title: Chemotherapy-induced CA-repeat DNA fragments of breast cancer triggers robust immune responses

first: Penghan

last: Huang

address: 107 Yan Jinag West Road

institute: Sun Yat-Sen University

summary: We found that cGAS has stronger binding ability with high CA-repeat DNA. The high high CA-repeat DNA has the potential to become a reliable biomarker for breast cancer immunotherapy and combination therapy strategies.

overall_design: Transcriptome sequencing of breast cancer tisuue

first: Xiaoqian

last: Zhang

first: Huiping

last: Chen

first: Jianing


title: Improving bulk RNA-seq protocols

status: Public on Aug 19 2025

city: Martinsried

first: Wolfgang

last: Enard

state: Bavaria

address: Grossshaderner Str.2, Anthropology Human Genomics, AG Enard

department: Anthropology and human genomics

country: Germany

institute: LMU Munich

type: Expression profiling by high throughput sequencing

summary: Bulk and single-cell RNA-seq are powerful tools for transcriptomic analysis, providing insights into many aspects of molecular and cellular phenotypes. Costs constrain the amount of biological insight obtainable within a given budget, and as sequencing prices decline, efficient library protocols have become a decisive factor. In this study, we introduce an approach to systematically optimize the number of usable reads that RNA-seq protocols generate. We applied this ”funnel strategy” to prime-seq, an early-barcoding bulk RNA-seq protocol, by systematically testing critical protocol steps totaling 1080 samples in 49 libraries. This resulted in the optimized prime-seq2 protocol that increases the number of usable reads by 60 % and improves one of the most cost-efficient bulk RNA-seq protocols available. Our study also suggests that monitoring the filtering of usable reads can serve as a valuable quality control for many RNA-seq protocols and sheds light on the complexity of the conditions and interactions that shape RNA-seq library composition and their interpretation.

overall_design: During different experiments various bulk-RNAseq protocol steps were altered and explored for their performance on a read count level.

first: Felix

last: Pförtner

first: Eva

last: Briem

first: Daniel

last: Richter


title: Recessive TMEM167A variants cause neonatal diabetes, microcephaly and epilepsy syndrome [scRNA-seq]

status: Public on Aug 18 2025

city: Bruxelles

first: Miriam

last: Cnop

address: Route de Lennik 808 CP618

department: Faculté de Medecine

country: Belgium

institute: Université Libre de Bruxelles

summary: Understanding the genetic causes of diseases affecting pancreatic β cells and neurons can give insights into pathways essential for both cell types. Microcephaly, epilepsy and diabetes syndrome (MEDS) is a congenital disorder with two known aetiological genes, IER3IP1 and YIPF5. Both genes encode proteins involved in endoplasmic reticulum (ER) to Golgi trafficking.  We used genome sequencing to identify 6 individuals with MEDS caused by biallelic variants in the novel disease gene, TMEM167A. All had neonatal diabetes (diagnosed <6 months) and severe microcephaly, five also had epilepsy. TMEM167A is highly expressed in developing and adult human pancreas and brain. To gain insights into the mechanisms leading to diabetes, we silenced TMEM167A in EndoC-βH1 cells and knocked-in one patient’s variant, p.Val59Glu, in induced pluripotent stem cells (iPSCs). Both TMEM167A depletion in EndoC-βH1 cells and the p.Val59Glu variant in iPSC-derived β cells sensitized β cells to ER stress. The p.Val59Glu variant impaired proinsulin trafficking to the Golgi and induced iPSC-β cell dysfunction.  The discovery of TMEM167A variants as a new genetic cause of MEDS highlights a critical role of TMEM167A in the ER to Golgi pathway in β cells and neurons.

overall_design: scRNA-seq profiling of wildtype and mutant carrying the V59E mutation in TMEM167A  iPSC-derived samples at week 9 of the differentiation protocol


title: Single-cell analysis of adult and aged mice meninges in between olfactory bulb

city: Daejeon

first: Cheolhwa

last: Jin

address: 291 Daehak-ro, Yuseong-gu

country: South Korea

institute: Korea Advanced Institute of Science and Technology

summary: To investigate the transcriptomic changes in the meninges located between olfactory bulb of adult and aged mice. Whole meningeal cells in adult and aged mice were FACS sorted and single-cell RNA seq was performed.

overall_design: CD45 depleted menigneal cells from adult and aged mice were sorted and single-cell libraries were generated.

first: Gou Young

last: Koh

first: Seon Pyo

last: Hong

first: Myung Jin

last: Yang


title: Single-cell profiling of blood and cerebrospinal fluid in tuberculous meningitis

city: Ho Chi Minh

first: HongThai

last: LeNguyen

address: 764, Vo Van Kiet

department: Tuberculosis Group

country: Viet Nam

institute: Oxford University Clinical Research Unit

summary: Tuberculous meningitis (TBM) is the most severe form of tuberculosis, with a fatality rate of 20-50% in treated individuals. Although corticosteroid therapy can increase survival in HIV-negative people with TBM, better antimicrobial and host-directed therapies are required to improve outcome. There is, therefore, a need to better understand local immunopathologic pathways. Despite its power in identifying disease-specific cellular profiles, single-cell RNA-sequencing (scRNA-seq) has been underutilized in cerebral samples in brain infection. We employed scRNA-seq to analyze fresh pretreatment cerebrospinal fluid (CSF) from four TBM patients, along with paired peripheral blood mononuclear cells (PBMCs). While 29 cell subtypes were present in both tissues, their relative abundance varied significantly. In particular, CSF was enriched with highly inflammatory microglia-like macrophages, GZMK+-expressing CD8+ T cells, and CD56bright NK cells. The latter two subsets exhibited features associated with dysfunctional cytotoxicity. Across multiple cell types, inflammatory signaling pathways were increased and oxidative phosphorylation was decreased in CSF compared to PBMCs. This study highlights the value of scRNA-seq for exploring CSF immunopathogenesis in TBM patients and offers a resource for future studies investigating the pathophysiology of TBM and other brain infections, including potentially targetable cell populations linked with immune-mediated pathology.

overall_design: To analyze the cell composition and transcriptional landscape of PBMCs and CSF in TBM, we performed scRNA-seq on fresh paired pretreatment samples from four Tuberculosis meningitis patients.

first: Tram

last: Trinh Thi Bich

first: Lucy

last: C. Garner

first: Nhat

last: Le Thanh Hoang

first: Thu

last: Do Dang Anh

first: Nghia

last: Ho Dang Trung

first: Van

last: Le Hong

first: Guy

last: E Thwaites

first: Ha

last: Vu Thi Ngoc

first: Paul

last: Klenerman

first: Thuong

last: Nguyen Thuy Thuong


title: Effect of fibulin-3 knockdown in glioblastoma stem cells

city: Syracuse

first: Mariano

middle: S

last: Viapiano

state: NY

address: 505 Irving Ave Rm 4604

department: Neuroscience and Physiology

country: USA

institute: SUNY Upstate Medical University

summary: Whole transcriptome comparison of two mesenchymal GBM stem cell lines transfected with control vs fibulin-3 (EFEMP1) siRNAs. GBM stem cell lines GBM09 and GBM34 developed in-house from freshly-resected primary GBM tumors, using standard procecures (Galli et al.; Cancer Res (2002) 64:7011). Cells were transfected with two fibulin-3 or control siRNAs and collected 48h after transfection. Gene expression was quantified by RNAseq using standard procedures. The results suggest that downregulation of fibulin-3 affects NF-kB-dependent GBM gene signatures associated with angiogenesis and immunosuppression.

overall_design: Three independent cultures for each cell line were transfected with two previously validated fibulin-3 siRNAs or control siRNA (Hu et al., Cancer Res (2012) 72:3873). Total RNA was extracted using column purification and poly-A mRNA was enriched and sequenced using Illumina HiSeq 2000. Analysis of gene expression was used to determine a gene signature correlated with fibulin-3 downregulation. Design: 2 GBM stem cell lines x 2 conditions per cell line (control or fibulin-3 KD) x 3 independent replicates.  Fibulin-3 mRNA knockdown was confirmed by qRT-PCR of the purified mRNA before RNA sequencing.

first: Soham

last: Mitra

first: Somanath

last: Kundu


title: Conservation of cis-regulatory codes over half a billion years of evolution [snATAC-Seq]

city: Saint Louis

first: Joseph

middle: C.

last: Corbo

state: MO

address: 660 S. Euclid

department: Pathology and Immunology

institute: Washington University School of Medicine

type: Genome binding/occupancy profiling by high throughput sequencing

summary: The identification of homologous cell types across species represents a crucial step in understanding cell type evolution. The retina is particularly amenable to comparative analysis because the basic morphology, connectivity, and function of its six major cell classes have remained largely invariant since the earliest stages of vertebrate evolution. We used comparative single-nucleus chromatin accessibility analysis of lamprey, fish, bird, and mammalian retinas, which began to diverge over half a billion years ago, to demonstrate cross-species conservation of cis-regulatory codes in all six retinal cell classes. In this study, we acquired retinal single-cell gene expression profiling (scRNA-seq) and single-nucleus chromatin accessibility (snATAC-seq) from sea lamprey (Petromyzon marinus), a jawless species. We also acquired long-read sequence data from lamprey retina and single-nucleus chromatin accessibility from chicken (Gallus gallus).

overall_design: A publicly available sea lamprey transcriptome assembly was updated using newly generated long-read sequencing data. Subsequently, single nuclei multiome profiles (comprising RNA and ATAC) of the downstream migrant lamprey retina were generated with the updated assembly. Furthermore, a single-nuclei chromatin accessibility profile was generated from the newly hatched (P0) chicken, which serves as a comparison of cis-regulatory features across diverse vertebrate species.

first: Yohei

last: Ogawa

middle: C


title: Human single nuclear RNA sequencing identifies CD47 as a therapeutic target for doxorubicin-induced cardiomyopathy

first: Zhen

last: Guo

address: 4939 Children's Place

department: Medicine

institute: Washington University in St. Louis

summary: Doxorubicin cardiomyopathy (DoxCM) remains a significant clinical problem, yet its underlying mechanisms remain incompletely understood. Identifying DoxCM mechanisms that can be translated into therapeutic interventions may improve patient outcomes. We performed single nuclear RNA-sequencing on left ventricular (LV) myocardial tissue from patients with DoxCM versus non-ischemic cardiomyopathy and non-failing donors. This approach aimed to elucidate the transcriptional changes associated with DoxCM. Additionally, we conducted immunostaining, flow cytometry, antibody neutralization, and cell depletion studies to validate our findings and define in vivo mechanisms.Compared to both donors and non-ischemic cardiomyopathy, LV myocardium from DoxCM patients exhibited increased periostin-positive (POSTN+) activated fibroblasts, down-regulation of genes involved in phagocytosis, and increased expression of the anti-phagocytic molecule CD47. Immunostaining of human cardiac sections and murine studies demonstrated increased POSTN+ cells and CD47 in DoxCM and in a murine breast cancer model. CD47 antibody neutralization both prevented and treated Dox-induced reduction in LV ejection fraction and fibrosis. Mechanistically, depletion of resident cardiac macrophages blocked the cardioprotective effects of CD47 neutralization and clearance of cardiac fibroblasts. Our data support CD47 as a disease-specific target and promising therapeutic approach for mitigating cardiac dysfunction in DoxCM

overall_design:
We conducted single-nuclear RNA sequencing (snRNA-seq) on left ventricular myocardial tissues collected from donors who died without a history of heart failure (HF), and from those with end-stage HF due to either doxorubicin (Dox) or non-ischemic cardiomyopathy (NICM) without Dox exposure.

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Submitter states that nine samples are missing raw files are due to file loss.
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first: Pan

last: Ma

first: Wenjing

last: Yu

first: Kory

last: Lavine

first: Ali

last: Javaheri


title: Conservation of cis-regulatory codes over half a billion years of evolution [multiome ATAC-Seq]


title: Single-cell gene expression of a glioma cell line (GL261) cultured adherently or as neurospheres

city: Caldwell

first: Richard

middle: Luke

last: Daniels

state: ID

address: 2112 Cleveland Blvd

department: Biology

institute: The College of Idaho

summary:
GL261 cells are a widely-used model system for glioma tumors and can be cultured adherently or as free-floating cell aggregates known as neurospheres. Neurospheres can be implanted into mice where they readily form tumors. This suggests that neurospheres may more closely resemble the in-vivo tumor phenotype. Our study has two primary objectives: 1) To determine differences in gene expression between adherent cells and the tumor-forming neurospheres and 2) To determine the extent of homogeneity in these cell populations.

This project was supported by an Institutional Development Award (IDeA) from the National Institute of General Medical Sciences of the National Institutes of Health (Grant #P20GM103408) along with a Murdock College Science Research Program Grant (SR-202119904) from the M.J. Murdock Charitable Trust.

overall_design: GL261 cells were cultured adherently in DMEM with 10% FBS and 1% penicillin-streptomycin. Adherent cells were trypsinzed, collected from culture flasks, and analyzed using scRNA-Seq. Neurosphere formation was induced with the addition of epidermal growth factor (EGF, 20 ng / ml), fibroblast growth factor (FGF, 20 ng / ml) and B-27 (1:50) to the culture media. Neurospheres were collected after 12 days, trypsinized, and analyzed using scRNA-Seq.

first: Emily

middle: A

last: Freko

first: Colton

middle: E

last: Troxel

first: Ruby

last: Olvera

middle: L


title: Expression data for 3D versus 2D cell culture

city: North Chicago

first: Vivian

last: Park

state: ILLINOIS

address: 1 North Waukegan Road

institute: AbbVie Inc.

summary:
Ferroptosis is a regulated non-apoptotic cell death process characterized by iron-dependent lipid peroxidation. This process has recently emerged as a promising approach for cancer therapy. Some evidence indicates that GPX4 may be a useful target for drug development, yet factors that govern GPX4 inhibitor sensitivity in vivo are poorly understood. We find that pharmacological and genetic loss of GPX4 function was sufficient to induce ferroptosis in multiple adherent (“2D”) cancer cell cultures. However, reducing GPX4 protein levels did not affect tumor xenograft growth when these cells were implanted in mice. Furthermore, sensitivity to GPX4 inhibition was markedly reduced when cells were cultured as spheroids (“3D”).
We utilized microarray to identify genome-wide expression changes in 3D versus 2D cell culture conditions.

overall_design: 3D and 2D cells were cultured for RNA extraction and hybridization on the Clariom D, human array. For 2D culture, cells were harvested at approximately 80% confluency. For 3D culture, 2,000 cells were seeded in 96-well ultra-low attachment microplates , spun at 1,200 rpm for 2 min for spheroid formation, then pooled and harvested 48 h post-seeding.


title: ZmPP2C45 and ZmBELL4 suppress maize biochemical defense against insect herbivores

city: Shenzhen

first: Mei

last: Luo

state: Gangdong

address: Dapeng

country: China

institute: Agricultural Genomics Institute at Shenzhen, Chinese Academy of Agricultural Sciences

summary: PP2Cs represent the largest gene family of protein phosphatases. Current research has predominantly focused on the regulation of the PP2C.A family in the abscisic acid (ABA) signaling pathway. However, there is currently no documented research regarding the involvement of PP2Cs in plant responses to biotic stressors. In this study, we found that maize (Zea may) ZmPP2C45 is an essential but insufficient negative regulator of benzoxazinoids. Since BZXs are important defensive metabolites against insect herbivores, we hypothesized that the genetic knock-out of ZmPP2C45 could affect the performance of insect herbivores on these plants.To further investigate how ZmPP2C45 depleted BZX contents, we performed a comparative transcriptomics analysis on the Zmpp2c45 mutants and the wildtype control. As a result, 789 genes were found significantly up-regulated in the mutant plants, whereas 198 genes were down-regulated. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses revealed that BZX biosynthesis-related genes were over-represented among the up-regulated genes in the Zmpp2c45 plants

overall_design: Maize inbred line KN5585 was used as the genetic background for genome editing of ZmPP2C45. The expression level were tested between maize inbred line KN5585 (WT) and  ZmPP2C45 knock-out line.  Leaves of two-week-old maize seedlings were used for RNAseq analyses

first: Shaoqun

last: Zhou

first: Shanshan

last: Zhang


title: Elevated PRDM13 disrupts photoreceptor function and survival in the mammalian retina.

city: Dallas

first: Katherine

middle: J.

last: Wert

state: TX

address: 5323 Harry Hines Blvd. E7.138

department: Ophthalmology and Molecular Biology

institute: University of Texas Southwestern Medical Center

summary: Degeneration of the retina is key to the pathogenesis of some of the most common causes of blindness, but there continues to be a gap in our understanding of the molecular mechanisms leading to retinal degeneration, which in turn has impeded progress towards effective treatments. PRDM13 has been associated with the development of the retina but little is known about the impact of elevated PRDM13 on the mammalian retina, which has been linked to human retinal disease. Here, we developed a mammalian model to induce PRDM13 expression outside of endogenous levels, in a controlled time-dependent manner. We discovered that systemic overexpression of PRDM13 in the adult mouse preferentially affects the retina and reduces photoreceptor function and survival over time. The removal of excess PRDM13 halted this degenerative phenotype and allowed for some restoration of photoreceptor function. Examination of the transcriptomic profile of the retinas prior to photoreceptor degeneration highlighted that genes involved in retinal development, phototransduction, and photoreceptor health were significantly altered by the overexpression of PRDM13. This model system can now be used to further elucidate the direct and indirect targets of PRDM13 that impact photoreceptor maturation, maintenance and function during mammalian retinal development and over adulthood.

overall_design: We generated a novel mouse model that carries a doxycycline (dox) inducible human PRDM13 gene in the Rosa26 safe harbor locus. This approximately 6 kilobase (kb) knock-in contained the EF-1α ubiquitous promoter driving reverse tetracycline-controlled transactivator (rtTA) expression as well as the TRE3G promoter to control expression of PRDM13. Mice carrying this insert (heterozygous) and wildtype littermates were untreated or treated with 2mg/mL dox + 10% sucrose in the drinking water for 72 hours. Neural retinas and the remaining eye cup (RPE, choroid, sclera) were dissected, flash frozen with liquid nitrogen, and RNA was isolated for RNA-sequencing. 3 biological replicates were sent for analysis for each group.

middle: J

middle: R

last: Nettesheim


title: Conservation of cis-regulatory codes over half a billion years of evolution [multiome RNA-Seq]

last: Corbo


title: Transcriptional analysis of dendritic cells upon TLR stimulation reveals an immunosuppressive profile (RNA-Seq)

city: Guangzhou

first: Ling

last: Wang

address: zhongshan road No.74

institute: Sun Yat-sen University

summary: Dendritic cells (DCs) simultaneously prime and dampen the immune response. The transcriptional program that regulates immunosuppression in DCs is currently unknown. Here we identified ETS homologous factor as a key transcription factor that regulates DC immunosuppression.

overall_design: Purified splenic DCs (~20%) were plated in complete RPMI-1640 (RPMI-1640 with 10% FCS, 1% L-glutamate, 1% penicillin/streptomycin, and 55 μM 2-mercaptoethanol), and stimulated with  100nM CpG-B at 37 ℃ for 9 hrs. Then, cDCs (Lin- MHC II+ CD11c+) were FACS-sorted and  RNA-seq library preparation.

first: Xiaoli

last: Liu

first: Cliff

middle: Y

last: Yang


title: Transcriptional analysis of dendritic cells upon TLR stimulation reveals an immunosuppressive profile (N685 N686 scRNA-Seq)

overall_design: Mice were immunized intraperitoneally (i.p.) with or without 60 µg TLR stimulation in 100 µL PBS. Splenic cells were collected 18 hrs after  injection for cDCs (live MHCII+ CD11c+) FACS-sorting for scRNA-seq library preparation.


title: Transcriptional analysis of dendritic cells upon TLR stimulation reveals an immunosuppressive profile (N279 scRNA-Seq)

overall_design: PBMCs of four male healthy volunteers were plated individually in complete RPMI-1640 (RPMI-1640 with 10% FCS, 1% L-glutamate, 1% penicillin/streptomycin, and 55 μM 2-mercaptoethanol), and incubated at 37 ℃ for 16 hrs. Then, DCs (Lin- CD123- CD11c+ HLA-DR+) were FACS-sorted and pooled for scRNA-seq library preparation.


title: Transplantation-induced reprogramming determines successful hepatocyte engraftment

city: Shanghai

first: Lijian

last: Hui

address: yueyang road 320

department: SIBCB

institute: CEMCS, CAS

summary: While demonstrated safety and efficacy in treating liver diseases, hepatocyte-based therapy faces the challenge of limited engraftment of transplanted hepatocytes (Tx-Heps) in clinical settings, akin to issues encountered in cell therapy for other solid organs. Here, we identified a conserved reprogramming state of Tx-Heps during engraftment, marked by the activation of liver progenitor genes and bipotential differentiation capacity. Transplantation reprogramming of Tx-Heps is crucial for successful engraftment, as proven by transplantation failure upon hepatocyte-specific ablation of Arid1a, which is required for Tx-Hep reprogramming. To validate translational potential, we artificially induced Tx-Hep reprogramming by in vivo treatment of either IL6 or IC7, a chimeric IL6 family protein, both of which significantly enhance hepatocyte engraftment. Our findings unveil early-stage cell fate reprogramming during transplantation and also propose a promising strategy to augment hepatocyte engraftment, which is an interesting framework to be studied in cell transplantation for other solid organs.

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: 37 samples, including fresh hepatocytes (Hep-1-3),fresh  cholangiocytes (Chol-1-3), fresh hepatoblast (HB-1-2),  Liver progenitor like cell (LPLC-1-3), fresh human hepatocytes(PHH-1-2),  transplanted hepatocytes (Tx-Heps) havested from FR recipient at day 1(Tx-Hep-D1-1-4), day3 (Tx-Hep-D3-1-2),  day7 (Tx-Hep-D7-1-2), Tx-Heps havested from c57 recipient at day 1(Tx-Hep（WT）-D1-1-2),  Tx-Heps havested from c57 recipient preconditioned with HIR at day 1(Tx-Hep（HIR）-D1-1-5),    Tx-Heps havested from FRG recipient at day 1(Tx-PHH-D1-1-5),   Tx-Heps derived from Arid1a∆li havested from FR recipientat day 1(Tx-Hep（Arid1aKO）-D1-1-3),  and Tx-Heps derived from Arid1af/f havested from FR recipient at day 1(Tx-Hep（Arid1aWT）-D1-1-3), these animals ranged in age from 8-12w

first: Zhen

last: Sun

first: Baihua

last: Wu

first: Shujie

last: Bao

first: Ludi


title: AVJ16 inhibits IGF2BP1 in lung adenocarcinomas and prevents tumor growth in mice

city: La Jolla

first: Brian

last: Yee

state: CA

address: 9500 Gilman Dr

department: Health

institute: UCSD

summary: Igf2bp1 is an oncofetal RNA binding protein that is expressed in a wide variety of tumors.  We have recently described a small molecule inhibitor of Igf2bp1, termed AVJ16, that prevents binding of the protein to its RNA targets by directly associating with the protein.  Here, using a multi-omics approach, we have analyzed the effects of this inhibition on RNA binding (by eCLIP), RNA expression (by RNAseq), and protein expression (by mass spectrometry).  RNAs encoding members of several pro-oncogenic signalling pathways, including Hedgehog, Wnt, and PI3K-Akt, are downregulated by AVJ16 treatment, with a high correlation between reduced Igf2bp1 binding directly to the RNA, reduced expression levels of the RNA, and reduced protein expression.  AVJ16 treatment of lung adenocarcinoma (LUAD) cells in culture causes a strong reduction in proliferation, colony formation, invasion, and spheroid growth while enhancing apoptosis and cell death.  All of these effects are limited to cells expressing Igf2bp1. Chemoresistance has also been positively correlated with Igf2bp1 expression in cancer cells.  LUAD cells treated with AVJ16 show a pronounced reduction in vital dye efflux, considered to be a proxy for enhanced chemosensitivity.  In syngeneic LUAD xenografts in mice, IP injection of AVJ16 prevents growth of tumors, and incubation with AVJ16 induces cell death in human organoids from Igf2bp1-expressing LUADs but not from healthy lung tissue.  Taken together, these results suggest that AVJ16 is a promising candidate for mono- and/or adjuvant precision therapy directed against tumors expressing Igf2bp1.

overall_design: To elucidate the mechanisms of action of AVJ16 as an inhibitor of IGF2BP1, we assessed the effects of AVJ16 treatment on lung adenocarcinoma (LUAD). A comprehensive RNA sequencing analysis was conducted to identify alterations in RNA expression, H1299 cell line were treted for 48 hour thereby revealing the inhibitor’s widespread impact on RNA expression.

first: Nadav

last: Wallis

first: Tehila

last: Gershon

first: Sojod

last: Shaaby

first: Froma

last: Oberman

first: Myriam

last: Gruenwald

first: Deborah

last: Duran

first: Gilad

last: Vainer

first: Vladimir

last: Spiegelman

first: Arun

middle: K

last: Sharma

first: Joel

last: Yisraeli


title: The nuclear interactome of 14-3-3zeta reveals its critical roles for genome accessibility during early stages of adipogenesis

city: Montreal

first: Gareth

last: Lim

state: Quebec

address: R08.482- 900 rue St Denis

country: Canada

institute: CRCHUM

summary: Little is known about the molecular factors that tightly coordinate sequential actions of adipogenic cellular pathways that occur during the early stages of adipocyte precursor cells (APCs) differentiation. We previously established the scaffold protein, 14-3-3ζ, as a critical regulator of adipogenesis (Lim et al., Nat Commun., 2015). Our proteomic analysis performed in the present study suggested functional interactions between 14-3-3ζ and epigenetic effectors, such as DNMTs and HDACs, during the intial stages of APC differentiation. To assess if or how 14-3-3ζ influences chromatin accessibility in differentiating APCs, we performed ATAC-seq on 3T3-L1 preadipocytes that were transfected with a control, non-targeting siRNA (siCon) or siRNA against Ywhaz (sizeta), the gene encoding 14-3-3ζ (using either a Ywhaz-targeting or a control siRNA), followed by differentiation with the adipogenic cocktail (MDI) for 0h, 24h and 48h. Our ATAC-seq analysis revealed that 14-3-3ζ depletion impacted the accessibility of up to 1,244 chromatin regions corresponding in part to adipogenic genes, promoters, and enhancers during the initial 48 hours of differentiation. In conclusion, we report 14-3-3ζ as a key epigenetic modulator during induction of adipogenesis.

overall_design: To explore how 14-3-3zeta may influence chromatin accessibility during adipogenesis, we used murine 3T3-L1 pre-adipocytes that were transfected with siRNA against Ywhaz, the gene encoding 14-3-3zeta, followed by isolation of nuclei for downstream ATAC-Seq.

first: Sabri

last: Rial


title: p53-activated colonic pioneers bridge injury to plasticity during regeneration

city: Beijing

first: Mengxian

last: Zhang

address: Beijing

institute: Tsinghua University

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

overall_design: Refer to individual Series


title: Macrophage Regnase-3 limits tissue inflammation and injury via alternative splicing of pre-mRNA

city: München

first: Chenyu

last: Li

department: Medizinische Klinik und Poliklinik IV

institute: LMU Klinikum

summary: RNA-binding proteins regulate posttranscriptional gene translation regulate but little is known about the cell type-specific functions of Regnase3. Here, we characterized the role of Regnase3 in macrophages using RankCre-Regnase3fl/fl mice. Single cell RNA sequencing demonstrated abundant Rank expression in kidney macrophages and a correlation with the induction of chemokines, macrophage phagocytosis and maturation upon kidney injury. In various kidney injury models, RankCre-Regnase3fl/fl mice showed more inflammatory macrophages, more kidney inflammation and injury, characterized by an increase in CCR2 positive leukocyte infiltration. Mechanistic in vitro studies revealed that Regnase3 suppresses macrophage polarization towards a pro-inflammatory phenotype modulates macrophage survival, migration and phagocytosis. In silico analysis suggests that Regnase-3 regulates the alternative splicing of inflammation-related pre-mRNAs such as pro-inflammatory cytokines/chemokines and chemokine receptors. Thus, macrophage Regnase-3 limits tissue inflammation and injury via alternative splicing of pro-inflammatory pre-mRNAs.

overall_design: To investigate the Regnase3's functions in Rank positive macrophages polarization

first: Hans-Joachim

last: Anders


title: Liver RNA-seq from male C57Bl/6J on a ketogenic diet

city: Salt Lake City

first: Amandine

middle: H

last: Chaix

state: Utah

department: NUIP

institute: University of Utah

summary: A ketogenic diet (KD) is a very low-carbohydrate, very high-fat diet recently proposed to treat obesity and type 2 diabetes. While KD grows in popularity, its effects on metabolic health are understudied. (here) We show that, while KD protects against weight gain and induces weight loss, over long-term, mice develop hyperlipidemia, hepatic steatosis, and severe glucose intolerance. Unlike HFD-fed mice, KD mice are not insulin resistant and have low levels of insulin. Hyperglycemic clamp and ex vivo GSIS revealed cell-autonomous and whole-body impairments in insulin secretion. Major ER/Golgi stress and disrupted ER-Golgi protein trafficking was indicated by transcriptomic profiling of KD islets and confirmed by electron micrographs showing a dilated and fragmented Golgi network compatible with defects in insulin granule biogenesis and secretion. Overall, our results suggest long-term KD leads to multiple aberrations of metabolic parameters that caution its systematic use as a health promoting dietary intervention

overall_design:
Mice were place on one of 3 diets for 9 months, a 10% low fat control diet, a 60% high fat diet, and an 89.9% fat ketogenic diet. At sacrifice, liver were snap frozen. RNA was extracted and sequenced to compare how a ketogenic diet affects gene expression in the liver.
20462X1_Liver_Control_ALF_replicate1 was contaminated and excluded from the analysis

first: Molly

last: Gallop


title: EZH2 reads DNA 6mA to regulate survival and drug resistance of human head and neck squamous carcinoma by suppressing RIOX2-CDKN1A-NRF2 signaling axis [RNA-seq]

city: wuhan

first: Joshua

last: Guo

address: shuiguohulu

institute: wuhan university

summary:
We performed short hairpin RNA (shRNA)-mediated knockdown (KD) experiments to abrogate ALKBH1 expression.
To comprehensively understand the underlying mechanism of ALKBH1 in HNSCC, we performed RNA-seq assay and profiled gene expression alteration of HNSCC cells upon ALKBH1 knockdown.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for HNSCC cells and its KD derivatives (shALKBH1).

first: Chengli


title: EZH2 reads DNA 6mA to regulate survival and drug resistance of human head and neck squamous carcinoma by suppressing RIOX2-CDKN1A-NRF2 signaling axis [MeDIP-ChIP-seq-shRNA]

type: Methylation profiling by high throughput sequencing

summary:
To determine whether 6mA has a role in guiding EZH2 recruitment, we focused on ALKBH1, the well-defined DNA 6mA demethylase in mammals, and knocked down ALKBH1 expression in HNSCC cells using shRNAs.
We performed MeDIP-seq and ChIP-seq using these cells, and found that ALKBH1 deletion led to an obvious gain of 6mA peaks, which accompanied with enrichment of EZH2 and H3K27me3.

overall_design: Chengli,Guo


title: EZH2 reads DNA 6mA to regulate survival and drug resistance of human head and neck squamous carcinoma by suppressing RIOX2-CDKN1A-NRF2 signaling axis


title: Transcriptome and Mutant Analysis of Neuronal Genes for Memory Formation and Retrieval in Caenorhabditis elegans

city: Taipei

first: Chun-Liang

last: Pan

address: Taipei , Taiwan (R.O.C.)

country: Taiwan

institute: National Taiwan University

summary: Although it is generally believed that the formation and retrieval of memory require distinct sets of genes, little is known about the identity and temporal specificity of genes that act at different memory stages. Here we characterize the transcriptomes for the formation and retrieval of stress-induced aversive memory in the nematode Caenorhabditis elegans. Our RNA-sequencing analysis show that neuronal genes for calcium homeostasis, membrane excitability, synaptic function and signaling are progressively activated during the formation of aversive memory. Stage-specific transcriptomes further reveal that memory formation and retrieval display distinct gene activation patterns. We carried out a candidate screen of mutants for these memory genes and verified the temporal requirement of memory function for several of them. Further in-depth characterization of casy-1/calsyntenin show that while the short CASY-1B isoform acts in memory retrieval, the long CASY-1A isoform functions during memory formation, and its shed extracellular N-terminus fragment is likely a critical signal for memory regulation. Our work uncovers gene expression patterns associated with distinct memory stages and provides a foundation for future mechanistic interrogation of memory functions.

overall_design: To investigate the important neuronal genes for stress-induced aversive learning and memory, we used atp-2 RNAi to disrupt core cellular function.We then perform gene expression profiling in memory formation, retrieval and during memory formation.

first: Shyang-Jen

last: Wu


title: Single-cell multi-omic dataset mapping chromatin modifications and transcriptome during zebrafish development

city: Utrecht

first: Vivek

last: Bhardwaj

address: Padualaan 8

country: Netherlands

institute: Utrecht University

summary: Establishing a cell-type-specific chromatin landscape is crucial for the maintenance of cell identity during embryonic development. However, our knowledge of how this landscape is set during vertebrate embryogenesis has been limited, due to the lack of methods to jointly detect chromatin modifications and gene expression in the same cell. In this study, we apply T-ChIC, a method for joint profiling of histone modifications and transcriptome of single cells, to study the early embryonic development in Zebrafish (4-24 hpf).

overall_design:
Wild-type TL embryos were collected 20 minutes after fertilization in a petri dish with E3 medium and kept at 28.5°C in an incubator. For early time points (4, 6, and 8 hpf), cells were dissociated with FACSmax cell dissociation solution at RT. For later time points (10, 12 and 24 hpf) cells were dissociated Protease solution on a shaker at 28°C and 400 rpm, resuspending vigorously every 2 minutes. Cells were washed and incubated with CellTrace (thermofisher) kit using different colors for each timepoint. They were then pooled in a 0.5-mL protein-low binding tube to end up with approximately 1 million cells in total. They were then processed using the tChIC protocol.

The detailed, step-by-step scT-ChIC protocol is available at: https://www.protocols.io/view/single-cell-tchic-for-zebrafish-q26g7pbe8gwz/v1

The data preprocessing pipeline (from .fastq to count tables and peaks) is available at: https://github.com/bhardwaj-lab/scChICflow . The processed data presented here was mapped to the genome version: GRCz11/danRer11, and gene annotations used were Ensembl v104.

first: Helena

last: Viñas Gaza

first: Alberto

last: Griffa

first: Peter

last: Zeller

first: Alexander

last: van Oudenaarden


title: Linolamide in Apoptotic Bodies: A Key Factor in Mesenchymal Stem Cell Immunotherapy for Two Abortion Models

status: Public on Aug 17 2025

city: Hangzhou

first: Songying

address: No.3 Qingchun East Road

department: Department of Obstetrics and Gynecology

institute: Sir Run Run Shaw Hospital

summary:
Background: Unexplained recurrent spontaneous abortion (URSA) is a distressing pregnancy disorder with no effective medical intervention. As a potential treatment for URSA, human umbilical cord mesenchymal stem cells (hucMSCs) undergo apoptosis and release apoptotic bodies (ABs) shortly after transplantation. However, the medical effects and the exact doses of ABs in the therapy for URSA remain unclear.
Methods: Staurosporine (STS) and ultraviolet (UV) induced apoptosis in hucMSCs. Differential centrifugation, transmission electron microscopy, immunofluorescent staining, and flow cytometry were used to isolate and characterize hucMSC-derived ABs (hucMSC-ABs), respectively. Two mouse abortion models (LPS-induced and CBA/J×DBA/2 immune-mediated) mimicked URSA. Flow cytometry, real-time quantitative PCR, immunofluorescence staining, and western blotting were used to analyze macrophage polarization and inflammatory pathways. Untargeted metabolomic analysis was used to detect the metabolic composition of hucMSC-ABs. RNA sequencing analysis was used to detect the transcriptome of macrophages (Macs). Dorsomorphin was used to inhibit the AMPK signaling pathway. Small interfering RNA (siRNA) was used to knock down Gys1 in raw246.7 macrophages.
Results: STS- and UV- induced hucMSC-ABs effectively alleviated abortion in both models, depended on Macs. However, excessive dosage of hucMSC-ABs induced pro-inflammatory Macs (pro-inflam Macs), worsening fetal loss. Appropriate doses suppressed the NF-κB pathway in Macs, while high doses activated it. Neither RNase nor trypsin fully abolished hucMSC-ABs' regulatory effects on macrophage polarization. Metabolomics identified linoleamide and palmitic acid (PA) as the dominant hucMSC-AB metabolites (~1:1 ratio). RNA-seq revealed hucMSC-ABs modulated Nfkb1 and Gys1 in Macs, linked to linoleamide. Appropriate doses of the 1:1 mixture of linoleamide and PA induced anti-inflam Macs, while high dosages of the mixture induced pro-inflam Macs. Linoleamide alone activated AMPK, suppressed NF-κB via Gys1, and protected pregnancy, whereas PA induced pro-inflam Macs and promoted abortion.
Conclusion: Appropriate doses of hucMSC-ABs induce anti-inflam Macs in the uterus and prevent fetal loss, while high doses promote the polarization of pro-inflam Macs and lead to fetal loss. The effects of hucMSC-ABs in regulating Macs and treating URSA are related to different doses of linoleamide and PA on Macs. Linoleamide activates AMPK and suppresses NF-κB via Gys1. This study revealed the effect and mechanism of hucMSC-ABs intervention in fetal loss and provided a new idea for the treatment of URSA.

overall_design:
RNA-seq of Mus musculus bone marrow macrophage:
Con: mock group
LPS: inflammation positive control
STSABs: STS-induced hucMSC-ABs, one of anti-inflammatory treatment
UVAB or UVABs: UV-induced hucMSC-ABs, one of anti-inflammatory treatment


title: Targeting Mediator MED23 inhibits HCC development by inhibiting compensatory proliferation and promoting ROS-mediated cell death [RNA-Seq]

first: zhang

last: yiyang

address: 2005 Songhu Road, Yangpu District, Shanghai, China

institute: Fudan

summary: Hepatocellular carcinoma (HCC) is frequently linked to compensatory proliferating hepatocytes in damaged livers, yet the underlying molecular mechanisms remain elusive. The Mediator complex precisely coordinates multiple transcription factors and cofactors to regulate diverse physiological and pathological processes. Here we discovered that Mediator subunit MED23 is involved in the progression of HCC. Both constitutive and inducible liver-specific ablation of Med23 effectively inhibited HCC development in diethylnitrosamine (DEN)-induced HCC mouse models. Mechanistically, MED23 deficiency significantly compromised hepatocyte cell viability by reducing the stability of the NQO1 protein, thereby leading to an increase in reactive oxygen species (ROS) production. Furthermore, MED23 collaborates with the transcription factor RFX5 to regulate a novel enhancer function for IGF2 expression, which thus influences hepatocyte viability and HCC development. Consistently, overexpression of IGF2 in MED23-deficient HCC cells stabilizes NQO1 and partially restored cell growth and reduced apoptosis. Collectively, our findings underscore the significance of the MED23-IGF2-NQO1 axis in HCC progression and propose a novel therapeutic strategy for the treatment of HCC.

overall_design: Whole liver tissues from Med23f/f and Med23Δli mice 48 hours after DEN treatment, used for RNA-seq profiling.

first: Zhichao

last: Wang

first: Xiaying

last: Zhao

first: Lihua

last: Min

first: Chonghui


title: The few-celled microspore embryo transcriptome of Brassica napus

city: Amsterdam

first: Charlotte

last: Siemons

address: tt. Vasumweg, 40W7

department: Molecular Biology

institute: Wageningen University & Research

summary: Haploid embryos can be induced from cultured immature pollen following a stress treatment. In Brassica napus (B. napus), application of the histone/lysine deacetylase (HDAC/KDAC) inhibitor trichostatin A (TSA) to pollen cultures enhances the production of differentiated embryos and embryogenic callus when applied together with heat stress (Li et al., 2014). To identify genes associated with the induction of B. napus haploid embryogenesis, we employed fluorescence-activated cell sorting on microspore cultures of the LEAFY COTYLEDON1 embryo reporter line (LEC1:LEC1-GFP, Li et al., 2014) to select for embryogenic structures developing in culture, followed by RNA-sequencing. Our transcriptome analysis of the 3-day-old enriched embryo populations and in vitro cultured pollen revealed different regulatory pathways underlying the early development of embryogenic structures. Comparing FACS-sorted embryogenic transcriptomes from cultures treated with heat stress combined with either a low or a high concentration of TSA allowed us to assign transcription profiles to embryogenic structures that have a low or high potential to develop into histodifferentiated embryos.

overall_design: 10 samples were analyzed (3 different treatments). For each condition, three or four biological replicates were analyzed (1 genotype)

first: Amit

last: Kumar

first: Kim

last: Boutilier


title: Transcriptomic profiling of oligodendrocytes, astrocytes, and microglia in an experimental autoimmune encephalomyelitis (EAE) model of demyelination

city: Sacramento

first: Hyun Kyu

last: Kim

address: 2425 Stockton Blvd

department: Neurology

institute: UCDAVIS

summary: The experimental autoimmune encephalomyelitis (EAE) mouse model is widely used to study the pathophysiology of multiple sclerosis (MS), including brain inflammation and demyelination. This study investigates cell-type-specific transcriptional changes in oligodendrocytes, astrocytes, and microglia at day 30 post-induction of EAE using MOG peptide (amino acids 35–55) emulsified in complete Freund’s adjuvant (CFA) containing Mycobacterium tuberculosis, followed by pertussis toxin injections. CFA control mice received only CFA and pertussis toxin, without MOG peptide. Oligodendrocytes, astrocytes, and microglia were isolated using magnetic-activated cell sorting (MACS) from brain and spinal cord of CFA-treated and EAE-induced mice. Bulk RNA sequencing was conducted to uncover transcriptional changes associated with EAE-induced demyelination. These findings will enhance our understanding of glial cell contributions to MS pathogenesis and help identify potential therapeutic targets.

overall_design: Three-month-old C57BL/6 mice were received CFA and pertussis toxin (CFA control mice), or MOG peptide (35–55) emulsified in CFA and pertussis toxin to induce EAE. At day 30 post-induction,brain cell suspensions were prepared, and oligodendrocytes, astrocytes, and microglia were isolated using magnetic-activated cell sorting (MACS) with cell type-specific markers. Experimental groups for RNA sequencing: (1) Oligodendrocytes from CFA control mice (CFA_Ctrl_OL); (2) Oligodendrocytes from EAE mice (MOG_Ctrl_OL); (3) Astrocytes from CFA control mice (CFA_Ctrl_Astro); (4) Astrocytes from EAE mice (MOG_Ctrl_Astro); (5) Microglia from CFA control mice (CFA_Ctrl_MG); (6) Microglia from EAE mice (MOG_Ctrl_MG). Bulk RNA sequencing was performed for all cell types and conditions. Each group has 3 or 4 repeats.

first: Meina

last: Zhu

first: Yan

first: Fuzheng


title: Targeting Mediator MED23 inhibits HCC development by inhibiting compensatory proliferation and promoting ROS-mediated cell death [ChIP-seq]

overall_design: CHIP-seq of H3K27ac and H3K4me1 in Tong cell with shRNA-mediated knockdown of Ctrl or MED23.

last: Li


title: Transcriptomic profiling of oligodendrocytes, astrocytes, and microglia in a cuprizone-induced demyelination model

summary: Demyelination is a central pathological feature of multiple sclerosis and many other neurodegenerative diseases, and the cuprizone diet is a widely used model for studying this process. This study examines the transcriptional changes in key glial cell types—oligodendrocyte and astrocytes—during demyelination induced by a 4-week cuprizone diet. Bulk RNA sequencing was performed on these cells isolated using magnetic-activated cell sorting (MACS) from mice on either a normal diet or a 0.3% cuprizone diet. The experimental groups included: (1) oligodendrocytes and astrocytes from mice on a normal diet, and (2) oligodendrocytes and astrocytes from mice on a cuprizone diet. This study provides a comprehensive transcriptomic view of how these glial cell types respond to demyelination and will enhance our understanding of their individual and collective roles in this pathological process.

overall_design: Two-month-old C57BL/6 mice were fed either a standard chow diet (Naive) or a 0.3% cuprizone-enriched diet (CPZ) for 4 weeks to induce demyelination. Brain cell suspensions were prepared, and oligodendrocytes, astrocytes, and microglia were isolated using magnetic-activated cell sorting (MACS) with cell type-specific MicroBeads. Experimental groups: (1) Oligodendrocytes from mice on a normal diet (Naive_OL); (2) Oligodendrocytes from mice on a cuprizone diet (CPZ_Ctrl_OL); (3)Astrocytes from mice on a normal diet (Naive_Ast); (4)Astrocytes from mice on a cuprizone diet (CPZ_Ctrl_Ast). Bulk RNA sequencing was performed for all cell types and conditions. Each group has 3 or 4 repeats.

last: Guo


title: Islets RNA-seq from male C57Bl/6J on ketogenic diet

first: Amandine

last: Chaix

summary: A ketogenic diet (KD) is a very low-carbohydrate, very high-fat diet recently proposed to treat obesity and type 2 diabetes. While KD grows in popularity, its effects on metabolic health are understudied. (here) We show that, while KD protects against weight gain and induces weight loss, over long-term, mice develop hyperlipidemia, hepatic steatosis, and severe glucose intolerance. Unlike HFD-fed mice, KD mice are not insulin resistant and have low levels of insulin. Hyperglycemic clamp and ex vivo GSIS revealed cell-autonomous and whole-body impairments in insulin secretion. Major ER/Golgi stress and disrupted ER-Golgi protein trafficking was indicated by transcriptomic profiling of KD islets and confirmed by electron micrographs showing a dilated and fragmented Golgi network compatible with defects in insulin granule biogenesis and secretion. Overall, our results suggest long-term KD leads to multiple aberrations of metabolic parameters that caution its systematic use as a health promoting dietary intervention.

overall_design: Mice were place on one of 3 diets for 9 months, a 10% low fat control diet, a 60% high fat diet, and an 89.9% fat ketogenic diet. At sacrifice, islets were isolated and snap frozen. RNA was extracted and sequenced to compare how a ketogenic diet affects gene expression in the in islets.

first: Molly

last: Gallop


title: EZH2 reads DNA 6mA to regulate survival and drug resistance of human head and neck squamous carcinoma by suppressing RIOX2-CDKN1A-NRF2 signaling axis [ChIP-MeDIP-seq]

first: Joshua

summary:
we attempted to comprehensively assess whether EZH2 recognizes 6mA modification at the global level.
We first performed chromatin immunoprecipitation following sequencing (ChIP-seq) in human HNSCCs using antibody that recognize EZH2 to determine its genome-wide occupancies.We further investigated 6mA profiling using methylated DNA immunoprecipitation following sequencing (MeDIP-seq).


title: The role of microglia in demyelination: insights into the impact of oligodendrocyte-secreted Serpina3n

summary: Microglia, the primary immune cells of the central nervous system, play critical roles in demyelination process. This study investigates the transcriptional changes in microglia associated with demyelination and examines the role of oligodendrocyte-secreted Serpina3n in modulating microglial responses during this pathological process. Bulk RNA sequencing was conducted on microglia isolated from mice subjected to a 4-week cuprizone diet, a model of demyelination. The experimental groups included: (1) normal control mice (Norm_Ctrl), (2) cuprizone-treated wild-type mice (CPZ_Ctrl), and (3) cuprizone-treated Olig2-Cre Serpina3n flox/flox mice (CPZ_cKO). Microglia were purified from mouse brains using magnetic-activated cell sorting (MACS). The results of this study aim to deepen our understanding of olidodendroglial Serpina3n’s role in shaping microglial behavior during demyelination and could inform potential therapeutic strategies for demyelinating diseases.

overall_design: Experimental groups: Norm_Ctrl: Microglia isolated from wild-type mice fed with normal diet; CPZ_Ctrl: Microglia isolated from wild-type mice after 4 weeks of cuprizone diet; CPZ_cKO: Microglia isolated from Olig2-Cre Serpina3n flox/flox mice after 4 weeks of cuprizone diet. Microglia were isolated from mouse brains in each group using magnetic-activated cell sorting (MACS). Bulk RNA sequencing was performed on the purified microglia to profile transcriptional changes associated with demyelination and the loss of Serpina3n. Each group has 3 or 4 repeats.


title: Single cell RNA-Seq mouse skin during the initial and exhaustion stage of mechanical stretch expansion

first: Qili

last: Qian

address: 320 Yueyang Road

institute: SINH

summary: Our understanding of how skin compartments coordinate in response to mechanical stretch induced regeneration is limited. After establishing a mouse scalp expansion model and defining the regenerative exhaustion phenotype, we collected corresponding expanded skin samples (Ctrl as DPE0, DPE8, DPE36) and performed single-cell RNA transcriptomic sequencing. We characterized the impaired proliferative and differentiation capacities, as well as compromised cellular adhesion in the basal stem cells of the interfollicular epidermis in the DPE36 samples. Additionally, we observed upregulation of Mmp2 and an imbalance in ECM degradation in the dermis of DPE36 samples. Our analysis provides a temporal transcriptomic atlas of the skin's mechanoresponsive mechanisms and sheds light on how a weakened dermal niche impacts stem cell stemness, ultimately leading to regenerative failure.

overall_design: Droplet Based Single Cell RNA sequencing libraries were generated for 3 control as DPE0, 3 DPE8 and 3 DPE36 adult moue skin samples using the 10x Genomics Chromium Platform and sequenced on the Illumina Novaseq 6000 and PE150.

first: Yidan

last: Sun

first: Qingfeng

first: Caiyue

last: Liu


title: A ketogenic diet prevents metabolic switching durng time restricted feeding


title: Changes in gene Expression in different tissues before and after mouse embryonic diapause

city: Fukuoka

first: Yasuyuki

last: Ohkawa

address: 3-1-1 Maidashi

country: Japan

institute: Medical Institute of Bioregulation

summary: To elucidate the characteristics of mural TE and, polar TE, epiblast, and PrE during diapause, we performed laser microdissection followed by RNA-seq analysis. Gene ontology (GO) analysis revealed increased expression of p53- and apoptosis-related genes. p21 was upregulated in diapause embryos, while Txnip was specifically elevated in mural TE cells. Neither gene was expressed in pre-diapause embryos, but both were induced in a diapause-specific manner.

overall_design: For tissue-specific RNA-seq analysis, tissues from diapause embryos were separated using the HTlasr system.

first: Katsuyoshi

last: TAKAOKA

first: Akihito

last: HARADA


title: Interbacterial AI-2 communication drives stage-specific genetic programs to support Salmonella colonisation in the murine gut

status: Public on Aug 16 2025

city: Bangalore

first: Anmol

last: Singh

state: Karnataka

address: Lab SA-10, New Biological Science Building,IISc.

department: Department of Microbiology and Cell Biology

country: India

institute: Indian Institute of Science

summary: The cooperative response through AI-2 allows Salmonella to coordinate and regulate its community behaviours crucial for its survival and infection. In this study, we report that Salmonella Typhimurium uses AI-2 signaling to modulate the expression of chemotaxis and motility-associated genes and the formation of flagella on the bacterial cell surface. The AI-2 acts as a chemoattractant, and the cascade mediates the chemotactic response of Salmonella. Such regulations assist in the attachment and invasion of Salmonella into intestinal epithelial cells both in vitro and in a murine model. Furthermore, we determined that HilD, known to regulate motility by induction of a chemoreceptor and SPI-1 in Salmonella, along with key SPI-1 genes, is underexpressed in the absence of LuxS/AI-2 signaling, which unravels a complex regulatory network by AI-2 in Salmonella. Beyond the initial phase, this signaling facilitates survival in the presence of polymyxin B and supports intracellular survival and persistence within epithelial cells by regulating the pmrD/AB system, thereby evading the antimicrobial peptide immune response. Additionally, our findings show that Salmonella activates its LuxS/AI-2 signalling cascade within the Caco-2 epithelial cells. Complementary observation through transcriptomic profiling revealed that LuxS/AI-2 signalling governs the coordinated regulation of genes implicated in distinct phases of Salmonella pathogenesis. Lastly, using a mouse model, we show that inhibition of LuxS/AI-2 signaling in combination with antibiotics can be an alternative therapeutic approach.  Thus, our study dissects an integrated regulatory mechanism by which AI-2 signaling mediates critical processes during multiple stages of Salmonella Typhimurium pathogenesis.

sample_organism: Salmonella enterica subsp. enterica serovar Typhimurium

overall_design: The STM WT and  STM ∆luxS, STM ∆lsrK, and STM ∆lsrB knockout strains were grown in vitro in LB media till mid-log phase at 37℃ under 170rpm shaking conditions, and then isolated RNA for sequencing

first: Abhilash

middle: V

last: Nair

first: R

last: Rajmani

first: Dipshikha

last: Chakravortty


title: Toxicity Evaluation of Glyphosate and Its Formulation Adjuvant, Polyoxyethylene Tallow Amine (POEA) on Cardiogenesis Using a Novel Human Heart Organoid Model

city: Nanjing

first: hao

last: sun

state: None Selected

address: longmian street

institute: nanjng medical university

summary: Based on morphological observations of animal models, people had reported that Glyphosate (Gly) herbicide exposure would cause cardiac abnormalities. However, multiple studies focused on developing toxicity of Gly-based herbicides (GBHs), which included not only Gly but also its adjuvant, causing molecule mechanisms hard to be clarified. To evaluate both the individual and combined exposure effects of Gly and its adjuvant, Polyoxyethylene tallow amine (POEA), on human heart development, we constructed a human pluripotent stem cells-derived model named human heart organoids (hHOs), which could imitate bona fide human cardiogenesis process. We conducted an exposure of Gly and POEA throughout the differentiation process, alone or in combination with hHOS, to hHOs from day 0 to day 16. Morphological, immunofluorescencet, and transcriptomic analyses showed that individual Gly exposure would result in epicardium hyperplasia, while single POEA exposure would induce cell apoptosis and restricted cardiomyocyte contraction. The combined exposure outcomes resembled POEA, where malformation mainly occurred in cardiomyocyte subtypes specification, atrioventricular septation formation, and heart contraction protein synthesis. To conclude, by employing a novel model, we demonstrated the adverse effects of Gly and proved the adjuvant POEA possessed stronger toxicity; we also depicted the similarities and differences between single and combined exposure. Moreover, we brought a new model method for human exposure toxicity evaluation.

overall_design: To further study the Gly and POEA’s influence on hHOs and clarify the underlying mechanism, we conducted transcriptome analysis on hHOs from high-dose groups containing 10μg/mL Gly, 3.33μg/mL POEA and combined exposure of 10μg/mL Gly with 3.33μg/mL POEA at day 16 of the differentiation, when the hHOs possessed distinct phenotype.

first: Yang

last: Yang

first: Hao

first: Yao

last: Gao


title: Deciphering the role of oligodendroglial Serpina3n in EAE pathology using single-cell RNA sequencing

first: Hyun Kyu

last: Kim

summary: This study employs single-cell RNA sequencing (scRNA-seq) to investigate cellular and transcriptional changes in the spinal cord at day 27 post-induction of experimental autoimmune encephalomyelitis (EAE). Samples were collected from three groups: (1) control mice treated with CFA only (Ctrl_CFA), (2) EAE-induced mice with MOG peptide administration (Ctrl_MOG), and (3) EAE-induced mice with oligodendrocyte-specific Serpina3n deletion (Olig2-Cre Serpina3n flox/flox, Serpina3n cKO_MOG). This approach aims to dissect the cellular diversity and molecular pathways affected by EAE, with a focus on the role of oligodendroglial Serpina3n in modulating neural cellular function and neuroinflammation. The findings provide insights into cell-specific contributions to spinal cord inflammation and demyelination, highlighting Serpina3n as a potential therapeutic target.

overall_design: Experimental Groups: (1) Ctrl_CFA: Spinal cord samples from control mice treated with CFA and pertussis toxin without MOG peptide. (2) Ctrl_MOG: Spinal cord samples from mice treated with MOG peptide (35–55) emulsified in CFA and pertussis toxin to induce EAE. (3) Serpina3n cKO_MOG: Spinal cord samples from EAE-induced mice with oligodendrocyte-specific Serpina3n deletion (Olig2-Cre Serpina3n flox/flox). At day 27 post-induction, spinal cords were extracted from mice in each group. Spinal cords from three mice were pooled and processed together for Single-cell RNA sequencing using the 10x Genomics Chromium platform.

first: Meina

last: Zhu

first: Yan

last: Wang

first: Fuzheng


title: CUT&Tag-seq of H3k27me3 in vehicle and DOPAC-treated CD8+ T cells

city: Jinan

first: Jing

last: Shen

address: Wenhua West Road 44

institute: Shandong University

summary: To investigate epigenetic alterations in vehicle and DOPAC-treated CD8+ T cells

overall_design: Sorted CD8+T cells from the spleen were cultured with αCD3/CD28. CUT&Tag experiments were performed using the antibody against H3k27me3.

first: Penghu

last: Han

first: Shuzheng

last: Chu

first: Yatai

last: Chen

first: Shiyang

last: Li

first: Detian

last: Yuan


title: Mechanosensory PNECs drive airway inflammation via secretoneurin-Slc23a2

city: chiba city

first: Masahiro

last: Kiuchi

state: chiba

address: cyuoku inohana1-8-1

institute: Chiba univercity

summary: The respiratory epithelium is the body’s most exposed internal surface to airborne antigens and pathogens. Beyond serving as a physical barrier, epithelial cells actively work to expel threats by secreting mucus and cough-mediated pressure dynamics and orchestrating an immune response1. However, the mechanisms by which epithelial cells transduce mechanical changes in the airway during allergic immune activation remain unclear. We demonstrated that pulmonary endocrine cells (PNECs), a specialized rare cell population, sense airway pressure fluctuations via the mechanosensitive ion channel Piezo2 and promote eosinophilic inflammation by secreting secretoneurin, a chromogranin family neuropeptide. Piezo2-expressing PNECs form clusters at bronchial bifurcation sites, and their anatomical locations tend to experience maximal mechanical stress2. PNECs actively secrete secretoneurin in response to positive pressure ventilation in vivo. Intratracheal administration of secretoneurin induces massive infiltration of eosinophils and eosinophil extracellular trap cell death (EETosis), a pathological process central to airway inflammation3. In a murine model of Aspergillus-induced severe asthma, conditional deletion of Piezo2 or secretoneurin-encoding Scg2 specifically in PNECs, significantly ameliorated eosinophilic inflammation in the lungs. Unbiased proteoliposome screening identified sodium-dependent ascorbate transporter SLC23A2 as a binding partner of secretoneurin in eosinophils. In human respiratory tissues, a spatial transcriptome analysis and immunohistochemistry confirmed the expression of both PIEZO2 and SCG2 in PNECs. Furthermore, patients with lung eosinophilic inflammation showed significantly higher secretoneurin concentrations in bronchoalveolar lavage fluid than other patients. These results revealed a previously unrecognized epithelial mechanosensory pathway that drives eosinophilic inflammation via the PIEZO2-secretoneurin-SLC23A2-EETosis axis, thereby providing potential therapeutic targets for eosinophilic airway diseases.

overall_design: We characterized the cytological characteristics of pulmonary neuroendocrine cells using scRNAseq of mouse lungs and Xenium spatial transcriptomics of human lung tissue, and elucidated the secretion mechanism of secretoneurin induced by pressure stimulation, as well as the function of secretoneurin and the identification of its receptors in vivo and in vitro using mouse eosinophils and human sample analysis.

last: Nemoto

first: Chiaki

last: Iwamura

first: Hiroyuki

last: Yagyu

first: Masaaki

last: Seki

first: Norie

last: Hamaguchi

first: Satoshi

last: Yasuda

last: Ogasawara

first: Kaori

last: Tsuji

first: Tsuguko

last: Tomita

first: Kanae

last: Ohishi

first: Takahisa

last: Hishiya

first: Atsushi

last: Sasaki

first: Kohei

last: Kusakari

first: Astushi

last: Onodera

first: Kazuhiro

last: Furuhashi

first: Keinosuke

last: Hizuka

first: Takeshi

last: Kawasaki

first: Motoko

last: Kimura

first: Shinichiro

last: Motohashi

first: Tomohisa

last: Sakaue

first: Tumes

last: Damon

first: Shigeharu

last: Ueki

first: Naoko

last: Mato

first: Takuji

last: Suzuki

last: Takeda

last: Murata

first: Toshinori

last: Nakayama

first: Kiyoshi

last: Hirahara


title: Expression data from rat hippocampus with chronic intermittent hypoxia exposure

city: Chongqing

first: Bing

last: Li

address: Chongqing medical university

department: Department of ENT

institute: First Affiliated Hospital of Chongqing Medical University

type: Non-coding RNA profiling by high throughput sequencing

summary: Obstructive sleep apnea syndrome (OSA) is a common sleep disorder. OSA is an independent risk factor for cognitive impairment. Chronic intermittent hypoxia (CIH) is the main characteristic of OSA and the main potential culprit of OSA-induced hippocampal damage. The mechanism of CIH in the development of cognitive impairment remains unclear  The microarray was used to investigate the differentially expressed long non-coding RNAs(lncRNAs), microRNAs (miRNAs) and mRNAs in the hippocampus of  control and CIH-exposed rats. The rats in control group and CIH group were exposed to normoxia for 4 weeks and CIH for 4 weeks, respectively.

overall_design: Examine the hippocampus of  control and CIH-exposed rats.  For RNA-seq, the total RNA was harvested using TRIzol reagent (Invitrogen, Carlsbad, CA, USA). The amount and quality of RNA were determined using a NanoAnalyzer and Agilent 2100 biological analyzer (Thermo Fisher Scientific, Ma, USA). The mRNA expression profiling was measured using BGISEQ-500/ MGISEQ-2000system (BGI Co., Shenzhen, China).

first: Yinpei

last: Huang


title: Comprehensive transcriptomic characterization of two melanoma cell lines with acquired dual resistance to BRAF and MEK inhibitors: toward understanding and reversing therapy resistance

city: Warsaw

first: Tomasz

last: Kobiela

address: Noakowskiego 3

department: Faculty of Chemistry

country: Poland

institute: Warsaw University of Technology

summary: To elucidate the molecular mechanisms underlying acquired resistance to dual BRAF and MEK inhibition, we performed transcriptomic profiling of two melanoma cell lines, Hs294T and WM9, rendered resistant to the combination of vemurafenib and cobimetinib.RNA-seq analysis revealed distinct resistance-associated gene expression signatures in each model, with only partial overlap, suggesting divergent adaptive responses to the same therapeutic pressure. Both resistant cell lines exhibited strong upregulation of extracellular matrix compo-nents, epithelial-mesenchymal transition (EMT) markers, and chemokine signaling genes, along with repression of melanocytic lineage markers. Inference of transcription factor and kinase activity uncovered line-specific regulatory rewiring, including activa-tion of MYOCD, SMAD3, and TP53, and suppression of immune regulators such as RFX5 and RFXANK. Network-based analysis identified key resistance hubs - IL6, FN1, COL1A1, and EGFR. WM9 cells showed broader transcriptional reprogramming and prominent engagement of inflammatory and immune-related pathways. At the same time, Hs294T resistance was marked by a more restricted program focused on stromal remodeling and impaired antigen presentation.

overall_design: RNA-seq profiling of Hs294T and WM9 cell lines with acquired dual resistance to to the combination of vemurafenib and cobimetinib and their respective controls (sensitive cells). Each group contained three biological replicates, resulting in six samples per cell line and twelve samples in total.

last: Kujawa


title: UV induced translation capacity is developmentaly regulated in fungi

city: Rehovot

first: Shay

last: Covo

address: po Box 12

department: Microbiology and Phytopathology

country: Israel

institute: Hebrew University of Jerusalem

summary: In fast-growing cells, most RNA molecules encode ribosomal subunits. During growth arrest caused by DNA damage, ribosome biogenesis is reduced because it is an highly energy demanding process. Here we report that, in two filamentous fungi, UV radiation significantly induces ribosome levels and translation capacity. This UV-induced response is developmentally regulated, occurring mosly after filament formation. Translation induction modestly enhances both UV survival and repair. Most of the mRNAs that are differentialy associated with ribosomes following UV exposure belong to modules involved in protein folding and gene expression, not only DNA repair. Furthermore, UV-induced translation is dependent on PKA signaling but remains unaffected by Target Of Rapamycin inhibition. These findings suggest a novel type of fungal response to DNA damage, where the primary aim is to protect the integrity of tgene expression from the detrimental effects of UVon transcription

sample_organism:
Fusarium oxysporum
Fusarium mangiferae

platform_organism:
Fusarium oxysporum
Fusarium mangiferae

overall_design: Germinating condia of Fusarium oxysporum strain Fol4287 or Fusarium mangiferae strain MRC7560 at 14 h post innoculation were irradiated with 50J/m2 and allowed to recover for additional 120 m. Total RNA and polysome high/low fractions were extracted and sequenced. 14 h untreated populations were used as a control. Each treatment includes three biological replicates.

first: Quyen

last: Hong

first: Shira

last: Milo

first: Dibya

last: Mukherjee


title: Effect of overexpression  different alleles C/G at locus rs149707223 of LINC02449 on gene expression in the mPFC of mice

city: Guangzhou

first: 杨

last: 腾飞

address: No.1023,South Shatai Road, BaiyunDistrict

department: Medical Genetics

institute: Southern Medical University

summary: Long non-coding RNA (LncRNA) is a significant epigenetic regulatory factor, and its allele-specific expression (ASE) may play an important role in mental disorders. Therefore, clarifying the relationship between allele-specific expression (ASE) of lncRNA and mental disorders is of great significance for an in-depth understanding of the molecular mechanism of mental disorders. We here report that ASE-driven allelic shift in LINC02449 in Bipolar disorder (BD) and schizophrenia (SZ) contributes to behavioral and synaptic abnormalities in mice. We found that when the alternative allele of LINC02449 was overexpressed in cells and mouse brain regions, the expression of differentially expressed genes would be significantly enriched in mental disorders, mediating enhanced synaptic excitability transmission. Taken together, our data supported that LINC02449 overexpression, driven by the rs149707223 alternative allele, affects the disease susceptibility of BD/SZ.

overall_design: RNA-seq profiling of over-expression the rs149707223 refence and alternative allele of LINC02449, and orresponding empty vector in mPFC brain region of male C57BL/6J mice.

first: Tengfei

last: Yang


title: TNG260, a novel small-molecule CoREST inhibitor, sensitizes STK11-mutant tumors to anti-PD-1 immunotherapy

city: New York

first: Yuan

last: Hao

address: Laura and Isaac Perlmutter Cancer Center

institute: NYU Langone Health

summary: Non-small cell lung cancer (NSCLC) patients with loss of the tumor suppressor gene STK11 are resistant to immune checkpoint therapies like anti-PD-1. Our in-vivo CRISPR screen identified HDAC1 as a target that, when inhibited, reversed anti-PD-1 resistance driven by loss of STK11. We developed TNG260, a potent small-molecule inhibitor of the CoREST complex, whose selectivity exceeds previously generated inhibitors in this class in preclinical studies. TNG260 led to increased expression of immunomodulatory genes in STK11-deficient cancer cells. When combined with anti-PD-1, TNG260 induced immune-mediated stasis and/or regression in STK11-deficient syngeneic tumor models and autochthonous NSCLC models. In the tumors of patients with STK11-deficient cancers, treatment with a combination of TNG260 and pembrolizumab (NCT05887492) increased intratumoral histone acetylation, PD-L1 tumor proportion scores, and T-cell infiltration to the tumor microenvironment. This study illustrates a new, promising treatment strategy for addressing immune evasion in STK11-mutant NSCLC patients.

overall_design: Bulk RNA sequencing profiling of STK11-null mouse KL cells treated with CoREST inhinbitor TNG260 and untreated control KL cells

first: Leanne

middle: G

last: Ahronian

first: Soumyadip

last: Sahu

first: Ayushi

last: Patel

first: Kwok-Kin

last: Wong


title: Counteracting Osteoclastic Resorption and Development of Osteoporosis via Rebalancing Gut Microbiota and thus Metabolite TMAO by Traditional Decoction Medicine

city: Kaohsiung

first: Wei

middle: Shiung

last: Lian

address: No.123, Dapi Rd., Niaosong Dist.,

department: Department of Medic al Research

institute: Kaohsiung Chang Gung Memorial Hospital

summary: Osteoporosis represents a significant health challenge, particularly in postmenopausal women. While traditional medicine offers potential solutions, the mechanisms underlying their efficacy remain elusive. This study demonstrates the bone-protective properties of Guilu Erxian gel decoction (GEX), a traditional medicine prepared from tortoise plastron, antler, and herbs, by elucidating its impact on gut microbiota and associated metabolites. Using an ovariectomized mouse model of postmenopausal osteoporosis, we demonstrate that GEX consumption significantly reduces key osteoporotic markers, including low bone mineral density, compromised trabecular microstructure, and reduced biomechanical strength. GEX intake profoundly reshapes the gut microbiome, enriching beneficial bacteria crucial for fatty acid metabolism and mineral absorption. Gut microbiota transplantation from GEX-fed mice to ovariectomized recipients reversed probiotic bacterial abundance, particularly Bifidobacterium and Akkermansia. This intervention effectively alleviated ovariectomy-induced colon inflammation, trimethylamine N-oxide (TMAO) overproduction, and osteoporosis progression. Excessive TMAO promotes osteoclastogenic differentiation in macrophages in vitro. Using μCT imaging, biomechanical testing, histological staining, and 16S rRNA sequencing, we provide compelling evidence for the complex therapeutic effects of GEX, including mitigation of osteoclast overburden, reduction of marrow adiposis, suppression of RANKL overproduction, and preservation of colon goblet cell mucin. This study demonstrates the interplay between gut microbiota, its metabolite TMAO, and bone health, offering new insights into the mechanism of action of GEX. Our findings not only validate the bone-protective potential of this traditional medicine but also open new avenues for developing microbiome-based strategies to combat osteoporosis.

overall_design: Mice with estrogen deficiency, treated with or without traditional medicine, were used to harvest feces for 16S rRNA analysis using Pacbio full-length sequencing and Multiplexed SMRTbell Library construction.

first: Re-Wen

last: Wu

first: Chao-Wei

last: Kao

first: Yu-Han

last: Lin

first: Cheng-Hsiu

last: Lu

first: Yu-Shan

last: Chen

first: Shao-Yu

last: Wang

first: Holger

last: Jahr

first: Csaba

last: Matta

first: Feng-Sheng

first: Wei-Shiung


title: Candida albicans drives colorectal cancer progression by inducing hypoxia signaling

city: Shenzhen

first: Kun

last: Sun

state: Guangdong

address: Rm A1921, Guangming International Innovation Center,

institute: Shenzhen Bay Laboratory

summary: Colorectal cancer (CRC) is the third leading cause of cancer-related mortality worldwide. Gut microbiota, including fungal species, are increasingly implicated in CRC progression, while the molecular mechanisms underlying host-fungal interactions in this context remain poorly understood. Here, we show that Candida albicans (C. albicans) activates pro-metastatic signaling pathways, MAPK and NF-κB, leading to upregulation of oncogenic transcription factors c-Jun and c-Myc. This cascade stabilizes and activates hypoxia-inducible factor 1α (HIF-1α), a central regulator of tumor metabolic reprogramming and angiogenesis, ultimately fostering a pro-tumorigenic microenvironment. Mechanistically, we identify candidalysin, a secreted peptide toxin of C. albicans, as a critical effector that engages epidermal growth factor receptor (EGFR) and toll-like receptor 2 (TLR2) in a species- and cancer cell type-dependent manner. These findings are further supported by patient-derived colonic organoids. Collectively, our study delineates a C. albicans-EGFR/TLR2-ERK/NF-κB-HIF-1α axis that promotes hypoxia-like responses in CRC, revealing a previously underappreciated role of fungal pathogens in shaping the tumor microenvironment and offering potential targets for therapeutic interventions.

overall_design: To identify the role of C. albicans in colorectal cancer progression, we cultured the colorectal cancer cell line without and with C. albicans under normoxia and hypoxia environment respectively, and performed RNA sequencing to analyze the transcriptome alteration.

first: Wanqiu

first: Fanglei

last: Gong


title: Large conjugative plasmid mediates chromosomal Type VI secretion system cross transcriptional regulation and diverse bacterial pathogenicity [ChIP-Seq]

city: Xi'an

first: Wenbo

last: He

state: ShaanXi

address: 76 Yanta West Road

department: The First Affiliated Hospital

institute: Xi'an Jiaotong University

summary: The type VI secretion system (T6SS) is a highly sophisticated nanomachine widely used by bacteria to achieve competitive advantage and to potentiate horizontal gene transfer. Plasmid conjugation plays crucial roles in bacterial evolution by driving adaptation to environmental stimuli and pathogenicity. The lethal effect mediated by T6SS is detrimental to horizontal gene transfer by conjugation, while bacteria have evolved T6SS repression mechanisms regulated by plasmid to accomplish conjugative transfer. Two TetR family regulators encoded by large conjugative plasmid (LCP) in Acinetobacter baumannii have been proved similar in T6SS restriction, which seems redundant in function. Here, the global regulation roles and multiple DNA binding sites of two plasmid-sourced TetRs were identified. The two TetRs showed distinct preferences in similar roles of T6SS inhibition and binding with DNA probes. Crystal structures of TetRs were solved for illuminating the regulatory mechanism and possible reasons for difference in functions. In addition, plasmid-sourced TetRs also significantly downregulated biofilm formation and bacterial colonization, as well as influenced bacterial virulence in cultured cells and murine pneumonia infection models. Taken together, this work comprehensively elucidates the roles and regulatory mechanisms of TetRs and clarifies their similarity and difference in function, providing insights into plasmid encoded chromosome regulation pathways.

overall_design: Chromatin immunoprecipitation DNA sequecing (ChIP-Seq) for plasmid encoded TetR1 and TetR2 in A. baumannii ATCC 17978 cells.

first: Yurong

last: Wen


title: Effect of overexpression  different alleles C/G at locus rs149707223 of LINC02449 on gene expression of SK-N-SH cells(Human neuroblastoma cell line)

first: 杨

last: 腾飞

overall_design: RNA-seq profiling of over-expression the rs149707223 refence and alternative allele of LINC02449, and orresponding empty vector in SK-N-SN cells.

first: Tengfei

last: Yang


title: Large conjugative plasmid mediates chromosomal Type VI secretion system cross transcriptional regulation and diverse bacterial pathogenicity [RNA-Seq]

overall_design: To investigate the roles of plasmid-sourced TetR1 and TetR2, encoded by large conjugative plasimd (LCP) in A.baumannii, we screened for strains losing LCP. Based on this, we established overexpression strains in which TetR1 and TetR2 have been overexpressed separately through supplement vector.


title: The Spontaneous Neoantigen-Specific CD4+ T Cell Response to a Growing Tumor is Functionally and Phenotypically Diverse

city: La Jolla

first: Vijayanand

last: Pandurangan

state: California

address: 9420 Athena Circle

institute: La Jolla Institute For Immunology

summary: CD4+ T cells play critical roles in the positive and negative regulation of cellular immunity through the many functional subsets they comprise. The progressive growth of immunogenic tumors in the face of mutation-specific T cells suggests that effective immune control may be avoided or suppressed at the level of the neoantigen-specific CD4+ T cell response. We used a tetramer specific for a validated neoantigen, CTLCH129>Q/I-Ek, to characterize the ontogeny of natural CD4+ T cell responses to an aggressive and poorly immunogenic Major Histocompatibility Complex Class II (MHCII)-deficient tumor, SCC VII, during progressive growth or following therapeutic peptide vaccination. We find that the natural CD4+ T cell response to a growing tumor is phenotypically and functionally diverse, with distinct subsets including type 1 helper (Th1), T follicular helper (Tfh)-like, and regulatory T cell (Treg) lineages appearing as early as 9 days after tumor implantation. Therapeutic vaccination using the CLTCH129>Q peptide in adjuvant plus -PD-1 sharply reduces the frequency of CLTCH129>Q-specific Treg frequency in both tumor and tumor-draining lymph node (tdLN). Single cell transcriptomic analysis of CLTC-specific CD4+ T cells recapitulated and extended the diversity of the response, with TCRs of varying affinity found within each functional subset. The TCR affinity differences did not strictly correlate with function, however, as even the lowest affinity TCRs isolated from Treg can mediate therapeutic efficacy against established tumors in the setting of adoptive cellular therapy (ACT). These findings offer unprecedented insight into the functional diversity of a natural neoantigen-specific CD4+ T cell response and show how immunotherapeutic intervention influences the phenotype, magnitude, and efficacy of the anti-tumor immune response.

overall_design:
To understand the endogenous neoantigen-specific CD4+ T cell response, we harvested tetramer-positive and tetrramer-negative CD4+ T cells from the draining inguinal lymph node of mice bearing SCC VII tumors injected subcutaneously on the left flank 17 days prior to cell harvesting.
Harvested lymph nodes were ground through a 70um filter and the resulting cells were moved into a single cell suspension which was stained, run through sorting, and then used for 10x sequencing.

first: Ryan

middle: Q

last: Griswold

first: Spencer

last: Brightman

first: Karla

last: Zavala

first: Manuel

last: Ordaz-Arias

first: Navid

last: Djassemi

first: Rukman

last: Thota

first: Martin

last: Naradikian

first: Hannah

last: Dose

first: Suzie

last: Alarcon

first: Pandurangan

last: Vijayanand

first: Bjoern

last: Peters

first: Aaron

middle: M

last: Miller

first: Ezra

last: Cohen


title: Replication Stress Causes Mitotic Nuclear Envelope Reassembly Defect

first: Kun

last: Sun

summary: Replication stress, if not effectively and timely addressed, could result in DNA damage in mitosis. However, it remains unknown the relationship between mitotic DNA damage and other mitotic events such as nuclear envelope (NE) breakdown and reassembly. Here we report that replication stress could generate NE rupture. Rather than de novo formation, the rupture per se is a result of nuclear envelope reassembly defect (NERD) in mitosis. Repair of mitotic DNA damage by DNA polymerase theta (Polθ), a key microhomology-mediated end joining (MMEJ) factor, suppresses NERD. Furthermore, exacerbated NERD is observed in multiple conditions of synthetic lethality, suggesting NERD might be a general consequence of synthetic lethality. In addition, genomic mapping of LADs identifies a population of RESS-LADs (replication stress-sensitive LADs). Replication stress causes the loss of CFSs at RESS-LADs, likely due to the sustained phosphorylation of Lamin A/C at the NE rupture sites. Altogether, our findings establish a novel link between replication stress-induced genome instability and nuclear vulnerability.

overall_design: Genome binding/occupancy of Lamin A/C and Lamin B1 under mild replicasion stress in HCT116 and RPE-1 cells profiling by high throughput sequencing.

first: Guojun

last: Ye

first: Yide

last: He

first: Fuhai

last: Liu

first: Lin

last: Deng

first: Haoyue

last: Zhang


title: CHLORELLA, chloroplast-targeted long noncoding RNA, mediates the chloroplast functional transition during leaf lifespan through anterograde signaling pathway

city: daegu

first: myeonghoon

last: kang

state: Daegu

institute: Daegu Gyeongbuk Institute of Science and Technology (DGIST)

summary: The transition of chloroplast function from biogenesis to degeneration upon leaf senescence is critical for a plant’s fitness, as nutrient relocation from leaves to reproductive organs is achieved through this process. The optimal timing of transition should be regulated by tight coordination between chloroplast and nucleus, but the underlying mechanisms remain elusive. Here, we describe the regulatory mechanism of this transition. Chloroplast-Related LONG NONCODING RNA 1 (CHLORELLA1) is highly co-expressed with genes coding for chloroplast functionality during leaf development. Leaves of chlorella exhibit precocious senescence symptoms and a decline in the expression of chloroplast-associated genes, indicating that CHLORELLA1 plays a role in maintaining chloroplast function. Mechanistically, nucleus-encoded CHLORELLA1 transcripts are translocated into the chloroplast and contribute to the assembly of the plastid-encoded RNA polymerase (PEP) complex. At aged leaves, decreased expression of CHLORELLA1 attenuates PEP complex assembly and transcription of photosynthesis genes, possibly triggering leaf senescence. Moreover, CHLORELLA1 is directly activated by GLK1/2, master regulators of chloroplast maintenance. Our study unravels a new layer of the regulation via chloroplast-targeted lncRNA as an anterograde signal in timely decision of leaf senescence.

overall_design: To compare  chlorella-1 mutant and Col transcriptome, we collected 14d,26d-old of each leaves, and performed differentially expressed gene analysis.

first: Myeong

last: Kang

first: Juhyeon

last: Lee

first: Jinkwang

last: Kim

first: Hazara

middle: B

last: Mohammad

first: Jeehye

last: Park

first: Min-Sik

first: Jong-Chan

first: Pyung

middle: O

last: Lim


title: Exosomes derived from 3D-cultured hUCMSCs exhibit superior hepatoprotection against ALF

status: Public on Aug 15 2025

city: Beijing

first: Yu

last: Chen

state: Select...

address: NO.8,xitoutiao road,youwai street,fengtai district

institute: 1.	Fourth Department of Liver Disease, Beijing Youan Hospital, Capital Medical University

summary: Researching exosomes derived from human umbilical cord mesenchymal stem cells (hUCMSCs) cultured in 2D and 3D environments, it was discovered that exosomes from 3D-cultured hUCMSCs exhibit superior hepatoprotective effects on acute liver failure by upregulating YAP/TAZ and autophagy signaling

overall_design: Identify differentially expressed miRNAs between 2D and 3D exosomes and their potentially regulated signaling pathways


title: PTEN controls alternative splicing of autism spectrum disorder-associated transcripts in primary neurons

city: Berlin

first: Marco

last: Preussner

address: Takustrasse 6

institute: FU berlin

summary:
Purpose: To identify alternative splicing events in primary Pten-/- neurons as a model for autism spectrum disorder (ASD).
Methods: RNA isolation from DIV14 control and cre-mediated Pten-/- primary cortical neuronal, glia-depleted cultures. PE RNA-Seq using Illumina4000 system. Identification of alternatively spliced transcripts in Pten-/- cultures using rMATS and iREAD.
Results: More than 900 alternative splicing events were identified in Pten-/- neurons. These are largely related to synaptic and gene expression regulatory processes. Importantly, more than 80 additional autism-associated risk genes were affected upon Pten loss.
Conclusion: PTEN-ASD seems to display a multifactorial condition rather than a monogenetic disorder.

overall_design: Analysis of alternative splicing in Pten-/- compared to wildtype mouse primary cortical neurons using rMATS and iREAD. Two biological replicates for each condition were analysed.

first: Sebastian

last: Rademacher

last: Preußner

first: Marie

middle: C

last: Rehm

first: Joachim

last: Fuchs

first: Bernd

last: Timmermann

first: Florian

last: Heyd

first: Britta

last: Eickholt


title: Characterization of WDR5 WIN-site Inhibition in Two Glioblastoma Cancer Stem Cell Models using Bulk RNAseq

city: Cleveland

first: Justin

last: Lathia

state: OH

department: Department of Cardiovascular & Metabolic Sciences

institute: Cleveland Clinic Research

summary: WDR5 inhibitors have been implicated as a therapeutic vulnerability in glioblastoma cancer stem cells (CSCs). We tested the transcriptional effects of two different WDR5 WIN-site inhibitors, the dihydroisoquinoline C16 and the triazole C3TD078, in two CSC models (L0 and DI318) by bulk RNAseq.These data are associated with Coker et al., "Development and Characterization of Triazole-Based WDR5 Inhibitors for the Treatment of Glioblastoma," bioRxiv, 2025, https://doi.org/10.1101/2025.07.29.667410.

overall_design: L0 and DI318 CSCs were treated for 72 hours with DMSO (0.1% v/v), 200 nM C16, or 200 nM C3TD078 (triplicate for all treatments). Total RNA was purified using a Qiagen RNeasy Plus kit and quality controlled for integrity and concentration on a Qubit® (Invitrogen). Bulk RNAseq was performed at MedGenome Inc. using the Illumina® Stranded mRNA Library Prep Kit and sequencing at 20M paired-end read-depth on a NovaSeq 6000 (PE100).

first: Amit

last: Gupta

first: Jesse

middle: A

last: Coker

first: Shaun

last: Stauffer

first: Feixiong

last: Cheng


title: Effect of SRPK1 inhibitor on gene expression of rat corpus cavernosum endothelial cells

first: Xiao-Hui

last: Tan

address: 8, Xishiku Street, Xicheng District

institute: Peking University First Hospital

summary: To investigate the effect of SRPK1 inhibitor on gene expression of rat corpus cavernosum endothelial cells (RCCECs), we used SRPK1 inhibitor SPHINX31 to treat primary cells, which were then subjected to RNA-seq.

overall_design: Gene expression profiling analysis of RNA-seq data for RCCECs treated with SPHINX31 or not.

first: Rui-Li

last: Guan


title: LCK-deficient CD8 T-cell show reduced proliferation but normal effector responses in vivo

city: Prague

first: Juraj

last: Michalik

address: Vídeňská 1083

country: Czech Republic

institute: Institute of Molecular Genetics of the Czech Academy of Sciences

summary: The overall study investigated the role of LCK and FYN in peripheral CD8⁺ T-cell responses using adoptive transfers of LCK- or FYN-deficient monoclonal T cells into polyclonal hosts. To assess the role of LCK in T-cell differentiation in greater detail, we performed a single-cell transcriptomics study of WT, LCK CA (knock-in mice with LCK unable to bind to CD4/CD8 co-receptors), and LCK KO OT-I CD8⁺ T cells responding to LM-OVA on day 5 post-infection. While the WT and LCK CA T cells were indistinguishable, LCK KO T cells exhibited a higher frequency of effector T cells and a lower frequency of memory T cells compared to the controls.

overall_design: The study presents three experimental conditions: CD8⁺ T cells extracted from either WT, KO, or CA monoclonal OT-I mice. Each condition includes two or three biological replicates.

first: Valeria

last: Uleri

first: Anna

last: Morales Mendez

first: Veronika

last: Niederlova

first: Ondrej

last: Stepanek


title: Global analysis of methylation by SETD7 in the MM genome

city: Shimotsuke

first: Sae

last: Matsuoka

state: Tochigi

department: Center for Molecular Medicine

institute: Jichi  Medical  University

summary: We analyzed methylation by SETD7  in multiple myeloma using ChIP-seq.

overall_design: We isolated fixed chromatin from KMS12BM,KMM1,MOLP8 cells and performed immunoprecipitation with anti-SETD7/9antibody, followed by deep sequencing.

first: Jiro

last: Kikuchi


title: scRNA-seq of microglia from Cx3cr1CreERT2(Litt) adult mice reveals gene expression profile after TAM treatment.

city: Fukuoka

first: Minako

last: Ito

address: 3-1-1 Maidashi, Higashi-ku

institute: Kyushu University

summary: The Cx3cr1CreERT2(Litt) mouse model is widely used for in-depth studies of myeloid cells, including microglia. In this study, we employed single-cell RNA sequencing (scRNA-seq) to characterize microglial responses to tamoxifen (TAM) administration in adult Cx3cr1CreERT2(Litt) mice. Our analysis revealed a prolonged TAM-dependent induction of CDKN1A in the microglial population, highlighting a effect of the Cre-induction system itself.

overall_design: Transcriptome profiles of microglia from whole brains of Cx3cr1-CreERT2(Litt) mouse models with TAM-treatment were generated, following the 10x Gemomics protocol.

first: Takahiro

last: Masuda

first: Ayato

last: Yamasaki


title: Ectopic recruitment of the CTCF N-terminal domain with two proximal zinc-finger domains as a tool for 3D genome engineering

city: Moscow

first: Artem

last: Luzhin

address: Vavilova 34/5

country: Russia

institute: Institute of Gene Biology RAS

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

overall_design: Refer to individual Series


title: BLIMP1 controls GC B cell expansion and exit through regulating cell cycle progression and key transcription factors BCL6 and IRF4.

city: Pittsburgh

first: Mark

last: Shlomchik

state: PA

address: The Assembly, 5051 Centre Avenue

department: Department of Immunology

institute: University of Pittsburgh

summary: In B cells BLIMP1 is required for plasma cell differentiation. BLIMP1 is also expressed in some dark zone (DZ) germinal center (GC) B cells (GCBCs), yet the role of BLIMP1 in GCBCs is not understood. Here we generated mixed bone marrow (BM) chimeric mice using Prdm1+/+ CD19Cre and Prdm1fl/fl CD19Cre BM, allowing us to examine the cell-intrinsic functions of BLIMP1 in GCBC, independent of antibody or antigen levels. Strikingly, BLIMP1-deficient B cells quickly dominate GCs and persist for a much longer time compared to the wild type cells. BLIMP1 deficiency promotes positive selection of GCBC and enhances cell-cycle progression. In addition, BLIMP1 deficiency enhanced class-switching. Mechanistically, BLIMP1-deficient GCBC fail to downregulate BCL6 and to upregulate IRF4, indicating that BLIMP1 controls the expression of these transcription factors that mediate exit from the GC. These studies revealed unique functions of BLIMP1 in regulating GCBC responses that impact long-lived immune compartments.

overall_design: Single Cell RNAseq expression profiling of Blimp1 KO and WT GCBC

first: Wei

last: Luo

first: Shuchi

last: Smita

first: Laura

last: Conter


title: Dynamic magneto-mechanical force in lysosomes instructs durable macrophage repolarization for antitumor immunity

city: Shanghai

first: Li

last: Yingze

address: Zhennan Road

institute: Tongji University

summary: Mechanical forces are the emerging physical cue to regulate biochemical signals of immune cells for antitumor immunity. Here we used single RNA sequencing to analyze the activations of different immune cells in tumor tissue after treated by magneto-mechanical force.

overall_design: The experiment is aim to illustrate the inflatration and activation of different immune cells (especially macrophages) of tumor tissue after treated by magneto-mechanical force for 14 days.

first: Yingze

last: Li

first: Mengge

last: Zheng

first: Zhenyan

last: Zhu

first: Yajuan

last: Zhang

first: Weiwei

last: Yang

first: Yichao

last: Tang

first: Haipeng

last: Liu

first: Chang

last: Chen

first: Yu

last: Cheng


title: TNG260, a novel small-molecule CoREST inhibitor, sensitizes STK11-mutant tumors to anti-PD-1 immunotherapy

first: Hideo

last: Watanabe

state: NY

address: One Gustave L. Levy Place

department: Department of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine

institute: Icahn School of Medicine at Mount Sinai

summary: Non-small cell lung cancer (NSCLC) patients with loss of the tumor suppressor gene STK11 are resistant to immune checkpoint therapies like anti-PD-1. Our in vivo CRISPR screen identified HDAC1 as a target that, when inhibited, reversed anti-PD-1 resistance driven by loss of STK11. We developed TNG260, a potent small-molecule inhibitor of the CoREST complex, whose selectivity exceeds previously generated inhibitors in this class in preclinical studies. TNG260 led to increased expression of immunomodulatory genes in STK11-deficient cancer cells. When combined with anti-PD-1, TNG260 induced immune-mediated stasis and/or regression in STK11-deficient syngeneic tumor models and autochthonous NSCLC models. In the tumors of patients with STK11-deficient cancers, treatment with a combination of TNG260 and pembrolizumab (NCT05887492) increased intratumoral histone acetylation, PD-L1 tumor proportion scores, and T-cell infiltration to the tumor microenvironment. This study illustrates a new, promising treatment strategy for addressing immune evasion in STK11-mutant NSCLC patients.

overall_design: The KL and KP cell lines were isolated and passaged from tumor nodules from intranasally CRE-recombinase-induced KL (KRAS+/LSL-G12D; LKB1fl/fl) and KP (KRAS+/LSL-G12D; Trp53fl/fl) genetically engineered mouse models. Mice were dosed daily with TNG260 (75 mg/kg of body weight) or the vehicle via oral gavage. They also received 200 mg anti-PD-1 (BioXCell; #BE0146) and isotype control anti-IgG2a (BioXCell; BE0089) antibodies three times a week via intra-peritoneal injection. Six- to seven-week-old female and male B6(Cg)-Tyrc−2J/J (B6-albino) mice (Jackson Laboratories; strain #000058) were injected subcutaneously with 1X106 KL or KP cells, respectively, on their right flanks. A slide caliper was used to measure tumor length and width, which was used to calculate tumor volume (length x width2)/2. Mice were randomized and divided into six treatment groups once the tumor volume reached approximately 100 mm3.

first: Reshmee

last: Bhattacharya

first: Soumyadip

last: Sahu

first: Kwok-kin

last: Wong