and sustained functional capacity. Strategies to enhance the longevity of both populations remain scarce. Here, we demonstrate that ablation of UBE2F, a neddylation E2 enzyme, induces a resilience program in CD8 T cells that operates across both TMEM and TEX compartments, resulting in improved viral and tumor control. This resilience state is characterized by enhanced self-renewal and survival without perturbing the conventional CD8 T cell differentiation trajectories. Mechanistically, UBE2F deficiency inhibited neddylation of CUL5, leading to accumulation of JUNB and upregulation of IL-2Rβ. The increased IL-2Rβ expression hypersensitizes CD8 T cells to physiological IL-15, thereby conferring the resilience features. Together, these findings identify the UBE2F-CUL5-JUNB-IL-2Rβ axis as a conserved post-translational mechanism regulating CD8 T cell longevity across memory and exhausted states, providing a novel strategy for enhancing antiviral and antitumor immunity.

overall_design: Naive wildtype (WT) or UBE2F KO (CKO) P14 cells were transferred into recipient mice infected with LCMV Armstrong. 14 days post-infection, donor P14 cells from spleens were sorted by FACS for Bulk RNA-seq analysis.


title: Single-cell RNA sequencing reveals that Epac1 deletion attenuates Müller glial pathological activation in ischemia-induced retinopathy

city: Galveston

first: Wenbo

last: Zhang

address: 301 University Blvd.

department: Ophthalmology

institute: University of Texas Medical Branch

summary: Here we report the single-cell RNA sequencing (scRNA-seq) analysis of retinas from WT and Epac1-knockout mice under Oxygen-Induced Retinopathy (OIR) and Room Air (RA) conditions. The OIR model was induced by exposing pups to 70% oxygen from postnatal day 7 (P7) to P12. This study aims to delineate the cellular heterogeneity and investigate the neuroprotective mechanisms associated with Epac1 deletion, with a specific focus on Müller glial pathological activation and retinal neurodegeneration. Retinal tissues were collected at postnatal day 17 (P17) to establish a comprehensive transcriptomic profile of the ischemia-induced retinopathy model.

overall_design: Retinal samples were harvested from WT and Epac1-knockout neonatal mice. The ischemia-induced retinopathy model was established using Oxygen-Induced Retinopathy (OIR) conditions (70% oxygen exposure from P7 to P12), with age-matched mice raised in standard Room Air (RA) serving as controls. Single-cell suspensions were prepared from retinas collected at P17. Libraries were constructed using the 10x Genomics Chromium platform and sequenced to assess transcriptomic dynamics and Müller glial responses.

first: Shuizhen

first: Fan

last: Xia

first: Zhongqiao

last: Lu

first: Erick

last: Palacios

first: Fang

last: Mei

first: Massoud

last: Motamedi

first: Xiaodong

last: Cheng

first: Hua


title: A community machine learning challenge to predict the effects of gene perturbations on T cell differentiation for cancer immunotherapy

city: Cambridge

first: Jiaqi

state: MA

address: 75 Ames St

institute: MIT; Broad Institute

summary: Perturbations of genes with functional importance in T cells could be used to change the distribution of CD8 T cell states to enhance anti-tumor functions for cancer immunotherapies. We launched a world-wide computational challenge to predict the effects of gene perturbations and to devise objective functions for prioritizing gene perturbations that lead to desired T-cell state distributions. We supported the challenge by generating a single-cell Perturb-seq dataset profiling the effect of knocking out 73 individual expert-defined genes in T cells transferred into a mouse melanoma model. We compared the top algorithms developed by participants, and found that performance was primarily determined by the prior data used for gene feature representation, with perturbational data derived features, proving most effective. Experimental validation of the top 61 genes nominated by the algorithms revealed that perturbation of Ndufv2 and Dimt1 reached the defined objective and biased differentiation toward desired states.

overall_design:
We used in vivo CRISPR to knockout each of 73 genes in naïve CD8+ T cells, followed by transfer of perturbed cells into mice. We restricted the CD8+ T cell repertoire using OT-1 TCR transgenic mice, in which CD8+ T cells express a TCR specific for the ovalbumin-derived peptide OVA257-264 (SIINFEKL) presented by H-2kb, enabling recognition of B16-OVA melanoma cells that express ovalbumin. Naïve Cas9-expressing OT1+ CD45.2+ CD8+ T cells were transduced with a library of 257 single guide RNAs (sgRNA). After five days, the modified naïve T cells were adoptively transferred to congenic CD45.1+ mice, which were then subcutaneously injected with B16-OVA melanoma cells 1 day after T cell transfer to examine how the individual loss of genes would affect T cells in the tumor microenvironment. The tumor-infiltrating perturbed T cells were then collected after 14 days (when exhausted T cells accumulate) and analyzed by single-cell RNA sequencing.

In the follow-up screen, we selected 57 target genes and designed 3 guides per gene. We performed a Perturb-seq of sgRNA knockouts following the same protocol and then the same steps as before, with additional hashtag staining to enable multiplexing of samples from individual mice.

first: Marc

last: Schwartz

first: Mohammed

last: Mutaher

first: Oluwatomisin

last: Olajide

first: Yuri

last: Pritkyin

first: Orr

last: Ashenbrg

first: Nir

last: Hacohen

first: Caroline

last: Uhler


title: Epigenetic control of microglial mitochondrial immunity by KAT7 drives Alzheimer’s disease pathogenesis [scRNA-Seq]

first: Yongqing

last: Liu

overall_design: FACS purified live microglia from 7-month-old mouse brain were sequenced for each group. scRNA-seq libraries were constructed using the using the 10x Genomics Chromium GEM-X Universal 3' Gene Expression v4 4-plex On-Chip Multiplexing (OCM) kit (CG000768, Rev A) according to the manufacturer’s protocol. Libraries were sequenced on an Illumina NovaSeq 6000 to a depth of ~20,000 reads per cell, targeting ~10,000 cells per sample.


title: Pristimerin enhances erastin-induced ferroptosis in AML cells via the ATF3/SLC7A11 axis

city: Chongqing

first: shan

last: chen

address: No. 439, Xuanhua Road, Yongchuan District

department: Yongchuan Hospital

institute: Chongqing Medical University

summary: Acute myeloid leukemia (AML) is a highly aggressive hematologic malignancy predominantly seen in adults, with chemotherapy remaining the primary modality for its clinical management. Nevertheless, the efficacy of chemotherapy is often compromised by issues such as drug resistance, toxicity, and long-term adverse effects, particularly in refractory and relapsed patients. Natural products have historically served as a vital source for the development of anti-cancer agents.

overall_design: In this study, we examined the therapeutic potential of pristimerin (PM), a natural bioactive compound derived from the Malvaceae and Portulacaceae families, against acute myeloid leukemia and explored its underlying mechanisms. Our findings indicate that PM effectively suppressed AML cell proliferation, triggered apoptosis, and arrested the cell cycle at the G0/G1 phase. Furthermore, PM was found to enhance erastin-induced ferroptosis via modulation of the ATF3/SLC7A11 axis, characterized by increased iron ( Fe2+) content, elevated malondialdehyde (MDA) levels, and , and decreased glutathione (GSH) levels. Mechanistically, PM augmented erastin-induced ferroptosis by regulating the expression of ATF3/SLC7A11 , and knockdown of ATF3 significantly attenuated the ferroptosis effec. In conclusion, our results elucidate a previously uncharacterized role of PM in erastin-induced ferroptosis through the modulation of ATF3/SLC7A11 pathway, indicating its potential as a naturally sourced therapeutic strategy for refractory and relapsed AML.

first: Shan

last: Chen


title: Epigenetic control of microglial mitochondrial immunity by KAT7 drives Alzheimer’s disease pathogenesis [Cut &  Tag]

overall_design: CUT&Tag was performed with Hyperactive Universal CUT&Tag Assay Kit for for Illumina Pro (TD904, Vazyme) according to the manufacturer’s instructions. In brief, BV2 cells were collected and counted same number for each group. Nuclei were isolated from BV2 cells and bounded to Concanavalin A (ConA)-coated beads. Subsequently, Nuclei were resuspended in antibody buffer and incubated with primary antibodies against H3K14ac (rabbit, Cell Signaling Technology, #7627), H3K4me3 (rabbit, Cell Signaling Technology, #9751) and IgG (rabbit, Cell Signaling Technology, #66362) at 4 °C overnight. On the next day, samples were incubated with goat anti-rabbit secondary antibodies (1:50, Cell Signaling Technology, #35401). The samples were incubated with pA/G-Tn5 transposase. After transposon activation and fragmentation, 0.5 pg Spike-in DNA was added to each sample and total DNA was isolated, amplified, and purified to construct library. The library for sequencing was constructed with TruePrep Index Kit V2 for Illumina (TD202, Vazyme) and VAHTS DNA Clean Beads (N411, Vazyme) were used for purification steps. The library was sequenced on an Illumina NovaSeq (PE 150) at Novogene.


title: The homeostasis of endoplasmic reticulum stress and autophagy regulates functional gene transcription in hepatocellular carcinoma cells

first: MENGJIAO

last: SHI

summary: Current studies have indicated an intricate and bidirectional regulatory interplay exists between autophagy and endoplasmic reticulum (ER) stress. Both processes collaborate to maintain cellular homeostasis and play critical roles in the development and progression of hepatocellular carcinoma. On one hand, autophagy alleviates ER stress by degrading misfolded proteins, acting as a complementary mechanism to the unfolded protein response (UPR) for restoring ER homeostasis. It can also directly mitigate ER stress by removing specific stressors. On the other hand, ER stress is capable of activating numerous associated functional proteins of autophagy. Upon activation, autophagy decreases the level of ER stress via multiple pathways. This feedback regulatory mechanism establishes the homeostasis between ER stress and autophagy by dynamically balancing stress responses and autophagic activities. Herein, we primarily examine the role of homeostasis between ER stress and autophagy throughout the functional gene transcription process in hepatocellular carcinoma cells.

overall_design: To assess the function of homeostasis between ER stress and autophagy, MHCC97-H cells were treated with autophagy inhibitor, chloroquine (CQ, 40 μM), and ER stress inhibitor, melatonin (MLT, 0.2 mM), for 16 hours. Then, CQ-treated, MLT-treated and untreated MHCC97-H cells were gathered for RNA sequencing analysis.

first: Pengfei

first: Mengjiao

last: Shi

first: Liangwen

last: Yan

first: Jiayi

last: Xu


title: Reciprocal Zeb1-Fgfr3 Regulation Controls Skeletal Development

city: NanJing

first: Chuyue

last: Pan

address: 639 Longmian Ave.

institute: China Pharmaceutical University

summary: Mesenchymal stem cell (MSC) lineage commitment during bone development is orchestrated by specific transcriptional factors, but the molecular drivers remain elusive. Here, we identify the zinc-finger transcription factor ZEB1 as a pivotal regulator of early skeletogenesis in perichondrial stem cells.

overall_design: To elucidate the molecular mechanisms underlying Zeb1 function in chondrocyte and osteoblast differentiation, Prx1+-MSCs were isolated from WT (Prx1-Cre+; ROSA-YFP; Zeb1wt/wt) and Zeb1Prx1 (Prx1-Cre+; ROSA-YFP; Zeb1fl/fl) mice for RNA-seq analysis.

first: Chenzi

last: Zang

first: Caiyun

last: Xiong

first: Cheng

last: Tang

first: Jiayue

last: Tian

first: Yuhang

last: Bao

first: Li

last: Deng

first: Yue

last: Gao

first: Stephen

last: Weiss

first: Zhaoqiu

last: Wu

first: Rong

last: Fu


title: FLCN-mutated oncocytic tumor in the thyroid defines a biologically distinct subset characterized by metabolic remodeling and canonical oncogenic signaling suppression [RNA-Seq]

city: Qingdao

first: liu

last: yanjun

state: shangdong

address: No. 1677 Wutaishan Road

department: Department of Pathology

institute: Qingdao University

summary: Birt-Hogg-Dubé (BHD) syndrome is a rare autosomal dominant disorder caused by germline pathogenic variants in FLCN. Here, we describe an oncocytic tumor in the thyroid harboring pathogenic FLCN alterations. The tumor showed indolent clinical behavior and was composed of solid sheets of oncocytic cells with abundant granular eosinophilic cytoplasm. Mitochondrial genome sequencing demonstrated preserved mitochondrial architecture without pathogenic mitochondrial DNA alterations. In vitro functional studies demonstrated that FLCN deficiency was associated with global attenuation of canonical phosphorylation–dependent signaling pathways, activation of AMPK signaling, upregulation of GPNMB, and increased expression of the mitochondrial marker Prohibitin, consistent with a cellular stress response. RNA sequencing analyses further indicated coordinated suppression of multiple metabolic and signaling pathways. These findings suggest that an FLCN-mutated oncocytic tumor in the thyroid represents a biologically distinct subset driven primarily by compensatory mitochondrial biogenesis rather than by classical oncogenic signaling activation or primary mitochondrial genome instability.

overall_design: We performed histopathological evaluation, mitochondrial genome sequencing, in vitro functional assays, and RNA sequencing on a FLCN-mutated oncocytic thyroid tumor from a patient with Birt-Hogg-Dubé syndrome, to characterize its clinical, molecular and transcriptomic features.

first: Weimao

last: Kong

first: Longnv

first: Jigang

last: wang


title: Individualised Treatment Approach for Advanced Meningeal Metastases: A Case Study of Ommaya Capsule Implantation

city: Jinhua

first: QI

last: TU

address: 365 Renmin East Road, Wucheng District

institute: Zhejiang University School of Medicine

summary: Leptomeningeal metastasis is a rare type of brain metastasis without effective therapeutic guidelines. Herein, we report emergency Ommaya capsule implantation performed for treating meningeal metastases from parathyroid carcinoma in a patient with intracranial hypertension. A 52-year-old woman was admitted to our hospital with recurrent headaches for 2 months and episodic vertigo for 2 days. The patient was hospitalised but did not exhibit abnormal intracranial signals. As her symptoms did not improve following transfer, the patient was diagnosed with a meningeal tumour, with a high suspicion of metastasis from parathyroid cancer. Conservative treatment was ineffective, and her symptoms worsened with severe headaches and shortness of breath.

overall_design: The patient underwent cerebellar hemispherectomy combined with Ommaya capsule implantation in the intensive care unit. Following surgery, she received intrathecal methotrexate injection combined with oral amlotinib. The patient recovered well post-treatment and continued chemotherapy. The patient survived for more than 12 months and ultimately died owing to disease progression. This case demonstrates that simple Ommaya capsule implantation is a safe and effective treatment for patients with advanced leptomeningeal metastasis.This approach is less traumatic and can rapidly control intracranial pressure, create conditions for subsequent treatment, and prolong survival.

first: Qi

last: Tu


title: Resolving cell-cell interaction networks and their molecular logic in complex tissues

first: Qiangfeng

middle: Cliff

last: Zhang

address: No. 1 Qinghuayuan Street

summary: Cells in complex organisms function through extensive interactions, yet mapping these interaction networks at scale remains challenging. Here, we present CCI-seq, a high-throughput method to unbiasedly capture cell-cell interactions by combining cell clump combinatorial indexing with single-cell sequencing. CCI-seq identified known interactions and fine-grained cellular organization in the mouse kidney and intestine, and uncovered aberrant interactions and disrupted spatial organization in adenomatous polyposis coli knockout (Apc-KO) mouse intestines. Its application to human colorectal cancer (CRC) revealed subtype-specific interactions linked to clinical classifications. Leveraging a single-cell RNA-seq backbone, CCI-seq achieves deep transcriptome coverage, enabling analysis of the molecular states arising from these interactions. This functional resolution revealed that interacting cells associate with distinct transcriptional programs—driving ion transport in the kidney, antigen presentation in Apc-KO villi, and NF-κB inflammatory activation in CRC. Thus, CCI-seq provides a scalable platform to unveil large-scale interaction networks and dissect their molecular and functional impacts, enhancing our understanding of complex multicellular systems.

overall_design:
This study utilizes CCI-seq (cell-cell interactions by combining cell clump combinatorial indexing with single-cell sequencing) to map large-scale cell-cell interaction networks and their associated single-cell transcriptomes across diverse complex tissues. The submission includes four main experimental groups: (1) In vitro 3D spheroids: Mixtures of human (HEK293T) and mouse (NIH/3T3) spheroids used for method validation and specificity assessment. (2) Mouse kidney: Healthy adult kidneys from wild-type C57BL/6J mice (3 biological replicates) to resolve homeostatic interaction networks. (3) Mouse small intestine: Intestines from wild-type C57BL/6J mice (3 biological replicates) serving as healthy controls, compared against precancerous intestines from a conditional Apc-knockout (Apc-KO) mouse model to investigate pathological interaction rewiring during adenoma development. (4) Human colorectal cancer (CRC): Primary tumor tissues collected from 5 patients, along with matched adjacent normal tissues from 3 of these patients serving as reference controls, to identify subtype-specific epithelial-immune networks.

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Raw files for human/patient samples are being made available in GSA (https://ngdc.cncb.ac.cn/gsa/search?searchTerm=PRJCA034558) for controlled access to the personally identifiable sequence data (PRJCA034558).
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