title: Aberrant mRNA Splicing and Impaired Hippocampal Neurogenesis in Grin2b Mutant Mice [grin2b_bulkRNAseq]

summary: NMDA (N-methyl-d-aspartate) receptor dysfunction is widely implicated in pathophysiology of autism spectrum disorder (ASD), a neurodevelopmental condition with a strong genetic basis. Here we investigated heterozygous mouse mutants carrying the ASD-linked C456Y mutation of Grin2b, a high-confidence ASD risk gene encoding the GluN2B subunit of the NMDA receptors. Comprehensive transcriptomic analyses across multiple brain regions and postnatal ages revealed large-scale gene expression changes, particularly in pathways related to oxidative phosphorylation and ribosome/translation, suggesting brain-wide alteration of energy metabolism and protein synthesis in Grin2b+/C456Y mice. Starting from transcriptomic evidence, we additionally discovered widespread splicing abnormalities, and impaired hippocampal neurogenesis in Grin2b mutants. Interestingly, the underlying genes and the spatial and temporal patterns of transcriptomic changes in Grin2b+/C456Y mice differed substantially from those observed in mutant mice lacking Grin2a, which encodes the GluN2A subunit of the NMDA receptor but is a schizophrenia risk gene. These findings underscore the distinct role of Grin2b in brain development and function and reveal potential mechanisms by which Grin2b loss of function may lead to neurodevelopmental disorders.

overall_design: Comparative gene expression profiling analysis of RNA-seq data from substantia nigra (SN) at 2, 4, 12 and 20 weeks of age in Grin2b mutant mice.

first: Farsi

last: Zohreh

first: Nicolella

last: Ally


title: Real-time quantitative PCR analysis of human glioblastoma and astrocytes

status: Public on Dec 31 2025

city: Isparta

first: Berrin

last: Ozdil

address: Cunur

department: Histology and Embryology

country: Turkey

institute: Suleyman Demirel University

summary: cell line of control and test groups

overall_design: qPCR gene expression profiling of glioblastoma and astrocyte cells with control and test group..  Cells were used and treated separately as indicated in the summary. Equal amount total RNA from each group was pooled prior to gene expression analysis.

first: Ozdil

last: Berrin

first: Kocaturk

last: Duygu


title: Based on single-cell sequencing analysis of CD4+ T cells and B cells in patients with lupus nephritis, the heterogeneity of these cells was investigated.

status: Public on Jan 01 2026

city: Hefei

first: lili

last: cheng

state: Anhui Province

address: No. 117, Meishan Road

country: China

institute: The First Affiliated Hospital of Anhui University of Chinese Medicine

type: Expression profiling by high throughput sequencing

summary: Utilizing single-cell technology to analyze the heterogeneity of CD4+ T cells and B cells in patients with lupus nephritis.We have delineated the immune cell profile of PBMC in LN patients, and focused on describing the heterogeneity characteristics of CD4+ T cells and B cells. Some specific cell subtypes and ligand-receptor pairs were identified, which indicate potential therapeutic targets for lupus erythematosus.

overall_design: Under the condition of informed consent, this study conducted single-cell transcriptome sequencing on PBMC samples from 3 patients with LN and 3 healthy controls (HC), aiming to explore the conditions of LN CD4+ T cells and B cells. Firstly, the cells were classified into immune cell clusters through cell dimensionality reduction and clustering. Then, further subdivisions were made for CD4+ T and B cells. Using differential analysis and public data, the Maker genes that affected LN CD4+ T and B cells were identified. Subsequently, GO, KEGG, and GSEA enrichment analyses were used to conduct functional analysis of the differentially expressed genes in LN patients.

first: Lili

last: Cheng

first: Zhongfu

last: Tang

first: Ming

last: Li

first: Shuangshuang

last: Shang

first: Junjie

last: Chen

first: Sidi

last: Liu

first: Chuanbing

last: Huang


title: Functionally heterogeneous intratumoral CD4+CD8+ double positive T cells can give rise to single positive T cells [bulkRNA-seq]

city: Seattle

first: Lawrence

last: Fong

state: Washington

address: 1100 Fairview Ave. N.

department: Immunotherapy Integrated Research Center

country: USA

institute: Fred Hutchinson Cancer Center

summary: Conventional single positive (SP) CD4+ and CD8+ T cells recognize tumor antigens and help mediate clinical responses with cancer immunotherapy. Double positive CD4+CD8+ (DP) T cells have also been described in human cancers, but their role in the tumor microenvironment (TME) remains unclear. By generating a multi-omic single cell atlas of DP and SP T cells, we find that DP T cells possess phenotypic heterogeneity similar to SP T cells that includes multiple clonally expanded populations of cytotoxic DP T cells in human renal cell carcinoma (RCC). These intratumoral DP T cells can mediate by both MHC class I- and class II-dependent killing of autologous tumor cells. In addition, transcriptional profiling of DP TCR-bearing T cells revealed a gene signature enriched for clinical responders to PD-1 blockade in advanced RCC. We confirm prior observations of SP T cells transitioning into DP T cells and more notably, demonstrate that intratumoral T cells are capable of bidirectional differentiation in which DP T cells serve as precursors to SP T cells in vivo.  In the latter scenario, intratumoral DP T cells are shown to express Rag2, suggesting that the tumor may act as an extrathymic site of T cell development. These findings reveal the multiple roles that DP T cells can possess in anti-tumor immunity.

overall_design: To characterize T-cell heterogeneity in renal cell carcinoma (RCC), we performed single-cell RNA sequencing (scRNA-seq) and single-cell TCR sequencing (scTCR-seq) using the 10x Genomics platform. Samples were collected from each patient’s tumor tissue, adjacent normal tissue, and peripheral blood mononuclear cells (PBMCs), along with PBMCs from healthy donors. To assign cells to their respective individuals following sequencing, we applied demuxlet, which leverages donor-specific genetic variants derived from bulk RNA-seq to enable genotype-based sample demultiplexing.

first: Tony

first: Arielle

last: Illano

first: Marcel

last: Arias-Badia


title: Akr1b7 functions as a master regulator in ovarian aging

status: Public on Jan 06 2026

city: Ube

first: Yoichi

last: Mizukami

state: Yamaguchi

department: Science Research Center

country: Japan

institute: Yamaguchi university

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

overall_design: Refer to individual Series


title: Single Cell Transcriptomics for Tbc1d23ΔE15/ΔE15 and wild-type mice bone marrow

city: Chengdu

first: chen

last: li

address: Renmin South Road

institute: Sichuan Univercity

summary: Compare bone marrow cell population and gene regulation changes in Tbc1d23ΔE15/ΔE15 and wild-type mice

overall_design: Bone marrow cells were isolated from 8-week-old female of C57BL/6J wild-type and Tbc1d23ΔE15/ΔE15 mice. The cells were sorted with  EasySep™ Mouse Hematopoietic Cell Isolation Kit for analysis with scRNA-seq.

first: Li

first: Xiao

last: Hu

first: JinRui

last: Wang

first: Qing

last: Yang


title: RBPscan: A Quantitative, In Vivo Tool for Profiling RNA-Binding Protein Interactions

city: Québec

first: Dmitry

last: Kretov

state: Québec

department: Oncology Division

country: Canada

institute: CRCHU de Québec - Université Laval

summary: RNA-binding proteins (RBPs) are essential regulators of gene expression at post-transcriptional level, yet obtaining quantitative insights into RBP–RNA interactions in vivo remains a challenge. Here we developed RBPscan, a method that integrates RNA editing with massively parallel reporter assays (MPRAs) to profile RBP binding in vivo. RBPscan fuses the catalytic domain of ADAR to the RBP of interest, using RNA editing of a recorder mRNA as a readout of binding events. We demonstrate its utility in zebrafish embryos, human cells, and yeast, where it quantifies binding strength, resolves dissociation constants, identifies high-specificity motifs for a variety of RBPs, and links binding affinities to their impact on mRNA stability. RBPscan also provide positional information of conserved and novel Pumilio-binding sites in lncRNA NORAD. With its simplicity, scalability, and compatibility across systems, RBPscan offers a versatile tool for investigating RBP–RNA interactions and complements established methods for studying post-transcriptional regulatory networks.

overall_design: RBPscan analysis of hsaPum2 binding to various PREs was performed in HEK293T cells. Expression of the hsaPum2-ADAR fusion protein was induced by doxycycline. The reporter mRNA library contained 1,000 distinct PREs and other control sequences. Each experiment was conducted in three biological replicates.

middle: A

first: Owen

last: Sanborn

first: Thora

last: McIssac

first: Elaine

last: Park

first: Imrat

last: Imrat

first: Marianne

last: Régis

first: Louis-Mathieu

last: Harvey

first: Samuel

last: Wu

first: Daniel

last: Cifuentes


title: Regulation of ABC Transporters and Ergosterol Biosynthesis by the Transcription Factor FvADS-1 Controls Azole Resistance and Virulence in Fusarium verticillioides

city: Tianjin

first: Yajing

last: Yin

address: No. 409 Guangrong Road

institute: Tianjin University of Commerce

summary: Fusarium verticillioides is a significant agricultural pathogen and an emerging causative agent of invasive fusariosis in clinical settings. Fusarium species frequently exhibit resistance to available antifungal agents, yet the molecular mechanisms underlying azole resistance remain poorly characterized. In this study, we identified the Zn(II)2Cys6 transcription factor FvADS-1 as a positive regulator of the azole stress response in F. verticillioides. The transcription of FvADS-1 was significantly induced by ketoconazole (KTC), and its deletion increased the susceptibility to multiple azole compounds. Mechanically, FvADS-1 positively regulates the KTC-induced expression of genes encoding ABC transporters and ergosterol biosynthesis enzymes, thereby modulating intracellular KTC accumulation and sterol homeostasis under azole stress. Furthermore, FvADS-1 positively regulates the transcriptional response of peroxisomal genes and contributes to fungal tolerance to oxidative stress. Notably, deletion of FvADS-1 attenuates the virulence of F. verticillioides on maize.

overall_design: For F. verticillioides, 107 conidia were inoculated in YPD liquid medium and cultured at 28°C with shaking (200 rpm) for 20 h. Then the mycelia were treated with or without 2 μg/mL KTC for 16 h. After harvest, the mycelia were finely grounded into powder in liquid nitrogen. RNA was extracted according to standard TRIzol method (Invitrogen, Carlsbad, CA, United States) and followed by sample analysis. Transcriptomic profiles of the F. verticillioides wild-type and FvADS-1 deletion strains, either treated with or without KTC, were analyzed by high-throughput RNA sequencing (RNA-seq).


title: Genome wide mapping of sni445-HTP binding sites in yeast by CRAC

city: Toulouse

first: Hussein

last: HAMZE

address: 118 Route de Narbonne  31062 TOULOUSE Cedex France

country: France

institute: Toulouse university - cnrs

summary: We report the application of the Cross-Linking and cDNA (CRAC) technique to identify binding sites of sni445, ribosome assembly factor, on RNAs in vivo. Once sequenced, RNAs associated have been aligned to the yeast genome and enrichment of specific RNAs has been studied in more details. Specifically, apparition of Mutations/deletions in the reads is center of interest since they mostly correspond to precise site of cross-link between bait protein and target RNAs. Here sni445-HTP is mostly bound to two snoRNAs, SNR4 and SNR45.

overall_design: We analyse the sequence enrichment of RNAs associated to sni445-HTP compared to a mock (un-tagged) control after protein/RNA cross-link in vivo.

last: Hamze

first: Jutta

last: Hafner

first: Anthony

last: Henras

first: Brigitte

last: Pertschy


title: Transport stress induces paradoxical increases in airway inflammatory responses in beef stocker cattle

city: Fort Collins

first: Grace

middle: Marie

last: Jakes

state: CO

address: 2500 Flintridge Pl

department: Microbiology, Immunology, Pathology

institute: Colorado State University

summary: The development of Bovine Respiratory Disease (BRD ) in beef cattle is associated with stressful events, including auction and transport. In addition to the effects of commingling on pathogen exposure, stress also impacts immune function and has classically been associated with an immunosuppressed state. Much of the research on cattle immunity in stress has focused on peripheral blood immune functionality rather than mucosal immune responses. To characterize immunity at the primary site of pathogen colonization in BRD, we evaluated stress responses  in lung cells from beef stocker cattle to understand mucosal immune changes. Stocker calves were sampled via bronchoalveolar lavage fluid collection within 24 hours of auction and transport to a new facility (Stressed, n=12), or allowed to acclimate for 2 months at the new facility before sampling (Acclimated, n=7). Lavage cellular RNA was extracted and sequenced for bulk RNA-seq gene expression. Differential gene expression analysis of RNA sequencing data demonstrated a profound  upregulation of inflammatory genes in Stressed calves compared to Acclimated calves, including expression of CXCL8, CSF3R, IL1B, and CCL22. Top pathway upregulation in Stressed calves involved neutrophil migration and chemotaxis, and cytokine signaling. To predict cellular population proportions from the data, CIBERSORTx was used to deconvolute bulk RNA-seq gene counts. This analysis showed that Stressed calves had significantly increased BALF neutrophils compared to Acclimated calves (p =0.003). Neutrophilic infiltration occurred in the absence of pathogen colonization of the lungs in most calves, as demonstrated by a multi-pathogen respiratory qPCR screen. As such, the stress induced an inflammatory response in lungs not explained by pathogen exposure. This study provides strong evidence that shipping stress in beef stocker calves can paradoxically  trigger increased rather than suppressed inflammatory pulmonary mucosal immune responses, which has important implications for the pathogenesis of BRD.

overall_design: RNA-seq profiling of Stressed beef calves immediately after auction and transport, and Acclimated calves on pasture for two months.

first: Dylan

last: Ammons

first: Randy

last: Hunter

first: Steven

last: Dow

first: Sarah

last: Raabis


title: Dasatinib resensitizes BRAF/MEK inhibitor efficacy in patient-derived xenografts from patients with progression on BRAF/MEK inhibitor treatment

city: Philadelphia

first: Yeqing

last: Chen

state: PA

address: 3601 Spruce Street

institute: The Wistar Institute

summary: Although BRAF/MEK inhibitor (BRAFi/MEKi) therapy initially shows high efficacy in patients with BRAFV600E/K cutaneous melanoma, resistance develops in over 75% of cases. We tested robustness of the umbrella trial strategy in this population by analyzing relationships between genomic status of a gene and associated downstream consequences at the protein level, which reveal poor relationships between mutations, copy number amplification, protein expression and activation.  An in vivo compound repurposing screen using 11 clinically relevant agents from an NCI-portfolio with pan-RTK, non-RTK and/or PI3K-mTOR specificity identified dasatinib as most capable of restoring sensitivity to BRAFi/MEKi in patient-derived xenograft (PDX) models originating from tumors that had progressed on BRAFi +/- MEKi. High baseline expression of BRAFi/MEKi resistance-associated proteins (e.g., AXL, YAP, HSP70, phospho-AKT) was predictive of response to BRAFi/MEKi plus dasatinib combination therapy. These findings suggest that adding dasatinib may help overcome resistance and restore anti-tumor activity in patients with BRAFi/MEKi-refractory cutaneous melanoma.

overall_design: Bulk RNAseq on melanoma patient-derived xenograft (PDX) models originating from tumors that had progressed on BRAF/MEKi.

first: Vito

middle: W

last: Rebecca

first: Min

last: Xiao

first: Meenhard

last: Herlyn


title: TM9SF1 aggravates liver ischemia-reperfusion injury by promoting autophagy

city: Zhengzhou

first: Tongtong

last: Wu

address: 1 Jianshe East Road

institute: Zhengzhou University

summary: Liver transplantation (LT) stands as the sole effective approach for addressing end-stage liver disease. Autophagy plays an indispensable role in liver ischemia-reperfusion（I/R）. Transmembrane 9 superfamily member 1 (TM9SF1) is a transmembrane protein that has been shown to be associated with autophagy. However, the role and mechanism of this protein in liver I/R injury have not been explored. We found that TM9SF1 expression increased in liver I/R injury mice and AML12 cells after hypoxia-reoxygenation (H/R). Then, we constructed TM9SF1 adeno-associated virus overexpression and knockdown (KD) mice and constructed a liver I/R injury model. The results showed that TM9SF1-overexpressing mice had increased liver damage, inflammation, and autophagy levels. The opposite changes were observed in knockdown mice. Mechanistically, we found that TM9SF1 and Annexin A2 (ANXA2) interacted and jointly affected the expression of autophagy levels during liver I/R injury. Based on the construction of TM9SF1-overexpressing mice , we interfered with the expression of ANXA2 and found that the degree of liver damage was reduced, the level of inflammation decreased, and the level of autophagy decreased. Finally, we performed virtual screening on the FDA-approved molecular library and found that lomitapide can reduce the expression of TM9SF1, thereby alleviating liver ischemia-reperfusion injury. In general, our findings indicated that TM9SF1 and ANXA2 interact with each other, affecting autophagy levels through the mitogen-activated protein kinase (MAPK) pathway, thereby aggravating liver I/R injury. Targeting TM9SF1-ANXA2 may be a potential therapeutic strategy.

overall_design: We constructed a liver ischemia-reperfusion model and detected the expression of TM9SF1. In vivo, we constructed TM9SF1 overexpression and knockdown mice, and detected the degree of liver damage and changes in autophagy through experimental methods such as TUNEL, DHE, and TEM. In vitro, we constructed knockdown and overexpression AML12 cell lines, and verified the changes in cell damage and autophagy through Hoechst 33342/PI, ROS, and TEM methods. At the same time, sequencing and mass spectrometry were performed on stably transfected cell lines to explore the mechanism of TM9SF1 in liver ischemia-reperfusion injury.

first: Wendong

last: Li

first: Ying

last: Zhu

first: Xudong

last: Liu

first: Hongwei

last: Tang

first: Mingjie

last: Ding

first: Wenzhi

last: Guo


title: Inflammatory proteomics of uterine fluid is potentially a non-invasive predictor for endometrial receptivity: a pilot study

city: Guangzhou

first: Hong

last: Zeng

state: Hunan

address: 87 Xiangya Street

department: Reproductive medicine center

institute: Xiangya Hospital Central South University

summary: Objective: To evaluate if the inflammatory proteomics of uterine fluid could define the endometrial receptivity phase. Methods: Inflammatory proteomics of uterine fluid were measured using the OLINK Target-96 Inflammation panel. Endometrial receptivity testing (ERT) combined with endometrial dating was a gold standard for defining the endometrial receptivity phase. A predictive model based on proteomics of uterine fluid was established to predict the endometrial receptivity phase. Results: The inflammatory factors in uterine fluid were differentially expressed between window of implantation (WOI) and displaced WOI groups, and the displaced WOI group was characterized by the increased expression of a variety of inflammatory factors. The predictive model established based on the top 5 differential proteins could accurately classify the endometrial receptive phase. Transcriptomic data from endometrial tissues showed that the differential gene sets between different receptive phases were mostly enriched in immune-related processes, and the expression of immune-related genes in the WOI group was significantly lower than that in the displaced WOI group. Conclusions: Detection of inflammatory proteins from the uterine fluid using the OLINK inflammation panel could be a novel non-invasive method to define the endometrial receptive phase. The inflammatory immune response during the embryo implantation window was inhibited to adapt to the implantation of the semi-alloimmune embryos.

overall_design: Observational study

first: Shuyi


title: Oriented Cell Divisions Induce Basal Progenitors and Regulate Neural Expansion Across Tissues and Species

city: Montreal

first: Benoit

middle: Charles

last: Boulan

state: Quebec

address: 110, avenue des Pins Ouest

institute: IRCM

summary: GPSM2 and SAPCD2 as major regulator of mitotic spindle orientation regulate basal progenitor production in retina and cortex

overall_design: scRNA-seq analysis of Gpsm2/Sapcd2 double-het versus double-KO in developing retina and cortex

first: Michel

last: Cayouette


title: Single cell RNA-seq reveals that the Vibrio cholerae Mak toxins are required for killing of Tetrahymena pyriformis and for survival in protozoan expelled food vacuoles

city: Sydney

first: M. Mozammel

last: Hoque

state: NSW

address: 15 Broadway, Ultimo

department: Australian Institute for Microbiology & Infection (AIMI)

country: Australia

institute: University of Technology Sydney

summary: Vibrio cholerae uses multiple strategies to resist predation by heterotrophic protozoa. For example, V. cholerae releases toxic compounds such as ammonium and pyomelanin, that can kill protists such as Tetrahymena pyriformis. V. cholerae also survives intracellularly and escapes as viable cells inside protozoan expelled food vacuoles (EFVs). We previously reported that V. cholerae encased in EFVs are hyperinfectious, establishing an important link between anti-protozoal strategies and bacterial virulence. Although the intracellular resistance and escape of V. cholerae in EFVs has been reported, the molecular mechanisms behind this remain poorly understood. Here, we used single cell transcriptomics of V. cholerae exposed to T. pyriformis and captured a total of 5,344 bacterial cells with heterogeneous gene expression. Cells with the same pattern of gene expression were grouped, resulting in eleven clusters of cells with a unique gene expression profile. Genes encoding outer membrane proteins, F1F0-Na+/H+ ATPase, metabolites and toxins showed differential expression among the clusters. Furthermore, the motility-associated killing factor (Mak) toxins (makA, makB and makC) were differentially expressed. Individual  V. cholerae ΔmakA, ΔmakB, and ΔmakE strains were not capable of killing T. pyriformis and ΔmakA and ΔmakE showed reduced survival inside EFVs compared to the wild type. Our findings reveal new insights into the grazing resistance mechanisms of V. cholerae, identify factors associated with the survival of V. cholerae within EFVs and more broadly, highlight the connection between antiprotozoal and virulence factors displayed by pathogenic bacteria.

overall_design: Intracellular Vibrio cholerae bacteria recovered from Tetrahymena pyriformis and from EFVs were fixed in 4% formaldehyde at 4 degc overnight and then the MicroSPLiT protocol was perfromed to individalluy tage the mRNA of the bacteria

first: M

middle: M

first: Diane

last: McDougald

first: Jonah

last: Moon

first: Gustavo

last: Espinoza-Vergara


title: An ultraconserved pseudo 5' splice site fine-tunes development by regulating alternative splicing within TOR-related pathways

city: Shanghai

first: Zhan

address: 300 Feng Lin Road

institute: CAS Center for Excellence in Molecular Plant Sciences

summary: Introns have expanded dramatically during evolution, in which ultraconserved RNA motifs may play essential regulatory roles. Sharing the sequence with the actual 5' splice sites (5'SSs), pseudo-5'SSs are widespread in introns but never spliced. We searched homologous introns and identified eight ultraconserved pseudo-5'SSs (UCP-5'SSs). The most conserved one resides in the animal ENOX1/Enox genes that are involved in plasma electron transport and cell enlargement. In vivo deletion of this 9-nt UCP-5'SS in Drosophila results in a significantly enlarged ovary and increased fecundity. We demonstrate that this UCP-5'SS is a silencer for alternative splicing (AS) regulation of an upstream ultraconserved essential exon through interaction with the U1 snRNP-core proteins. The AS changes are observed in all the tested Drosophila mutants from the dTOR and Insulin-like pathways. Remarkably, loss of this UCP-5'SS significantly mitigates the changes. Conservatively, multiple-source human cells treated with the mTOR/Insulin pathway inhibitors also change the AS and specifically increase the translation of U1-70K. This study reveals an ultraconserved regulatory network in which a short intronic RNA motif functions as a sensor of TOR-related pathways during ovarian development.

overall_design: To investigate the function of conserved motifs in the enox gene of fruit flies, we established strains with deletions in the enox motif and the enox gene, followed by RNA-seq analysis.

first: Zhuo-Ya

last: Fang

first: Hao

first: Yong-Zhen

last: Xu


title: Next Generation Sequencing Facilitates Quantitative Analysis of keratocytes sorted from Prrx1-creERT;Ptch1 and ctrl mice

first: qian

last: yu

address: 1665 Kong Jiang Road

institute: Xinhua Hospital affiliated to Shanghai Jiao Tong University School of Medicine

summary: We had one goal to perform this study: transcriptome of keratocytes sorted from Prrx1-creERT;Ptch1 and ctrl mice

overall_design: Comparison of transcriptome of keratocytes  sorted from Prrx1-creERT;Ptch1 and ctrl mice

first: Qian

last: Yu


title: Next Generation Sequencing Facilitates Quantitative Analysis of Epithelial cells sorted from Prrx1-creERT;Ptch1 and ctrl mice

summary: We had one goal to perform this study: transcriptome of Epithelial cells sorted from Prrx1-creERT;Ptch1 and ctrl mice

overall_design: Comparison of transcriptome of Epithelial cells sorted from Prrx1-creERT;Ptch1 and ctrl mice


title: Differential Epithelial Responses to GII.3 HuNoV Infection in Jejunal Human Intestinal Organoids (HIOs)

status: Public on Dec 30 2025

city: Houston

first: Mary

last: Estes

state: TX

address: 1 Baylor Plaza

department: Microbiology and Virology

institute: Baylor College of Medicine

summary:
We performed RNA-seq to compare the epithelial transcriptomic response to GII.3 HuNoV infection to gamma-irradiated inactivated HuNoV (gGII.3) and media controls in parental HIE lines (J2 and J4) and genetically modified HIOs (J2STAT1-KO and J4FUT2-KI), which support enhanced viral replication due to STAT1 knockout and FUT2 knock-in, respectively.  HIEs were harvested and analyzed at 24 hours post-infection/treatment.

NCBI grant:
Grant ID: U19 AI144297
Consortium name: Texas Medical Center Genomic Center for Infectious Diseases (TMC GCID)
URL: https://gcid.research.bcm.edu/

overall_design: HIOs from two different individuals and their genetically modified counterparts were used for total RNA sequencing

first: Sue

middle: E

last: Crawford

first: Gurpreet

last: Kaur

first: Hoa

last: Nguyen-Phuc

first: Khalil

last: Ettayebi

first: Muzny

last: Donna

first: Doddapaneni

last: Harshavardhan

first: Cristian

last: Coarfa

first: Sasirekha

last: Ramani

middle: K


title: NIT2 epigenetically restrains oxidative phosphorylation to overcome fluorouracil resistance in gastric cancer

first: Ziyang

last: Wang

state: --- Select One ---

address: 58 Zhongshan 2nd Road

institute: Ziyang Wang, Doctor, The First Affiliated Hospital, Sun Yat-sen University

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Fluorouracil (5-FU) chemoresistance is an important reason for the postoperative recurrence and poor prognosis of gastric cancer, but there is still no effective way to overcome chemoresistance. Here, by using the CRISPR/Cas9 system, we identify nitrilase family member 2 (NIT2) reverses chemoresistance, regardless of its metabolic function. NIT2 depletion causes H3K14 acetylation (H3K14ac) increase and NF-κB signalling activation, in turn upregulating oxidative phosphorylation (OXPHOS) and promoting chemoresistance. Mechanistically, NIT2 prevents BRD1 from binding histones and releases ING4 to degrade the transcription factor RELA. Upon 5-FU stimulation, the E3 ligase CCNB1IP1 interacts with NIT2 to cause autophagic degradation of NIT2. In addition, NIT2 downregulation correlates with poor prognosis in gastric cancer patients, and this is probably related to the promotion of OXPHOS. Our finding highlights the nonenzymatic function of NIT2 in chemoresistance and show that the blockade of OXPHOS by metformin can enhance chemosensitivity to 5-FU upon loss of NIT2.

overall_design: Control and shNIT2 MKN45 cells were crosslinked with formaldehyde and quenched with 125 mM glycine. The fragmented chromatin fragments were pre-cleared and then immunoprecipitated with Protein A + G Magnetic beads coupled with anti-H3K14ac antibodies. After reverse crosslinking, ChIP and input DNA fragments were end-repaired and A-tailed followed by adaptor ligation. The DNA libraries were amplified for 15 cycles and sequenced.

first: Yuqin

last: Di

first: Xiongjun

first: Weiling

last: He


title: Deciphering the Neurological Puzzle in ALG13-CDG Through Cutting-Edge Brain Organoid Modeling.

city: New York City

first: Rameen

last: Shah

address: 1425 Madison Avenue

institute: Mount Sinai

summary: Asparagine-linked glycosylation 13 (ALG13) is an X-linked congenital disorder of glycosylation (CDG). Our study addresses the urgent need for deeper insights into ALG13-CDG characterized by significant gaps in our understanding of its pathobiology and the absence of effective treatment options. Despite extensive research on various CDG, investigations into ALG13-CDG have been hindered by the lack of observable glycosylation defects in patient samples, particularly in blood and fibroblasts. However, the profound neurological symptoms associated with ALG13-CDG strongly suggest a primary impact on the brain. To test this hypothesis, we established a brain model of ALG13-CDG using induced pluripotent stem cells derived from fibroblasts, which were subsequently differentiated into human cortical cortical organoids(hCOs). Contrary to previous reports of random X-inactivation in individuals with ALG13-CDG, we observed X-inactivation skewing within ALG13-CDG cell lines. Our multi-omics approach, encompassing single-cell RNA-seq, proteomics, glycoproteomic, and metabolomics analyses, revealed significant reductions in glycosylation and expression of key proteins essential for axon growth, neuronal migration, and synaptic plasticity. Additionally, alterations in protein abundances associated with neuronal migration and nucleotide synthesis were also observed, along with distinctive changes in genes linked to epilepsy risk and lipid metabolism. Metabolomic analyses ALG13-CDG hCOs showed elevated GlcNAc levels and decreased nucleotide synthesis metabolites. Importantly, our study sheds light on the previously unrecognized protein glycosylation defect in ALG13-CDG, offering valuable insights into the brain-related disturbances underlying the disease pathology. Furthermore, our findings hold promise for guiding the clinical management of seizures in ALG13-CDG patients, addressing a critical unmet medical need.

overall_design: 3 ALG13-CDG cortical brain organoids and 3 control brain organoids were seperated into a single cell suspension using Neurosphere Dissociation Kit and ran through scRNAseq

first: Silvia

last: Radenkovic


title: Analysis of A375 and SKMEL-103 cells after treatment with with DMSO as control or BAY-850

city: Birmimgham

first: Romi

last: Gupta

state: Alabama

address: 720, 20th street south

institute: University of Alabama at Birmingham

summary: To identify the gene expression changes in NRAS mutant cell line SKMEL-103, and BRAF mutant cell line A375 upon BAY-850 treatment, we analyzed these cell line with either control DMSO or BAY-850 treatment via RNA sequencing.

overall_design: SKMEL-103 and A375 cells were plated, samples were either treated with DMSO or BAY-850 (5-micromolar for 24 hours), cells were harvested and were used to prepare the total RNA, followed by RiboRNA depletion with random priming and RNASeq Illumina Hi-Seq 2500 platform, with three biological replicates for each sample.


title: High-resolution single-nematode transcriptomic datasets of plant-parasitic nematodes from juveniles to adults

city: wuhan

first: xuemeng

last: han

address: shizishan street

institute: HZAU

summary: Plant-parasitic nematodes (PPNs) pose major agricultural threats, yet their transcriptional regulatory mechanisms remain poorly understood. Deciphering these mechanisms is critical for advancing knowledge of nematode development and host interactions, and for guiding the rational design of integrated control strategies. However, the lack of reliable synchronization of nematode development within plant hosts, together with the stringent requirements of high-throughput sequencing library preparation, hinders comprehensive transcriptomic profiling across distinct developmental stages. To overcome this limitation, high-resolution, single-nematode RNA-seq data was generated for eight developmental stages of Meloidogyne incognita (from second-stage juveniles to adults) using a low-input Smart-seq2 approach. The resulting dataset comprises 75 high-quality transcriptome libraries with at least five biological replicates per stage, enabling robust and reproducible analyses.

overall_design: The high-resolution, single-nematode RNA-seq data was generated for eight developmental stages of Meloidogyne incognita (from second-stage juveniles to adults) using a low-input Smart-seq2 approach. The resulting dataset comprises 75 high-quality transcriptome libraries with at least five biological replicates per stage, enabling robust and reproducible analyses.


title: LXR agonism elicits a pre-effector state in naïve CD8+ T cells [RNA-seq]

city: Berlin

first: Benjamin

middle: N

last: Ostendorf

address: Augustenburger Platz 1

country: Germany

institute: Charité University Medicine

summary: Here, we analyze transcriptional profiles of naïve CD8+ T cells with versus without exposure to the synthetic LXR agonist RGX-104 in the absence of TCR stimulation.

overall_design: Differential gene expression analysis of naïve CD8+ T cells after 24 hours of treatment with the  synthetic LXR agonist RGX-104 versus DMSO.


title: LXR agonism enhances T cell activation upon crosspresentation by LXR-DKO BMDCs.

summary: Here, we analyze transcriptional profiles of OT-I CD8+ T cells co-cultured with LXR-/- bone marrow-derived dendritic cells pulsed with the SIINFEKL peptide in the absence or presence of the synthetic LXR agonist RGX-104.

overall_design: Differential gene expression analysis of flow cytometry-sorted OT-I CD8+ T cells after co-culture with LXR-/- bone marrow-derived dendritic cells in the presence or absence of the synthetic LXR agonist RGX-104.


title: scRNA-seq and TCR-seq of T cells and APCs in tumor-draining lymph nodes with versus without pharmacological LXR activation.

summary: Here we assessed the impact on the transcriptomes of T cells and APCs in tumor-draining lymph nodes from mice administered control chow versus chow containing the synthetic LXR agonist RGX-104. In addition, TCR-seq was performed to assess the impact on clonal expansion of T cells upon LXR activation.

overall_design: T cells and antigen-presenting cells (APCs) were isolated from tumor-draining lymph nodes from mice by flow cytometry and subjected to scRNA-seq and TCR-seq.


title: KNSTRN knockdown impairs autophagy flux and inhibits bladder cancer progression through ROS- mediated lysosomal dysfunction

city: nanchang

first: Yaoyi

last: Xiong

state: jiangxi

address: No. 17 Yongwai Zhengjie, Donghu District, Nanchang City, Jiangxi Province, China

institute: Nanchang University

summary: Bladder cancer (BLCA) is a prevalent cancer affecting the urinary tract, the mitochondria-localized Astrin-binding protein (KNSTRN) has been shown to be strongly associated with the development of several cancers. In addition, abnormal levels of autophagy have been shown to have a dramatic impact on tumor development. However, the potential mechanisms of BLCA autophagy regulation by KNSTRN remain poorly understood. In this research, we found that knockdown of KNSTRN inhibited the autophagic flux of BLCA. Mechanistically, knockdown of KNSTRN leads to reactive oxygen species (ROS)-dependent disruption of the lysosomal acidic environment and reduction of protease activity, hindering autophagosome-lysosome fusion. Clioquinol reactivates lysosomal activity by normalizing lysosomal pH, which in turn reinstates autophagic flux. Intracellular ROS production is also critical for this process, as ROS scavengers (NAC) reverse lysosomal dysfunction and reactivate autophagic flux. Additionally, the autophagy activator rapamycin (Rapa) effectively protected against KNSTRN knockdown-induced cell death in vitro and in vivo. Thus, we demonstrate that knockdown of KNSTRN leads to intracellular ROS accumulation and lysosomal dysfunction, which impairs autophagic flux and inhibits BLCA progression.

overall_design: T24 cells were inoculated into 6 cm dishes and cultured for 24 hours until the cells were fully adherent to the wall, then treated with si-NC or si-KNSTRN for 24 h. subsequently, total RNA was extracted using RNA extraction solution and transcriptome sequencing was performed. Three biological replicates per group.

first: Xianbin

last: Huang


title: Transcriptomic analysis of chemotherapy-associated oropharyngeal candidiasis reveals a novel role of indigenous mucosal bacteria in pathogenesis

city: Farmington

first: Roberto

last: Vazquez-Munoz

state: Connecticut

address: 263 Farmington Avenue, Main building, room L6008

department: General Dentistry

institute: UConn Health

summary: This work reports a new mechanism of pathogenic synergy between C. albicans and E. faecalis, which may be responsible for increased epithelial barrier damage and mucosal invasion by C. albicans hyphae in cancer chemotherapy.

overall_design: Tongue tissues (stored in RNAlater at -80oC) were thawed on ice for 15 min and RNA isolation was carried out using the RNeasy Kit (Qiagen) with few modifications. Briefly, thawed samples were homogenized in 800µl of RLT buffer containing 1% of βeta-mercaptoethanol (Biorad) using a tissue homogenizer. Subsequently 800µl of Phenol:chloroform:isoamyl-alcohol (Invitrogen) was added to the homogenate in 2ml screw-capped tubes. Following centrifugation, the aqueous phase was collected, and an equal volume of 70% molecular-grade ethanol was added. Kit instructions were followed for subsequent column separation steps. DNAse treatment was performed using the TURBO DNA-free kit (Invitrogen). RNA was analyzed for quality using the Experion automated gel electrophoretic system (Biorad) and only samples with RNA integrity value (RIN) >7 were used for RNA seq. For the RNA sequencing, cDNA libraries were prepared using the TruSeq RNA kit (Illumina) and subjected to poly(A) enrichment according to kit protocol. cDNA fragments (one hundred nucleotides from each end) were sequenced using the Illumina NextSeq platform. To analyze the RNA sequences, we combined the raw reads from each sample and performed a quality check using FASTQC (https://www.bioinformatics.babraham.ac.uk/projects/fastqc/). Next, we used Sickle to trim the reads and QC them again with FASTQC (https://github.com/najoshi/sickle). Reads were aligned using HISAT2 (Hierarchical Indexing for Spliced Alignment of Transcripts) against the Mus musculus (GRCm38) index (Kim et al., 2015). The aligned reads were then converted into binary format using samtools and the duplicates were removed using the tool PICARD (Li et al., 2009). The counts were calculated using HTseq-count program and comparisons were done between the antibiotics and non-antibiotics oropharyngeal candidiasis groups (Anders et al., 2015). False discovery rate adjusted p-values ≤ 0.05 were applied to identify significant differentially expressed (DE) genes using the DESeq2 package. Samples within a group were compared using principal component analysis and sample-to-sample distance matrix. Finally, the R software was used to compare the two groups and DE genes were tabulated and subjected to further downstream analysis.

first: Vazquez-Munoz

last: Roberto

first: Ranjan

last: Amit

first: Bertolini

last: Martinna

first: Thompson

last: Angela

first: Pegah

last: Mosharaf Ghahfarokhy

first: Alannah

last: Harnden

first: Clarissa

last: Nobile

first: Takanori

last: Sobue

first: Paola

last: Vera-Licona

first: Anna

last: Dongari-Bagtzoglou


title: Genomic correlates of LXR activation in dendritic cells and T cells

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

overall_design: Refer to individual Series


title: LXR agonism elicits a pre-effector state in naïve CD8+ T cells [ATAC-seq]

status: Public on Dec 29 2025

summary: Here, we assess chromatin accessibility profiles of naïve CD8+ T cells after 24 hours of exposure to either the LXR agonist RGX-104 or DMSO in the absence of TCR stimulation.

overall_design: ATAC-seq of naïve CD8+ T cells in absence or presence of a synthetic LXR agonist.


title: Piezo1 Knockdown Activates PI3K/AKT and Enhances SPP1 to Drive M2 Macrophage Polarization and Reduce Cardiac Inflammation

city: kunming

first: yunnhan

last: zhang

address: 528 Shahe Road

institute: Fuwai Yunnan Cardiovascular  Hospital

summary: We have successfully established a mouse model with myeloid cell-specific knockdown of Piezo1.   The intraperitoneal injection of lipopolysaccharide (LPS) resulted in a significant increase in cardiac macrophage infiltration, as well as an increase in the expression of inflammatory factors and the inflammatory response.   However, myeloid cell-specific knockdown of Piezo1 impaired this response, leading to an increase in macrophage polarization towards the M2 type and the decreased inflammatory response.   As a result, myocardial injury caused by sepsis was attenuated.   We have also demonstrated that the PI3K/AKT pathway is significantly activated after Piezo1 knockdown, resulting in reduced myocardial dysfunction.

overall_design: RNA-sequencing profiling of macrophages from Piezo1^flox/flox and Piezo1^flox/flox Lyz2-Cre C57BL/6J mice following lipopolysaccharide (LPS) treatment.

first: Yunhan

last: Zhang

first: Ying

first: Jiaoyan

last: Song

first: Ziwen

last: Zhao

first: Wenhao

last: Ju

first: Hao

first: Shuang

last: Li


title: Single-cell transcriptomic and spatial subcellular landscape of the articular disk synovium in mouse temporomandibular joint osteoarthritis

city: Sinagawa-ku

first: Kazuhiro

last: Shibusaka

state: Tokyo-to

address: 1-5-8, Hatanodai,1st building, 343

institute: showa university

summary: This study aimed to elucidate the molecular mechanisms underlying TMJ-OA by integrating subcellular spatial transcriptomics with single-cell RNA sequencing analysis in TMJ-OA mouse models.

overall_design: The TMJ-OA model mouse experiments were conducted using 9-week-old female C57Black/6J mice. The TMJ-OA models were divided into three groups: Control (n=7), Mechanical Stress (MS) model (n=7), and Articular Disc Displacement (ADD) model (n=4). scRNA-seq was performed on cells obtained from the articular disc, including the synovium, three weeks after establishing the TMJ models.

first: Asuka

last: Terashima

first: Soichiro

last: Negishi

first: Masahiro

last: Hosonuma

first: Miki

last: Maemura

first: Hiroshi

last: Yoshida

first: Nobuhiro

last: Sakai

first: YoungKwan

last: Kim

first: Yutaka

last: Suzuki

first: Hiroyuki

last: Okada

first: Fumiko

last: Yano


title: Epigenetic Signatures of Brain Aging by Single Nucleus Methylation Sequencing [FC-9mo-m-020]

city: La Jolla

first: Joseph

middle: R

last: Ecker

state: CA

address: 10010 North Torrey Pines Road

department: Genomic Analysis Laboratory

institute: HHMI-Salk-Institute

type: Methylation profiling by high throughput sequencing

summary: Illustrating aging effects on the epigenomic features of brain is critical to understand brain functional decline and neurodegeneration. Single nucleus methylation sequencing was applied to brain regions of both male and female mouse at the age of 2, 9 and 18 months. We use these data to identify the epigenomic changes with aging in mouse brains.

overall_design:
Apply snmC-seq3 to mouse brain regions to identify aging effects on epigenomics

Processed data for these samples are available at:

https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE313770

first: Q

last: Zeng

first: Wei

last: Tian

first: Anna

last: Bartlett

first: J

last: Nery

first: Rosa

last: Gomez Castanon

first: Julia

last: Osteen

first: Jordan

last: Altshul

first: N

middle: D

last: Johnson

first: M

last: Kenworthy

first: C

last: Valadon

first: Huaming

last: Chen

last: Behrens


title: Circadian and Light Perturbed Circadian Gene Expression in Prochlorococcus marinus MED4

city: Richland

first: Lindsey

last: Anderson

state: WA

address: 3300 Stevens Dr

department: Biological Sciences Division

institute: Pacific Northwest National Laboratory

summary: A circadian gene expression study in model marine cyanobacteria Prochlorococcus marinus MED4 was performed in order to evaluate circadian gene expression and identify genes which were regulated dependent on circadian photoperiod or light intensity.

overall_design: Prochlorococcus marinus MED4 was cultured in adapted Pro99 media prepared using Salish Seawater (Sequim, Washington) and 2X standard concentrations of Pro99 N/P sources, while maintaining 1× concentration of Pro99 trace metals. Cultures were acclimated to a circadian photoperiod of 12:12 h light:dark at an incident white-light intensity of 45 µmol photons m⁻² s⁻¹ and a temperature of 22 °C for XX days / generations prior to sampling. Accimaltion was performed in a single XL batch flask before splitting samples into individual 50mL tubes. Circadian perturbed samples were exposed to extended periods of light during circadian night (ZT = 14, 16h) or dark during circadian day (ZT = 2, 4h). Destructive sampling was performed for three biological replicates every two-hours across a full circadian cycle. At each time point, biological replicates were harvested via rapid filtration and flash-frozen in liquid nitrogen.

first: Pavlo

last: Bohutskyi

first: Zachary

first: Xialou

last: Li

first: Natalie

last: Sadler

first: Margaret

middle: S

last: Cheung

first: Weijun

last: Qian


title: Phagocytosis of necroptotic cells optimizes type 1 conventional dendritic cells for induction of a cytotoxic T-cell response

city: Leiden

first: Jannie

last: Borst

address: Albinusdreef 2

department: Immunology

country: Netherlands

institute: Leiden University Medical Center

summary: Whether a T-cell response to dead cells arises depends on whether they harbor recognizable  antigens, but also how dead cell debris impacts conventional dendritic cells (cDCs). In all tissues, cell debris is continuously phagocytosed by cDCs that can migrate to lymph nodes (LNs) and initiate T-cell responses, depending on their maturation state. The cDC1 lineage excels at antigen cross-presentation, which is required for induction of the cytotoxic CD8+ T-lymphocyte (CTL) response. At steady state, cDC1s undergo homeostatic maturation, which leads to T-cell non-responsiveness. This cDC1 state has recently been defined by ex vivo transcriptomics as resulting from phagocytosis of apoptotic cell debris. Necroptotic (tumor) cell death has been described as more immunogenic than apoptotic cell death, but its impact on cDC maturation has not been defined. In this study, we use an in vitro model to compare side-by-side the impact of well-defined apoptotic versus necroptotic tumor cell debris on the CTL response induced by cDCs, as well as on phenotype and function of both cDC1s and cDC2s. We confirm that cDC2s are less efficient than cDC1s in dead cell phagocytosis and find that they minimally respond to it in terms of gene expression. Apoptotic cell debris is more efficiently phagocytosed by cDC1s than necroptotic cell debris and induces a cDC1 cell state in vitro that has an evident transcriptomic relationship to the homeostatic maturation state defined ex vivo, thus validating our approach. We identify necroptosis as more potent than apoptosis in inducing a CTL response and attribute this to the ability of necroptotic cell debris to induce a specific, transcriptomically defined maturation state in cDC1s, characterized by cytokine and phosphoinositide signaling, cytoskeletal and metabolic activity and functional differentiation. We suggest that this cDC1 signature may be used to diagnose immunogenicity of necroptosis ex vivo.

overall_design: Bulk RNA sequencing of murine primary splenic cDC1 and cDC2 co-cultured for 6 h with medium from wildtype TC-1 cells, or medium from apoptotic TC-1-iBimS cells, or medium from necroptotic TC-1-iRIPK3 cells.

first: Mo

last: Staal

first: Zhixian

last: Wang

first: Douwe

last: Bosma

last: Busselaar

first: Ellen

last: Schrama

first: Evert

last: de Vries

first: Yanling

last: Xiao


title: Essential role of NONO-HOXA1-Wnt axis in cardiomyocyte differentiation

first: Feizhen

last: Wu

state: Shanghai

address: Zhangheng Road 825, Pudong

department: Intelligent Medicine Institute

institute: Fudan Univ, Shanghai, China

summary: NONO is recognized as a critical molecular scaffold involved in both transcriptional and posttranscriptional regulation. Mutations in NONO are frequently linked to congenital heart diseases (CHDs) in humans. However, the mechanisms by which NONO regulates cardiac development remain elusive. Here, we identified NONO as a pivotal dual-function regulator of cardiomyocyte differentiation in human induced pluripotent stem cells (hiPSCs). NONO deficiency in hiPSCs results in a distinct defect in early cardiomyocyte differentiation. Mechanistically, NONO interacts with HOXA1 and regulates the dynamic expression of key genes during early cardiomyocyte differentiation. ChIP-seq analysis reveals that NONO loss reduces HOXA1 occupancy at target genes, compromising its transcriptional regulation. Additionally, NONO and HOXA1 cooperatively activate the Wnt signaling. Taken together, these findings establish the NONO-HOXA1-Wnt axis as a key molecular mechanism in cardiomyocyte differentiation and provid insights into the etiology of CHDs associated with NONO mutations.

overall_design: We performed ChIP-seq of NONO in Day2-differentiated cells. We performed ChIP-seq of HOXA1 in WT and NONO-KO Day2-differentiated cells overexpressing Dox-induced HOXA1-HA using anti-HA tag antibody, Input of ChIP-seq in Day2-differentiated cells, mRNA-seq of WT,  NONO-KO Day2, 5, 7, 9-differentiated cells and HOXA1-KO Day2-differentiated cells.

first: Wei

last: Sheng

first: Guoying

last: Huang

first: Zhiyu

last: Feng

first: Yuan

last: Gao


title: CRATER tumor niches facilitate CD8+ T cell engagement and correspond with immunotherapy success [Spatial transcriptomics]

city: Boston

first: Leonard

last: Zon

state: MA

address: 1 Blackfan Circle

department: Oncology/Hematology

institute: Boston Children's Hospital

summary: T cell-mediated tumor killing underlies immunotherapy success. Here, we used long-term in vivo imaging and high-resolution spatial transcriptomics of zebrafish endogenous melanoma, as well as multiplex imaging of human melanoma, to identify domains facilitating the immune response during immunotherapy. We identified cancer regions of antigen presentation and T cell engagement and retention (CRATERs) as pockets at the stroma-melanocyte boundaries of zebrafish and human melanoma. CRATERs are rich in antigen-recognition molecules, harboring the highest density of CD8+ T cells in tumors. In zebrafish, CD8+ T cells formed prolonged interactions with melanoma cells within CRATERs, characteristic of antigen recognition. Following immunostimulatory treatment, CRATERs expanded, becoming the major sites of activated CD8+ T cell accumulation and tumor killing. In humans, elevation in CRATER density in biopsies following immune checkpoint blockade (ICB) therapy correlated with a clinical response to therapy. CRATERs are structures that show active tumor killing and may be useful as a diagnostic indicator for immunotherapy success.

overall_design: A 10um slice of BRAF(V600E)/p53mitfa specific null/Tyrosinse mitfa specific null zebrafish melanoma tumor was analyzed using Slide-SeqV2 spatial transcriptomics.

first: Georgia

last: Stirts

first: Sophia

last: Liu

first: Qiyu

last: Gong

first: Irving

last: Barrera

first: Aya

last: Ludin

first: Fei

last: Chen


title: Pathophysiological Significance of Impaired KAT7-Dependent Histone H3K14 Acetylation During Zinc Deficiency [ChIP-seq_Hela]

city: Tokyo

first: Takao

last: Fujisawa

address: 7-3-1, Hongo, Bunkyo-ku

institute: The University of Tokyo

summary: Zinc is an indispensable micronutrient for optimal physiological functions, and zinc deficiency has been implicated in the pathogenesis of various human diseases. One potential mechanism underlying such pathogenic effects is the alteration of gene expression caused by zinc deficiency; however, the details of this process remain largely unexplored. Here, we show that during zinc deficiency, the histone acetyltransferase KAT7 loses its enzymatic activity, leading to the attenuated acetylation of histone H3 at Lys14 (H3K14ac) at enhancer regions. Physiologically, the decrease in H3K14ac leads to the upregulation of the expression of ZIP10, a plasma membrane-localized zinc transporter, thereby facilitating the import of extracellular zinc to maintain cellular zinc homeostasis. Moreover, prolonged zinc deficiency in mice induced by a zinc-deficient diet or high-fat diet, accompanied by decreased H3K14ac levels in the liver, upregulated the expression of genes associated with intracellular lipid droplet formation, leading to the accumulation of lipids within liver tissue. Our findings demonstrate that cells respond to zinc deficiency by converting it into an epigenetic signal that drives physiological or pathophysiological biological processes.

overall_design: HeLa cells were culutred with the indicated medium (zinc-normal or zinc-defieicnt) or treated with each siRNA (non-targeting or KAT7). Then DNA was isolated using SimpleChIP Enzymatic Chromatin IP Kitand subjected to ChIP-seq

first: Satoshi

last: Takenaka


title: Chromatin Accessibility Dynamics Suggest Immune-Modulatory Effects of Vitamin D3 In Vivo

city: Olsztyn

first: Maciej

last: Rybiński

state: Warmian-Masurian Voivodeship

address: Trylińskiego 18

country: Poland

institute: Institute of Animal Reproduction and Food Research of the Polish Academy of Sciences.

summary: Vitamin D₃ is a key micronutrient known to support innate immunity and modulate adaptive responses, with in vitro studies suggesting the involvement of epigenetic mechanisms. However, in vivo evidence remains limited. In this study, we investigated genome-wide epigenomic responses to vitamin D₃ supplementation in a cohort of 38 individuals from a Polish population. Peripheral blood mononuclear cells (PBMCs) were collected at baseline (day 0) and 24 hours after supplementation (day 1). ATAC-seq analyses revealed widespread vitamin D₃-induced changes in chromatin accessibility.

overall_design: ATAC-seq libraries of PBMCs obtained from a Polish cohort of 38 individuals before supplementation (day 0) as well as 24 hours after (day 1).

first: Rybiński

last: Maciej

first: Carlberg

last: Carsten


title: Reduction of the HIV-1 reservoir in T cells from people with HIV-1 on suppressive antiretroviral therapy using expanded natural killer cells

city: Cleveland

first: Konstantin

last: Leskov

state: OHIO

address: 2109 Adelbert Rd, Wood W200

department: Molecular Biology and Microbiology

institute: Case Western Reserve University School of Medicine

summary: Treatment with latency-reversing agents (LRAs) alone has been ineffective in reducing HIV-1 reservoirs in people living with HIV-1 (PLWH) who are on antiretroviral therapy (ART), due to inefficiencies in reservoir reactivation and adaptive immune responses. However, NK cells activated with cytokines may be able to target HIV-1 reservoirs more effectively. To explore the therapeutic potential of NK cells, we expanded blood NK cells from multiple donors ex vivo into CD56brightCD16+ “eNK” cells using artificial antigen-presenting cells (aAPCs) expressing membrane-bound IL21. eNK cells express multiple activating receptors and are highly cytotoxic against specific target cells. They can also kill HIV-infected CD4+ T cells via antibody-dependent cell-mediated cytotoxicity (ADCC) using broadly neutralizing antibodies (bNAbs) against HIV-1 Env gp120/gp41. Notably, eNK cells from PLWH on ART efficiently killed autologous HIV-1+ T cells reactivated by a combination of vorinostat (SAHA) and IL-15 or an IL-15 superagonist (N-803), as evidenced by declines in proviral load, inducible HIV-1 mRNA, and virus release. Adoptive immunotherapy with eNK cells combined with LRA treatment thus presents a promising strategy to reduce the latent HIV-1 reservoir in PLWH.

overall_design: NK cells were isolated from cryopreserved PBMCs of PLWH. Non-expanded NK cells are referred to as primary NK cells while NK cells expanded with C9.K562-mbIL21 aAPCs for 2 weeks are referred to as "eNK". In this experiment we are comparing the transcriptional profiles of primary NK cells vs eNK cells.

first: Mary Ann

last: Checkley

first: Cheryl

last: Cameron


title: Thrombospondin 1 Aggravates the Progression of Heart Failure with Preserved Ejection Fraction by Inhibiting Mitophagy

city: Taiyuan

first: Xingpeng

last: Bu

address: No. 85, Jiefang South Road

institute: Shanxi Medical University

summary: Heart failure with preserved ejection fraction (HFpEF) accounts for over half of all heart failure cases, yet its underlying mechanisms remain poorly understood. Recent evidence suggests that mitochondrial dysfunction and impaired mitophagy play pivotal roles in HFpEF pathogenesis. Thrombospondin 1 (Thbs1), a matricellular protein, is implicated in cardiovascular remodeling, but its role in HFpEF has not been elucidated. Here, we demonstrate that Thbs1 expression is significantly elevated in the myocardium of HFpEF mice and that Thbs1 exacerbates cardiac dysfunction by suppressing mitophagy. Using a well-established "two-hit" mouse model (high-fat diet and L-NAME), we show that AAV9-mediated knockdown of Thbs1 alleviates diastolic dysfunction, cardiac fibrosis, and myocardial inflammation. RNA sequencing and proteomics analyses revealed enrichment of the PI3K/Akt/mTOR pathway in HFpEF hearts, which was attenuated by Thbs1 silencing. Mechanistically, Thbs1 knockdown restored autophagic flux, promoted mitochondrial clearance, and improved mitochondrial homeostasis in cardiomyocytes. These findings establish Thbs1 as a key regulator of impaired mitophagy in HFpEF and suggest that targeting Thbs1 may provide a therapeutic avenue for treating this complex syndrome.

overall_design: Male C57BL/6 mice were fed a high-fat diet (HFD; 60% kcal from fat, D12492, Research Diets) and received L-NAME (0.5 g/L, Sigma-Aldrich) in drinking water (pH 7.4) for 12 consecutive weeks. Control mice were fed standard chow and given regular drinking water. After 12 weeks, cardiac function, body weight, and blood pressure were assessed.


title: Pathophysiological Significance of Impaired KAT7-Dependent Histone H3K14 Acetylation During Zinc Deficiency [RNA-seq]

overall_design: Mice were fed a normal diet or a zinc-deficient diet for two weeks. Then RNA was isolated from the liver using ISOGEN and subjected to RNA-seq.


title: PUM2 knockdown regulates the expression and alternative splicing of genes associated with myocardial fibrosis in H9C2 cells

city: Urumqi City

first: Jie

last: Li

address: No. 91, Tianchi Road

institute: People's Hospital of Xinjiang Uygur Autonomous Region

summary: Myocardial fibrosis (MF) represents a major pathological alteration observed in the progression of numerous heart conditions. The presence of excessive myocardial fibrosis is instrumental in the worsening of different heart diseases, which can ultimately lead to heart failure. It has been found that abnormal expression of Pumilio RNA-binding family member 2 (PUM2), an RNA-binding protein, is a contributing factor in the development of a variety of diseases. This study aims to investigate how PUM2 affects the expression and alternative splicing of genes associated with MF in H9C2 cells, thereby elucidating the role of PUM2 in this context.

overall_design: Inhibition of PUM2 expression in H9C2 cardiomyocytes was achieved through siRNA transfection. Cell proliferation was assessed using the Cell Counting Kit-8 (CCK-8)   assay, while apoptosis was detected via flow cytometry. RNA-seq was utilized to analyze the differential gene expression profiles and alternative splicing events in H9C2 cells regulated by PUM2. The sequencing results were confirmed through real-time quantitative polymerase chain reaction (RT-qPCR) experiments.

first: Zilong

last: Zhang

first: Hangyu

last: Zhou

first: Wei

last: Zhu

first: Adili

last: Diliyaer

first: Yong

first: Wenzheng

first: Zhao

last: Wang


title: Transcriptomic analyses of mouse livers from an 18-month oral carcinogenicity study of HFPO-DA with a 9-month chronic toxicity phase

city: Asheville

first: Melissa

last: Heintz

state: NC

address: 31 College Place, Suite B118

institute: ToxStrategies

summary: Transcriptomic anlayses were conducted on liver tissue from male and female CD-1 mice  orally exposed to 0, 0.05, 0.1, 0.5 or 5 mg/kg-bw/day HFPO-DA (ammonium 2,3,3,3-tetrafluoro-2-(heptafluoropropoxy)-propanoate; CASRN 62037-80-3) in a 18-month carcinogencity study that included a 9-month chronic toxicity phase in support of an investigation of the mode of action for HFPO-DA-mediated liver toxicity. This combined chronic toxicity and carcinogenicity study complied with Good Laboratory Practice (GLP) and Organization for Economic Co-operation and Development (OECD) 453 test guidelines for combined chronic toxicity/carcinogenicity studies. Transcriptomic responses in exposed mice were compared to time-matched control mice. Pathway enrichment of differentially expressed genes, as well as benchmark dose modeling and functional classification of dose-responsive genes were conducted. A low hepatic transcriptomic response was observed in mice exposed to 0.05 or 0.1 mg/kg-bw/day HFPO-DA for 9 or 18 months. In mice exposed to 0.5 or 5 mg/kg-bw/day, the top most significantly enriched gene sets were similar in male and female mouse livers regardless of exposure duration. Upregulated gene sets were related to b-oxidation of fatty acids and fatty acid metabolism, PPAR signaling, and peroxisome signaling. Downregulated gene sets were related to innate immune responses and amino acid metabolism. Results from benchmark dose-response analysis indicate livers from male mice exposed to HFPO-DA for 9 months had the greatest transcriptomic response.

overall_design: Comparative gene expression profiling analysis of RNA-seq data from FFPE liver tissue of male and female CD1 mice orally exposed to 0, 0.05, 0.1, 0.5 or 5 mg/kg-bw/day HFPO-DA (n= 3-5 per treatment group) once daily for a total of 9 or 18 months.

first: William

last: Klaren

first: Amanda

last: Buerger

first: Chad

last: Thompson

first: Laurie

middle: C

last: Haws


title: LXR agonism enhances T cell activation upon crosspresentation.

first: Benjamin

last: Ostendorf

summary: Here, we analyze transcriptional profiles of OT-I CD8+ T cells co-cultured with bone marrow-derived dendritic cells pulsed with the SIINFEKL peptide in the absence of presence of the synthetic LXR agonist RGX-104.

overall_design: Differential gene expression analysis of flow cytometry-sorted OT-I CD8+ T cells after co-culture with bone marrow-derived dendritic cells in the presence of absence of the synthetic LXR agonist RGX-104.


title: Investigating the Therapeutic Potential of the Antioxidant Epigallocatechin Gallate in Fetal Alcohol Spectrum Disorders: Cognition and RNASeq

status: Public on Dec 28 2025

city: Barcelona

first: Anna

last: Ramos-Triguero

address: C/ del Rosselló, 149

country: Spain

institute: FRCB-IDIBAPS

summary: Prenatal alcohol exposure (PAE) impacts fetal development, leading to Fetal Alcohol Spectrum Disorders (FASD) characterized by cognitive, behavioral, and physical impairments. This study explores Epigallocatechin Gallate (EGCG), a potent antioxidant and modulator of neuronal plasticity, as a therapeutic intervention for FASD improvement. In a 12-month pilot study, patients with 40 FASD received 9 mg/kg/day of EGCG, with outcomes assessed through RNA sequencing of blood samples and neurocognitive evaluations (WISC-IV, CBCL 6-18, and NEPSY-II). Reduced levels of oxidative stress were observed after 6 months of daily treatment with EGCG, to maintain the bioavailability of the molecule in the body, with decreased levels of MDA and 8-isoprostane and increased activity of LDH. Significant neurocognitive improvements were shown after one year of treatment in Perceptual Reasoning Index (PRI) and Working Memory Index (WMI) using the WISC-IV test. CBCL test revealed an improvement in aggressive behavior scores after EGCG treatment. NEPSY-II assessment showed improvements in face memory, and delayed face memory. Interestingly, no significant improvements were observed in intelligence quotient, attention, anxiety, or depression, which affect a proportion of individuals diagnosed with FASD. Additionally, EGCG modulates molecular pathways associated with neuroinflammation, oxidative stress, immune response, and neurogenesis. This study highlights EGCG as a potential therapeutic candidate to ameliorate cognitive and behavioral deficits caused by PAE in children affected by FASD, revealing potential pathways and biomarkers that contribute to these improvements. These advancements ultimately aim to enhance the quality of life for FASD patients and their families.

overall_design: RNA-seq analysis was conducted in 8 FASD patients at baseline (t0) and following 12 months of EGCG treatment (t12)

first: Marta

last: Astals-Vizcaino

first: Elisabet

last: Navarro-Tapia

first: Melina

last: Vieiros

first: Adriana

last: Bastons-Compta

first: Leopoldo

last: Martínez

first: Vicente

last: Andreu-Fernández

first: Óscar

last: García-Algar


title: LXR agonism promotes T cell effector chromatin landscapes upon crosspriming by dendritic cells.

address: Augustenburger Platz 1

institute: Charité University Medicine

summary: Here, we assess chromatin accessibility profiles of OT-I CD8+ T cells upon co-culture with antigen-pulsed BMDCs in the presence or absence of the synthetic LXR agonist RGX-104.

overall_design: ATAC-seq of OT-I CD8+ T cells after co-culture with BMDCs in absence or presence of a synthetic LXR agonist.


title: Ketogenic diet dampens excitatory neurotransmission by shrinking synaptic vesicle pools

status: Public on Dec 27 2025

city: Saint Louis

first: Marion

middle: Isabelle

last: Stunault

state: MISSOURI

address: 660 S Euclid Ave

institute: Washington University School of Medicine

summary: The ketogenic diet (KD) is a common dietary intervention for treating seizures in intractable childhood epilepsies and has been proposed to improve disease outcome in neurodegenerative disorders. Despite its clinical applications, we know little about how this diet impacts brain circuitry and neuronal function to elicit its protective effects. Here, we examined the impact of the KD on hippocampal function through integrative analysis of gene expression, epigenetics and neurotransmission.  We found that KD induces profound transcriptional reprogramming of the hippocampus, including altered expression of numerous synaptic genes. Proteomic analysis of histone variants and post-translational modifications also revealed significant changes in activating and repressive epigenetic marks in the hippocampus of KD mice. To determine how transcriptional and epigenetic rewiring of the hippocampus under KD impacts neurotransmission, we performed electrophysiological recordings to examine synaptic dynamics and synaptic summation at CA3-CA1 synapses. We found that KD diminishes synaptic gain and dampens short-term plasticity at excitatory synapses, resulting in reduced summation of synaptic inputs at the circuit level. We determined that the dampening of synaptic gain was due to a reduction in size of the readily releasable as well as the total of synaptic vesicles in excitatory but not inhibitory synapses. Our findings show that the ketogenic diet triggers synaptic remodeling in the hippocampus, driven by broad transcriptional and epigenetic changes that reduce synaptic vesicle pools and short-term plasticity at excitatory synapses ultimately dampening excitatory synaptic gain and integration at the circuit level. These synaptic adaptations may represent a major mechanism underlying the anti-epileptic effects of this diet.

overall_design: RNAsequencing analysis of the hippocampus of young and Adult mice fed either a chow or ketogenic diet.

middle: I

first: Pan-Yue

last: Deng

first: Anjali

last: Yadav

first: Erica

last: Periandri

first: Francisca

last: de Luna Vitorino

first: Michael

last: Thomsen

first: Jasmin

last: Sponagel

first: Amelia

middle: J

last: Barfield

first: Renzelle

last: Ponce

first: Layla

last: Foroughi

last: Garcia

first: Gabor

last: Egervari

first: Vitaly

last: Klyachko

first: Ghazaleh

last: Ashrafi


title: Transcriptional profiles of tumor-draining lymph node resident CD11c+ cells in wildtype versus APOE-KO mice

city: Berlin

first: Benjamin

last: Ostendorf

summary: Here, we analyze transcriptional profiles of CD11c+ enriched cells from the lymph nodes draining E0771-cOC tumors in either wildtype or APOE-KO mice.

overall_design: Differential gene expression between CD11c+ cells from APOE-KO versus wildtype mice.


title: Gene regulatory programs underlying diversification of facial ligaments and tendons in zebrafish

city: Los Angeles

first: Gage

last: Crump

address: 1425 San Pablo St.

department: Stem Cell

institute: USC

summary: The musculoskeletal complex is held together by ligaments connecting skeletal elements and tendons bridging the musculature with the skeleton. How connective tissues of the right type and function are specified in distinct regions of the developing body remains understudied. To understand the gene regulatory programs specifying connective tissue subtypes, we generated single-cell datasets of RNA expression and chromatin accessibility for scxa:mCherry+ connective tissue cells of the developing zebrafish face. We identified cell clusters corresponding to tendon, ligament, periligament, perichondrium, and other connective tissue types, which we validated by in situ hybridization. We also uncovered tendon and ligament cells sharing an osteogenic signature, which may explain the remodeling of ligament-bone interfaces and the formation of sesamoid bone from tendons. This osteogenic potential of tendon and ligament cells is further reflected by co-enrichment of transcription factor-binding motifs for Scx and the osteogenic factor Runx2 in their enhancers. Moreover, several enhancers drive spatially-restricted transgenic activity in distinct ligaments, periligament tissue, perichondrium, and other jaw mesenchyme types, which we used to express a photoconvertible nlsEOS protein and reveal posterior-directed growth of the major jaw-stabilizing ligament. At the anterior end of this same ligament, we show that Nkx3.2 is required for its attachment to the jaw joint. Our study reveals gene regulatory programs for jaw connective tissue diversification and provides a mechanism underlying the propensity of tendons and ligaments to ossify in normal and pathological contexts.

overall_design: Tg(scxa:mCherry)+ single cells or nuclei were extracted and sorted from 5 and 14dpf zebrafish embryos. ScRNA, snRNA, and snATAC libraries were prepared using the 10X Genomics platform.

first: Ryan

last: Roberts

first: Hung-Jhen

last: Chen

first: Kuo-Chang

last: Tseng

first: J

last: Gage Crump


title: Vincristine induces spermatogenic impairment in a B-ALL PDX mouse model via downregulation of Tssk4 and Ccdc159: RNA-seq transcriptomic profiling

status: Public on Dec 26 2025

city: Fuzhou

first: Meng

last: Fu

state: Fujian

address: 310 Yangqiao Middle Road

institute: Fujian Children's Hospital

summary: This dataset contains RNA sequencing (RNA-seq) data generated from testicular tissues of a B-cell acute lymphoblastic leukemia (B-ALL) patient-derived xenograft (PDX) mouse model treated with vincristine (VCR). The study aimed to elucidate the molecular mechanisms underlying VCR-induced reproductive toxicity. Samples were collected from multiple experimental groups, including normal controls (NC), leukemia-bearing controls (ALL), and VCR-treated groups with varying leukemia infiltration levels. Transcriptomic analysis revealed widespread gene expression perturbations following VCR exposure, with significant downregulation of genes crucial for spermatogenesis and sperm flagellar assembly. This data provides a comprehensive resource for understanding the genetic pathways affected by VCR in the testicular microenvironment.

overall_design: RNA-seq profiling of testicular tissues from five experimental groups of PDX mice: Normal control (NC), B-ALL model control (ALL), VCR-only treated, and VCR-treated with low (Low-VCR) and high (High-VCR) peripheral blood leukemia infiltration.

first: Chaoming

last: Zhou

first: Suyun

first: Shengqi

last: Zheng

first: Xu

last: Cui


title: Pathophysiological Significance of Impaired KAT7-Dependent Histone H3K14 Acetylation During Zinc Deficiency [ChIP-seq_Mice]

first: Takao

last: Fujisawa

overall_design: Mice were fed a normal diet or a zinc-deficient diet for two weeks. Then DNA was isolated using SimpleChIP Enzymatic Chromatin IP Kit and subjected to ChIP-seq.

first: Satoshi

last: Takenaka


title: Single embryo total RNA sequencing to map the effect of maternal SETDB1 on the 2-celll and 8-cell transcriptome

city: Grand Rapids

first: Piroska

last: Szabó

state: MI

address: 333 Bostwick Ave NE

department: Department of Epigenetics

institute: Van Andel Insitute

summary: Embryos with maternal mutation of the H3K9 methyltransferase SETDB1 die before implantation. We tested the role of maternal SETDB1 in the timely processes of the preimplantation stage embryo. Using single embryo total RNA sequencing from 2-cell and 8-cell embryos, we found that maternal SETDB1 is required for switching off maternal transcripts by the 2-cell stage, minor ZGA transcripts by the 2-cell stage, and major ZGA transcripts by the 8-cell stage. By timely extinguishing of endogenous retroviruses, oocyte-specific ERVL-MaLRs, many oocyte-specific genes, MERVLs, MERVL LTR-driven chimeric transcripts and ZGA genes as well as KRAB ZF genes, maternal SETDB1 secures the proper transition from totipotency to pluripotency.

overall_design: Setdb1 maternal mutant (Zp3Cre +) and control (Zp3Cre -) 2c and 8c stage mouse embryos were collected at 1.5 dpc and 2.5 dpc, respectively. Single embryo total RNA-seq was done using biological replicates.

first: Tie-Bo

last: Zeng

first: Zhen


title: Sustained STING-IRF7 signaling aggravates LPS-induced endometrial inflammation via excessive neutrophil extracellular traps generation

city: Yantai

first: Min

last: Chu

state: Shandong

address: No. 20 Yuhuangding Estern Road

institute: Yantai Yuhuangding Hospital

summary: The stimulator of interferon genes (STING) is a central mediator of innate immune sensing and represents a critical regulator of chronic inflammation. Upon persistent infection, excessive neutrophil activation leads to the formation of neutrophil extracellular traps (NETs) that damage the tissues. However, the mechanism by which STING signaling regulates NETs formation under chronic inflammatory conditions remains poorly understood. In this study, using LPS-induced murine endometritis models in wild-type and STING-deficient mice, we demonstrated that STING deficiency significantly suppressed myeloperoxidase activity, and diminished NETs formation. We identified neutrophil surface molecular CD11b as a key downstream target of STING, whose expression was transcriptionally regulated via IRF7. Furthermore, the STING-IRF7 axis was found to drive lipocalin-2 (LCN2) expression, which acted through its receptor MC4R to upregulate intracellular adhesion molecule-1 (ICAM-1), thereby facilitating neutrophil recruitment and NETosis during LPS stimulation. The role of this pathway was validated both in vitro using isolated neutrophils and in vivo using Lcn2-/- mice. Moreover, STING deficiency reprogramed the endometrial immune microenvironment by reducing inflammatory infiltration and restoring receptivity transcription factor homeobox A10 (HOXA10). Our findings revealed a novel mechanism in which the STING-IRF7 pathway exacerbated endometrial inflammation and tissue damage by coordinately upregulating CD11b and activating the LCN2-ICAM-1 axis. Consequently, targeting the STING signaling pathway may offer a promising therapeutic strategy for chronic endometritis.

overall_design: For LPS-induced endometritis, uterine tissues were collected from two groups: LPS-treated STING-deficient mice and LPS-treated WT mice. Each group included three biological replicates to ensure statistical robustness. In this study, using LPS-induced murine endometritis models in wild-type and STING-deficient mice, we demonstrated that STING deficiency significantly suppressed myeloperoxidase activity, and diminished NETs formation.

first: Ding

last: Ma

first: Zhan

last: Song

first: Li

last: Liang

first: Fengjuan

last: Xing

first: Hongchu

last: Bao


title: cMaf supports Zeb2 expression for primitive hematopoiesis (TRM RNA-seq)

first: Jing

last: Chen

state: MO

address: 600 S Euclid Ave

institute: Washington University in St. Louis

summary: Tissue-resident macrophages (TRMs) are essential for tissue homeostasis and play a key role in disease and pathology. They originate from distinct waves of hematopoietic progenitors, including primitive, transient-definitive, and definitive hematopoiesis. We found that loss of the Zeb2 ‒165kb enhancer impairs monocyte development and alters TRM transcriptional landscapes, with only HSC-derived monocytes requiring Zeb2 for their development. In Zeb2∆‒165kb mice, primitive TRMs persist in tissues due to the lack of replacement by later hematopoietic waves, and Maf is required for maintaining Zeb2 expression in primitive macrophages.

overall_design: TRMs were isolated from the lung, liver, brain and spleen of wildtype and Z165KO mice and performed bulk RNA-seq.

first: Theresa

middle: L

last: Murphy

first: Kenneth


title: cMaf supports Zeb2 expression for primitive hematopoiesis (FL mono RNA-seq)


title: Analysis of local mucosal immune dysregulation to guide pilot directed therapy for long-COVID olfactory loss [TCR-seq]

status: Public on Dec 25 2025

city: Durham

first: Sarah

last: Kim

address: 481 MSRB1

institute: Duke University

summary: To further define local mechanisms impacting peripheral olfactory structures, we obtained olfactory biopsies from subjects with post-COVID olfactory loss (hyposmia) or controls for viral, single cell and T cell receptor assays. Here we identified clonally expanded T cell subsets with a pro-inflammatory profile.

overall_design: Biopsies of human olfactory epithelium collected from three long-COVID hyposmics and three normosmic control patients and processed for 5' GEX and TCR sequencing

first: Vincent

last: D'Anniballe

first: John

middle: B

last: Finlay

first: Tiffany

last: Ko

first: Michael

last: Wang

first: Bradley

last: Goldstein


title: Inflammation in a severe model of dystrophic cardiomyopathy contains a high proportion of T-cells that contribute to onset of pathology

city: Columbus

first: Jill

last: Rafael-Fortney

state: OH

address: 460 W. 12th Ave

department: Physiology & Cell Biology

institute: The Ohio State University

summary: Duchenne muscular dystrophy (DMD) is a severe neuromuscular disorder characterized by progressive muscle degeneration and cardiomyopathy leading to heart failure. While the inflammatory environment in dystrophic skeletal muscle has been well-studied, little is known about inflammation in the progression of DMD cardiomyopathy due to the lack of adequate animal models. To address this, we developed the Fiona/dko mouse model, which exhibits severe, isolated dystrophic cardiomyopathy. In this study, we used Fiona/dko mice to characterize the immune cell composition in dystrophic heart and investigated the contribution of T-cells to the onset and progression of cardiac pathology. Flow cytometry analysis revealed that T-cells constitute a significant proportion of the immune cell population in Fiona/dko hearts, in contrast to the predominantly myeloid signature observed in dystrophic skeletal muscle. Furthermore, we demonstrated that T-cell infiltration precedes the development of cardiac fibrosis and dysfunction in Fiona/dko mice and that depletion of circulating CD3+ T-cells ameliorates early pathology, suggesting a role for T-cells in the initiation and persistence of dystrophic cardiomyopathy. These findings highlight the distinct inflammatory environment in the dystrophic heart and provide new insights into the pathogenesis of DMD cardiomyopathy, paving the way for the development of targeted anti-inflammatory therapies.

overall_design: To investigate gene expression differences between more severe cardiomyopathy in Fiona/dko mice compared to less severe Het/Fiona mice, 9-month-old mice of each genotype, including males and females for each, were dissected and RNA was extracted from heart ventricles to send for bulk RNA sequencing.

first: Arden

last: Piepho

first: Swathy

last: Krishna

middle: A


title: Epigenetic Signatures of Brain Aging by Single Nucleus Methylation Sequencing [FC-9mo-m]

city: La Jolla

first: Joseph

last: Ecker

address: 10010 North Torrey Pines Road

institute: HHMI-Salk-Institute

summary: Illustrating aging effects on the epigenomic features of brain is critical to understand brain functional decline and neurodegeneration. Single nucleus methylation sequencing was applied to brain regions of both male and female mouse at the age of 2, 9 and 18 months. We use these data to identify the epigenomic changes with aging in mouse brains.

overall_design:
Apply snmC-seq3 to mouse brain regions to identify aging effects on epigenomics

Processed data for these samples are available at:

https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE313770

first: Q

last: Zeng

first: Wei

last: Tian

first: Anna

last: Bartlett

first: J

last: Nery

first: Rosa

last: Gomez Castanon

first: Julia

last: Osteen

first: Jordan

last: Altshul

first: N

last: Johnson

first: M

last: Kenworthy

first: C

last: Valadon

first: Huaming

last: Behrens


title: Analysis of local mucosal immune dysregulation to guide pilot directed therapy for long-COVID olfactory loss [5' GEX]

first: Sarah

last: Kim

first: Vincent

last: D'Anniballe

first: John

last: Finlay

first: Tiffany

last: Ko

first: Michael

last: Wang


title: Evaluation of Metaplastic Triple-Negative Breast Cancer Extracellular Matrix Structure and Protein Composition

status: Public on Dec 24 2025

city: New Orleans

first: Elizabeth

middle: Carol

last: Martin

state: LA

address: 1430 Tulane Avenue

department: Medicine

institute: Tulane University

summary: Alterations in the tumor extracellular environment and matrix stiffness promotes tumor progression. Furthermore, correlational studies have identified enrichment of extracellular matrix (ECM) proteins (glycoproteins, collagens) in breast tumors. Despite these findings, there has yet to be an interdisciplinary analysis of both ECM composition and structural architecture in rare breast tumors, such as metaplastic breast cancer. Here, we explored changes in ECM protein expression and architecture in a triple-negative breast cancer (TNBC) metaplastic tumor through SEM, proteomics, and RNA sequencing. SEM revealed tumor pore size was larger compared to control adipose tissue. Oscillating rheometry demonstrated increased ECM stiffness in the tumor compared to control adipose breast adipose. Proteomic analysis of the metaplastic TNBC tumor showed significant enrichment for ECM proteins, notably glycoproteins compared to control adipose. Interestingly, these samples showed no observed changes in expression for major fibrillar collagens COL1A1 and COL1A2, and a reduced expression of COL3A1. To determine the impact of less characterized ECMs in metaplastic TNBC, we overexpressed MFAP2 in primary metaplastic breast cancer cells and performed RNA sequencing. MFAP2 overexpression was associated with upregulation of epithelial-to-mesenchymal transition related genes . Overall, our results establish an extracellular signature and onco-architecture for the metaplastic triple-negative tumor type.

overall_design: Metaplastic TNBC (TU-BcX-4IC)  cell line constructed to overexpress the matrix protein MFAP2 or control vector. Overexpression (OE) was chieved through the transfected with 5 μg of pCMV6-Entry Mammalian Expression Vector DNA (Origene, MA, USA) and MAGP1 5ug (MFAP2) (NM_017459) Human Tagged ORF Clone (Origene, MA, USA). Following stable selection of MFAP2 overexpressing cell lines, RNA sequencing was performed. For RNA sequencing, metaplastic TU-BcX-4IC and TNBC cell line with pCMV6 Vector or MFAP2 OE cells were cultured in a T75 flask (Thermo Scientific, Waltham, Massachusetts, USA) grown to 80% confluency and collected for RNA extraction.

first: Jorge

last: Belgodere

first: Matthew

last: Burow

first: Katherine

last: Hebert


title: The effect of TASL knockout on murine B cells following TLR9 stimulation

city: Oxford

last: Johnstone

address: Kennedy Institute of Rheumatology, Roosevelt Drive

country: United Kingdom

institute: University of Oxford

summary: TLR signalling and the IRF5 pathway play a critical role in the activation of inflammatory pathways in B cells. The recently identified innate immune adaptor, TASL, plays an essential role in this pathway, enabling the phosphorylation of IRF5 and thereby the activation of downstream inflammatory pathways. We here identify the role of TASL in primary ex vivo murine B cells, finding that in the absence of TASL, key Interferon stimulated genes (ISGs) and genes involved in cytokine production are downregulated after stimulation by the TLR9 ligand, CpG ODN.

overall_design: RNA-seq profiling of splenic B cells isolated from WT or TASL-KO mice, stimulated in vitro with 100nm CpG.

first: Alexander

last: Clarke


title: Adipogenic Transcriptional Regulation Mediated by PARP7 Through NAD+ Sensing Mechanism [ATAC-seq]

city: Dallas

first: W. Lee

last: Kraus

state: TX

address: 5323 Harry Hines Blvd.

institute: UT Southwestern Medical Center

summary: The process of differentiating from a preadipocyte into a mature, fat storing, adipocyte (adipogenesis) is a complex and tightly regulated process vital to human health. The molecular mechanisms regulating adipogenesis are incompletely understood, although key facets of the signaling and regulatory pathways have been defined. Here we have identified a mono(ADP-ribosyl)transferase (MART), PARP7, that plays a pivotal role in adipogenesis. ADP-ribosylation – the process whereby specific members of the poly(ADP-ribosyl)polymerase (PARP) family facilitate the covalent transfer of  ADP-ribose moieties from NAD+ to substrate proteins – has been shown to control multiple components of the adipogenic regulatory machinery. Herein we have found that PARP7 is required for modulation of the adipogenic transcriptional program during adipogenesis, and that the loss of PARP7 results in a decrease of the adipogenic process. Contrary to previous studies, the ability to modulate the adipogenic transcriptional program is independent of PARP7 catalytic activity. However, the catalytic activity of PARP7 plays a vital role in regulating protein stability, in a time and space specific manner, which is required for modulation of the adipogenic transcriptional program. This study has found a novel pathway which utilizes NAD+ compartmentalization to stabilize PARP7 at a specific time during the adipogenic process allowing for the regulation of adipogenic genes, through modulation of the well-known adipogenic transcription factor C/EBPß, in a time sensitive manner. Therefore, acting as another check and balance to the adipogenic differentiation process.

overall_design: 3T3-L1 cells were exposed to various treatments and culture conditions for the experiments described herein.  For treatment with MG-132 (10 μM, Sigma, M7449), the cells were grown as described above, cells were then treated with 10 µM MG-132 for 6 hours before collection.  For treatment with RBN2397, the cells were grown as described above upon differentiation of 3T3-L1 cells using differentiation cocktail the cells were treated with 400 nM RBN2397. The treatment continued every other day with media changes until specified collection time.  For PARP7 MAR immunoprecipitation assays, the cells were treated with RBN 2397 for 16hrs

first: MiKayla

last: Stokes

first: Yoon Jung

first: Sneh

last: Koul

first: Josue

last: Zuniga

first: Shu-Ping

last: Chiu

first: Tulip

last: Nandu

first: Kraus

last: W Lee


title: Adipogenic Transcriptional Regulation Mediated by PARP7 Through NAD+ Sensing Mechanism

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

overall_design: Refer to individual Series


title: Adipogenic Transcriptional Regulation Mediated by PARP7 Through NAD+ Sensing Mechanism [RNA-Seq]

overall_design: 3T3-L1 cells were seeded in 6-well plates and treated as described above. The cells and tissues were collected, and total RNA was isolated using Trizol Reagent (Invitrogen) according to the manufacturer's protocols. Total RNA was reverse transcribed using oligo (dT) primers and MMLV reverse transcriptase (Promega) to generate cDNA. The cDNA samples were subjected to qPCR using gene-specific primers, as described below. For the reverse transcription quantitative real-time PCR (RT-qPCR) analyses, “relative expression” was determined in comparison to a value of the control sample.

last: Kim


title: Single-cell atlas in the living fossil Yangtze sturgeon provides insight into the evolution of fish

status: Public on Dec 23 2025

city: Chengdu

first: Yeyu

last: Chen

state: --- Select One ---

address: The Fishery Institute of The Sichuan Academy of Agricultural Sciences, No.1611 Xiyuan Street

institute: Fisheries Research Institute, Sichuan Academy of Agricultural Sciences

summary: We constructed a fish cell atlas at the whole-body scale. We investigated the heterogeneity and functional diversity of cells in the digestive, immune and nervous systems. The tissue included heart, liver, spleen, head kidney, midkidney, pyloric caecum, stomach, duodenum (smallintestine), spiral intestine, rectum, skin, muscle, gill, brain, eye, gonad, and blood samples.

overall_design: We constructed a fish cell atlas by scRNA-seq, including heart, liver, spleen, head kidney, midkidney, pyloric caecum, stomach, duodenum (smallintestine), spiral intestine, rectum, skin, muscle, gill, brain, eye, gonad, and blood samples.


title: A streamlined nanopore-compatible 5PSeq protocol for rapid phenotypic antimicrobial sensitivity testing (FigS4D-F_mixed_MinION)

city: Solna

first: Honglian

last: Liu

address: Tomtebodavägen 23

department: Department of Microbiology, Tumor and Cell Biology

country: Sweden

institute: Karolinska Institutet

summary: Antimicrobial resistance (AMR) poses a significant threat to public health. Rapid and accurate antimicrobial sensitivity testing is essential to guide effective treatment. Here, we present “simplified 5PSeq” (s5PSeq), a streamlined protocol for profiling 5’ monophosphorylated (5’P) mRNA degradation intermediates that reflect ribosome dynamics in vivo. By capturing antibiotic-induced, context-specific ribosome stalling events, s5PSeq provides a molecular proxy for bacterial growth inhibition—offering a molecular phenotypic readout without the need for culturing. s5PSeq reduces library preparation time to under four hours and incorporates a novel rRNA blocking strategy. We demonstrated its clinical utility by identifying erythromycin-resistant and sensitive Clostridioides difficile clinical isolates. Combining s5PSeq with real-time nanopore sequencing enables fast AMR diagnosis with as few as 3000 reads. In addition to simplifying the study of 5’P co-translational mRNA decay, our work suggests that utilizing information-rich phenotypic molecular readouts can significantly improve AMR diagnostics.

sample_organism:
Staphylococcus aureus
Enterococcus faecalis
Bacillus subtilis
Clostridioides difficile

overall_design: s5PSeq library were prepared using 100ng extracted total RNA from exponetially growing (OD600=0.6-0.8) C.difficile clinical isolates that are resistant or sensitive to erythromycin. Bacteria cells are treated with erythromycin(1ug/ml) for 10min or without treatment. C.difficile RNA is mixed with equal amount of RNA from untreated B.subtilis, E.feacalis and S.aureus respectively.

first: Susanne

last: Huch

first: Ryan

last: Hull

first: Fabricio

last: Garcia

first: Lilit

last: Nersisyan

first: Wei-Hua

first: Juan

last: Du

first: Vicent

last: Pelechano


title: A streamlined nanopore-compatible 5PSeq protocol for rapid phenotypic antimicrobial sensitivity testing (FigS4B-C_mixed_illumina)

platform_organism:
Staphylococcus aureus
Enterococcus faecalis
Bacillus subtilis
Clostridioides difficile

overall_design: s5PSeq library using mixture of 100ng of total RNA extracted from exponetially growing (OD600=0.6-0.8)B.subtilis, S.aureus, E.faecalis and erythromycin treated C.difficile clinical isolates(resistant and sensitive respectively)


title: Expression data from HEK-293 cells treated with different CDK8/19 inhibitors

city: Heidelberg

first: Angga

last: Prawira

address: Im Neuenheimer Feld 344

department: Molecular Virology

institute: University Hospital Heidelberg

summary: Hepatitis delta virus (HDV) enters hepatocytes via the receptor NTCP and requires CDK8/19 Mediator kinases to establish its infection by RNA Polymerase II. Here, we are interested in assessing the class effect of various CDK8/19 inhibitors and investigating the possible off-target effects caused by them.

overall_design: HEK-293 cells overexpressing the NTCP receptor were treated with 500 nM MSC2530818, 2 µM SEL120, or 50 nM CCT251545 between d1-5 post-seeding. Cells were harvested for RNA extraction and subjected to the human Clariom S assay, ThermoFisher.

first: Yi

last: Ni