title: Patient-derived organoid – immune cell co-culture platform for therapeutics discovery in high-grade endometrial cancer

city: Jammu

first: Santhilal

last: Subhash

state: Jammu and Kashmir

address: Jagti, NH-44, PO Nagrota

department: Biosciences and Bioengineering

country: India

institute: Indian Institite of Technology Jammu

summary: We established a biobank of 85 patient-derived organoids (PDOs) generated from 44 individuals, encompassing a broad range of endometrial cancer (EC) subtypes, including a majority of high-grade endometrial cancer (HGEC) PDOs from African American patients. From these same patients, we isolated autologous immune cells, enabling the creation of PDO–immune cell co-cultures that reflect each patient’s unique characteristics without evoking allogeneic immune responses. To dissect the roles of antigen presentation pathways and evaluate proof-of-principle immunotherapeutic interventions, we performed bulk RNA sequencing, flow cytometry, and live-cell imaging.

overall_design: Bulk RNA-seq profiling of endometrial cancer patient-derived organoids (PDOs) and matched normal (CTL).

first: Charlie

last: Chung

last: Yueh

first: Onur

last: Eskiocak

first: Semir

last: Beyaz


title: Topology-informed regulatory element collections coordinate cell identity gene expression programs

status: Public on Feb 15 2026

city: Memphis

first: Brian

middle: J

last: Abraham

state: TN

address: 262 Danny Thomas Blvd

department: Computational Biology

country: USA

institute: St. Jude Children's Research Hospital

type: Genome binding/occupancy profiling by high throughput sequencing

type: Expression profiling by high throughput sequencing

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

overall_design: Refer to individual Series


title: Estrogen receptor β target gene expression reveals novel repressive functions in aggressive breast cancer [ChIP-Seq]

city: Houston

first: Christoforos

last: Thomas

state: Texas

address: 6670 Bertner Avenue

department: Department of Medicine

institute: Houston Methodist Research Institute

summary: Inflammatory breast cancer (IBC) is a highly metastatic breast carcinoma with high frequency of estrogen receptor a (ERα) negativity and limited treatment options. We previously explored the second ER subtype, (ERβ) and reported correlation of its tumor expression with reduced metastasis in patients and in preclinical models of the disease. We initially associated the anti-metastatic function of the receptor with the inhibition of actin-based cell migration and the associated Rho GTPase signaling in IBC cells. We have now followed an integrated genomics approach to fully delineate the signaling underlying the anti-metastatic effects of ERβ. Through mapping binding sites in IBC cells that express endogenous and transfected ERβ in the presence of an agonist and interrogating this information with altered expression of protein coding mRNAs and miRNAs we have defined the interaction of a biologically active receptor with the cancer genome that controls metastatic signals. We reveal key  regulatory chromatin binding sites and motifs and identify direct target genes and miRNAs and the associated biological functions. Our new findings implicate the regulation of metabolic pathways and signaling in development and tumor microenvironment in anti-metastatic activity of ERβ. Through a rigorous analysis of target genes in clinical datasets we also associate downstream factors with patient outcomes reporting new molecules with targeting potential and strengthening the relevance of ERβ signaling for the metastatic process in breast cancer. Our findings thus offer an opportunity to validate the tumor repressive role of ERβ through a better understanding of its mechanism of action.

overall_design: Analysis of breast cancer cells with different ERβ levels and after with treatment with the ERβ agonist. KPL4 cells without ERβ (ERβ knockout cells) vs. KPL4 cells with ERβ (ΕRβ knockout cells with transfected ERβ). Wild-type SUM149 cells with endogenous ERβ (Control cells) vs. SUM149 cells with overexpressed ERβ (Control cells with transfected ERβ). KPL4 ΕRβ knockout cells with transfected ERβ after treatment with vehicle (DMSO) or the ERβ agonist LY500307 for 2 hours

first: Spyros

last: Tastsoglou

first: Ilias

last: Karagounis

first: Marios

last: Miliotis

first: Harika

last: Nagandla

first: Kristina

last: Zambo

first: Maria

last: Liousia

first: Naoto

last: Ueno

first: Amit

last: Maity

first: Artemis

middle: G

last: Hatzigeorgiou


title: Development and Characterization of an Inducible Tensin1 Deficient Transgenic Murine Model

status: Public on Feb 14 2026

city: Madison

first: Nathan

last: Sandbo

state: WI

address: 600 Highland Avenue

institute: University of Wisconsin-Madison

summary: Tensin1 (TNS1) is a key component of focal and fibrillar adhesions, mediating fibrillogenesis, as well as the transduction of mechanical cues and adhesive signaling. To enable further TNS1 characterization, we have developed a novel transgenic mouse that allows for temporally controlled and lineage specific knockout of TNS1. We found no differentially observed effects of TNS1 knockout on mouse health, breeding capacity, or vital organ histopathology. In contrast, RNA sequencing analysis identified 171 differentially expressed genes with Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis demonstrating differential expression in osteoclast differentiation and a number of pathways involved in host immune response. Furthermore, STRING pathway analysis showed differential regulation of genes involved in B-cell and myeloid-related signaling pathways, a number of which were validated by reverse transcription-quantitative polymerase chain reaction (RT qPCR). These findings were corroborated by impaired function of TNS1 siRNA monocytes and increased detection of lymphocytes in the bronchoalveolar lavage within days following TNS1 knockout. This study provides a novel understanding of the phenotypic and genotypic changes that occur following knockout of TNS1 that may lead to subsequent understanding of its role in disease.

overall_design: RNA sequencing profiling of TNS1 expressing (TNS1+/+) and inducible, conditional deletion TNS1 knockout mice (TNS1-/-) whole lung lysates. All animals were given tamoxifen for 7 days, and the left lung from each animal was flash frozen, lysated and processed for RNA sequencing 14 days after the completion of tamoxifen treatment.

first: Ksenija

last: Bernau

first: Kelsey

last: Holbert

first: Ivy S.

last: McDermott

first: Babita

last: Rahar

first: Kade W.

last: Coulter

first: Madalyn A.

last: Osterhaus

first: Thomas J.

last: Harr

first: Carson

last: Gehl

first: Angie T.

last: Oler

first: Christopher

last: Huffman

first: Beth

last: Gray

first: Trevor S.

last: Langel

first: Kenneth M.

last: Chan

first: Amir

last: Forati

first: Sandra

last: Splinter BonDurant

first: Mark

last: Berres

first: Kathy J.

last: Krentz

first: C. Dustin

last: Rubinstein

first: Andres F.

last: Mejia


title: Carbohydrate fatty acid monosulfateester enhances the immunogenicity ofinfluenza antigens via TLR4/2-dependent mechanisms

status: Public on Feb 13 2026

city: Palakkad

first: Jagadeesh

last: Bayry

state: Kerela

address: IIT Palakkad

institute: IIT palakkad

summary: Adjuvants are critical for optimizing the efficacy of influenza subunit vaccines, yet currently approved formulations fail to elicit durable and broad protection. Here, we dissect the immunostimulatory mechanisms of a synthetic carbohydrate fatty acid monosulphate ester (CMS), a key immunogenic component of a squalane-in-water emulsion adjuvant currently in phase I clinical trials. Using human peripheral blood mononuclear cell (PBMC)-based assays, we show that CMS markedly enhances antigen‑specific T cell responses to influenza hemagglutinin (HA) peptides. While recombinant H7N9HA alone poorly activated antigen‑presenting cells, co‑formulation with CMS induced robust dendritic cell (DC) activation, cytokine secretion, and a balanced polyfunctional effector and regulatory T cell response. Bulk RNA sequencing of CMS‑stimulated DC revealed strong induction of toll‑like receptor (TLR)-driven innate inflammatory pathways. Furthermore, functional blockade experiments confirmed that CMS adjuvanticity depends on TLR4 and TLR2 receptors. These results define the molecular basis of CMS‑driven immune activation and highlight this adjuvant as a promising platform for next‑generation influenza vaccines targeting emerging pandemic strains.

overall_design:
We treated  dendritic cells derived from the peripheral blood monocytes of healthy donors with CMS (n=3 donors). Untreated dendritic cells maintained in cell culture medium were used as control  (n=3)

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first: Sruthi

middle: V

last: Retnakumar

first: Suraj

middle: C

last: Singh


title: LncRNA NAS1 deficiency drives cisplatin resistance in non-small cell lung cancer

city: nanjing

first: Zhou

last: Jun

state: jiangsu

address: longmiandadao

department: College of life science and technology

country: China

institute: China Pharmaceutical University

summary: Cisplatin resistance remains a major obstacle in non-small cell lung cancer (NSCLC) treatment. Long non-coding RNAs (lncRNAs) have been implicated in chemotherapy resistance, yet their specific roles and mechanisms are not fully understood. This study reveals that low expression of lncRNA NAS1 drives cisplatin resistance via NR2F1-mediated TGFB1/NF-κB signaling in NSCLC.

overall_design: Total RNA-seq profiling of three distinct cisplatin-resistant NSCLC cell lines (H226/DDPr, H460/DDPr, PC9/DDPr) and their corresponding parental cells.

first: Xianrong

last: Lin

first: Wenjun

last: Tao


title: Repeat-rich RNA Clusters Repetitive Genomic Elements into Biomolecular Condensates for Heterochromatin Organization and Muscle Integrity

city: Suwon-si

first: Jinmi

last: Choi

state: Gyeonggi-do

address: Seoburo 2066, Jangan-gu

country: South Korea

institute: Sungkyunkwan University

summary: Biomolecular condensation is a pivotal mechanism in chromatin organization and nuclear compartmentalization. However, the molecular mechanism that drives heterochromatin organization and selectively partitions heterochromatin components in muscle cells remains unclear. Furthermore, its pathological implications remain unexplored. Here, we demonstrate that ChRO1, a muscle-specific RNA enriched with simple dinucleotide repeats, is associated with static heterochromatin foci containing similar repetitive elements in C2C12 mouse muscle cells. Through its CU-repeat-rich region, ChRO1 promotes heterochromatin clustering and facilitates the selective partitioning of heterochromatin proteins, as shown in vitro and in cells. Consequently, chromatin interaction stablized at ChRO1-bound regions, reinforcing TAD boundaries and promoting inactive chromatin states. The enhanced intra- and interchromosomal interactions secure the heterochromatinization of non-muscle genes, highlighting ChRO1’s role in establishing chromatin interaction hubs. Disruption of ChRO1 or perturbation of condensate organization induces chromocenter disintegration and muscle atrophic phenotypes, underscoring the importance of these processes in maintaining muscle integrity. Notably, ChRO1 mitigates chromocenter disintegration and atrophic phenotypes in chemically induced atrophy models, emphasizing its protective role. These findings reveal a novel repeat-rich RNA-based mechanism of repetitive DNA condensation that safeguards heterochromatin organization and muscle integrity, providing mechanistic insight and therapeutic implications for muscle-related disorders.

overall_design: HiChIP experiments performed with an anti-H3K9me3 antibody (Abcam, ab8898) in C2C12 WT and ChRO1 KO cells, differentiated for 4 days.

first: Eun-Jung

last: Cho


title: Microglia gene-expression after a transient ischemic attack (TIA)

city: München

first: Gemma

last: Llovera

address: Feodor-Lynen-Straße 17

country: Germany

institute: Institut für Schlaganfall- und Demenzforschung (ISD)

summary: Analysis of more than 700 genes using the Neuroinflammation panel (NS_Mm_NeuroInflam_v1.0) of Nanostring technologies from isolated microglial cells in naive and TIA animals revealed that they have an activated phenotype even 3d after TIA.

overall_design: In the study presented here, 3 animals per group and 65ng of microglial RNA per sample were used.


title: Human U2 snRNA BSL sequence mediates splicing efficiency driven by branchpoint sequence complementarity

city: Santa Cruz

first: Melissa

last: Jurica

state: CA

address: 1156 High Street

institute: University of California Santa Cruz

summary: To investigate the global effects of perturbing U2 snRNA sequence on splicing and gene expression, we carried out transcriptomic analysis of HEK293T cell lines stably expressing U2 snRNA mutants C28U in the branchpoint interacting stem loop or T34A/ A35C/G36T to create an orthogonal branch point recognition sequence. With both mutants, the expression of many genes is generally repressed, potentially by nonsense mediated decay (NMD) arising from a global decrease in splicing efficiency. However, we also see upregulation of genes important for pre-mRNA processing, translation and protein folding. In several cases, the upregulation of certain genes can be linked to a shift in alternative splicing that favors the productive isoform relative to an NMD-targeted isoform.

overall_design: Short-read RNA-seq of HEK293T cell lines engineered for stable expression of empty vector (783) or RNU2-1 expression locus harboring either C28T (U2-C28U), TAG36ACT (U2-UCA) using lentiviral integration


title: TGF-β and IL-4+IL-13 induce neuroplasticity in an in vitro model of hPSC-derived sensory neurons

city: Groningen

first: Reinoud

last: Gosens

address: Antonius Deusinglaan 1

department: Molecular Pharmacology

country: Netherlands

institute: University of Groningen

summary: Asthma is a chronic inflammatory disease of the airways characterized by airway hyperresponsiveness. Recent studies using mouse models, bronchial biopsies of asthma patients, and lung tissue of patients with fatal asthma have implicated neuroplasticity as a pathological feature of severe asthma, possibly contributing to airway hyperresponsiveness. Currently, we lack the models to study the mechanisms behind sensory neuroplasticity in vitro. Here, we describe the differentiation of sensory neurons from human pluripotent stem cells. Generation of sensory neurons was validated using immunofluorescence, flow cytometry and RNA-sequencing, as well as functional responsiveness to capsaicin using calcium imaging. We exposed these hPSC-derived sensory neurons to TGF-β or Th2-cytokines IL-4 together with IL-13, both of which have important roles in asthmatic airway remodelling. Both treatments induced neuroplasticity-related changes such as increased network density and neuronal sensitivity in the sensory neurons, albeit TGF-β more strongly than IL-4+IL-13. Our results show that hPSC-derived sensory neurons can be generated robustly and reproducibly and provide a good model to investigate the mechanisms behind neuroplasticity. Furthermore, our findings support a role for the asthmatic airway microenvironment, most notably TGF-β, in the development of neuroplasticity.

overall_design: H9WAO9 human Pluripotent Stem cell (hPSC)-derived sensory neurons were used to study neuroplasticity development. Mature hPSC-derived sensory neurons exposed to TGF-β or IL-4+IL-13 for 5-days were subjected to RNA-sequencing.

first: Carli

middle: S

last: Koster

first: Sophie

middle: T

last: Bos

first: Chiara

last: Lavitola

first: Mihaly

last: Balogh

first: Barbro

middle: N

last: Melgert


title: Caspases 3 and 7 restrict intestinal inflammation by regulating stem cell function and gsdmd-mediated pyroptosis

city: Ghent

first: Bruno

last: Verstraeten

state: Oost-Vlaanderen

address: Technologiepark 71

country: Belgium

institute: Ghent University

summary: Aberrant intestinal epithelial cell (IEC) death is a hallmark of inflammatory bowel disease (IBD), observed in patient samples and animal models of colitis. While multiple cell death pathways contribute to disease pathogenesis, the dominant modalities and their regulatory mechanisms in IBD remain poorly defined. In this study, we demonstrate that mice with intestinal epithelial cell-specific deletion of caspase-3 and -7 (Casp3/7 Tg) exhibit exacerbated colitis, increased mortality, and impaired epithelial regeneration, phenotypes not observed in other cell death-related knockout models. These findings highlight a previously unrecognized protective role of caspase-3/7 in controlling inflammation and tissue regeneration following intestinal injury. Mechanistically, caspase-3/7 deficiency negatively affects intestinal stem cell proliferation and promotes GSDMD-dependent pyroptosis, compromising barrier integrity and return to steady state conditions. Together, our results identify caspase-3/7 as key regulators of epithelial integrity and inflammation and suggest their modulation as a promising therapeutic strategy in IBD and colorectal cancer.

overall_design: Two sets of mRNA seq samples: The first set of samples are mural colon tissue samples from 4 conditions (0 or 8 days post DSS treatment of Casp3/7 transgenic and wild type mice). The second set of  samples were derived from mural intestinal epithelial cells of Casp3/7 transgenic and wild type mice. The samples were taken 0 or 3 days post DSS treatment.

first: Xie

last: Wei

first: Verstraeten

last: Bruno

first: Vandenabeele

last: Peter


title: Trimetazidine delays autoimmune diabetes in mice by transiently suppressing CD8⁺ T-cell fatty-acid oxidation

city: Vienna

first: Manuel

last: Salzmann

address: Lazarettgasse 14

department: Department of Medicine II, Division of Cardiology

country: Austria

institute: Medical University of Vienna

summary: Type 1 Diabetes Mellitus (T1D) is an organ specific autoimmune disease, which is characterized by persistent hyperglycemia due to immune-mediated destruction of pancreatic islet β cells. Shifting immune cell metabolism is an emerging therapeutic concept. Therefore, we tested whether the fatty acid oxidation (FAO) inhibitor trimetazidine (TMZ) can restrain autoreactive immunity and delay T1D in a non-obese diabetic mouse model. Of note, TMZ is one of only three approved drugs directly targeting cellular metabolism. TMZ acutely increased mitochondrial membrane potential, suppressed FAO and curtailed activation and proliferation of human CD8⁺ T cells. In dysglycemic NOD mice, a clinically approved dose of TMZ delayed progression to T1D, lowered mean glycaemia and reduced islet CD4⁺/CD8⁺ infiltration. scRNA-seq revealed depletion of FAO-high, stress-responsive secretory cells and mitochondrially active stromal cells, indicating improved pancreatic health. However, prolonged exposure elicited compensatory up-regulation of carnitine-palmitoyl-transferase-1A in CD8⁺ subsets, normalized T-cell infiltration and nullified protection. We conclude that TMZ delivers a dampening of initial T-cell pressure and pancreatic stress. Adaptive upregulation of FAO within cells counteracted observed benefits thereby only transiently delaying disease onset. Our work demonstrates that drugs targeting cellular metabolism needs to retain sufficient potency to not be outpaced by immune cells upscaling metabolic pathways.

overall_design:
Pancreatic tissue was collected from five control mice and five TMZ-treated mice after one week of treatment, initiated when fasting blood glucose reached 150-180 mg/dL.
Pancreatic heads were dissected, snap-frozen, and stored in liquid nitrogen until processing. Tissue dissociation and fixation were performed using the Chromium Next GEM Single Cell Fixed RNA Sample Preparation Kit (PN-1000414, 10x Genomics, Pleasanton, CA, USA). Nuclei and single cells were isolated following the protocol “Tissue Fixation & Dissociation for Chromium Fixed RNA Profiling” (CG000553). Samples from each group (control and TMZ-treated) were pooled and assigned one barcode per group for multiplexed analysis.
Library preparation was performed using the “Chromium Fixed RNA Profiling for Multiplexed Samples” protocol (CG000527, protocol version F), with the Chromium Fixed RNA Profiling Kit - Mouse Transcriptome (4 reactions × 4 barcodes, PN-1000496), Hybridization & Library Kit (PN-1000415), and the Chromium Next GEM Chip Q Single Cell Kit (16 reactions, PN-1000422), all from 10x Genomics. Sequencing was performed on an Illumina NextSeq 2000 instrument using a NextSeq 2000 P4 flow cell (100 cycles, PN-20100994, Lot #20879630, Illumina, San Diego, CA, USA).
Sequencing data were demultiplexed and aligned using Cell Ranger software version 8.0.1 (10x Genomics), with the Mus musculus mm10 (Ensembl 98). Cell Ranger Loupe Browser output files were imported into R (version 4.4.1) for downstream processing. Nuclei with >45% mitochondrial transcript content, nFeature_RNA ≤ 500, or nCount_RNA ≥ 500 were excluded from analysis. Filtered data were normalized, log-transformed, and the resulting matrix was used for all downstream analyses.
Data integration was performed using RPCA-based batch correction implemented in Seurat v5 (https://satijalab.org/seurat/articles/seurat5_integration). Principal component analysis was conducted using the first 20 components, and clustering was performed with a resolution of 0.1. The final annotated dataset was exported as a cloupe file and reloaded into the Loupe Browser (10x Genomics) for visualization and manual inspection of clusters.
Pseudo-bulk differential expression analysis was performed using the DElegate package (https://github.com/cancerbits/DElegate).

first: Laura

last: Boccuni

first: Philipp

last: Hohensinner


title: Transcriptome changes in C57BL/6 mice after ischemia/reperfusion injury

city: Zhengzhou City

first: Yang

last: Bai

state: Henan Province

address: 1 Jianshe Dong Road, Erqi District, Zhengzhou City, Henan Pr

institute: Zhengzhou University

summary: Renal warm ischemia-reperfusion (I/R) injury drives acute kidney injury and transplant dys-function through endoplasmic reticulum (ER) stress. Although Activating Transcription Factor 6 (ATF6) modulates ER stress resolution via the unfolded protein response, its functional role in re-nal IRI remains undefined. Using murine model of warm renal I/R and hypoxia-reoxygenation (H/R)-treated HUVECs/HK-2 cells, we systematically investigated the expression of ATF6 and molecular mechanisms through RNA-seq, ChIP, and dual-luciferase assays. IRI significantly up-regulated the expression of ATF6 in renal tissues, especially in proximal tubule epithelial cells. Functionally, ATF6 activation reduced Cr, BUN, and inflammatory cytokines, whereas genet-ic/pharmacological suppression aggravated renal tubular damage. Mechanistic studies revealed ATF6 transcriptionally represses FHL2 by direct promoter binding. The interaction between FHL2 and TRAF6 promoted the TRAF6/NF-κB signaling pathway, and the phosphorylation levels of p65 and IκBα were increased. ATF6 overexpression effectively counteracted FHL2-mediated NF-κB hyperactivation, establishing a protective axis where ATF6 mitigates inflammation via FHL2 sup-pression. This study identifies ATF6 as a renoprotective factor that suppresses FHL2 to inhibit TRAF6/NF-κB inflammation during IRI. The ATF6/FHL2/NF-κB axis provides mechanistic in-sights and therapeutic targets for ischemic renal injury and transplant complications.

overall_design: We randomly assigned C57BL/6N mice to sham-operated (Sham, n=6) or I/R (n=6) groups. The I/R group received pentobarbital sodium anesthesia followed by renal pedicle occlusion. After 60 minutes of ischemia, we restored blood flow for 6h reperfusion before euthanasia and sample collection

first: Xuan

last: Wu


title: Postmitotic transcription and 3D regulation show locus-specific and differentiation-specific sensitivity to cohesin depletion [ChIP-exo]

status: Public on Feb 16 2026

city: New York

first: UkJin

last: Lee

state: NY

address: 413 E 69th St

department: Sanford I. Weill Department of Medicine

institute: Weill Cornell Medicine

summary: Structural loops are known to collapse in the absence of cohesin, whereas regulatory loops largely persist with only minor transcriptional changes, leaving unresolved questions about cohesin’s role in establishing regulatory interactions during cell state transitions. To investigate this, we degraded RAD21, a core cohesin subunit, in mouse embryonic stem cells (ESCs) transitioning from mitosis to G1 under self-renewal or differentiation conditions. We performed ChIP-exo for H3K4me3 to map marked regions and for CTCF and RAD21 to map binding regions in ESCs.

overall_design: Characterization of H3K4me3-marked regions and CTCF and RAD21 binding regions with ChIP-exo in ESCs.

first: Effie

last: Apostolou

first: Alejandra

last: Laguillo-Diego


title: SLC33A1 exports oxidized glutathione to maintain endoplasmic reticulum redox homeostasis [KPK_Slc33a1_KO_TUNC]

status: Public on Feb 12 2026

first: Shanshan

last: Liu

address: 430 East 63rd Street,

institute: The Rockefeller University

summary: Endoplasmic reticulum stress and redox homeostasis influence protein folding and unfolded protein response signaling. To examine transcriptional responses associated with Slc33a1 loss and complementation, we performed RNA sequencing of KPK cells with Slc33a1 knockout and cells complemented with either empty vector or cDNA constructs. Cells were treated with either DMSO or tunicamycin to induce ER stress, and total RNA was collected for sequencing. This dataset provides transcriptome profiles that enable comparison of gene expression changes across genotypes and treatment conditions.

overall_design: KPK cells with Slc33a1 knockout and complemented lines were cultured and treated with either DMSO or tunicamycin. Total RNA was extracted and libraries were prepared for RNA sequencing. Biological replicates were generated for each condition to compare transcriptional responses to ER stress in different genetic backgrounds.

first: Alon

last: Millet

first: Kivanc

last: Birsoy


title: Host-pathogen relationships in aoudad (Ammotragus lervia) and bighorn sheep (Ovis canadensis) with respiratory disease agents

city: Canyon

first: Matthew

last: Scott

state: TX

address: 3201 Russell Long Blvd

institute: Texas A&M University

summary: To evaluate transmission propensity of Mycoplasma ovipneumoniae and leukotoxigenic Pasteurellaceae from aoudad and bighorn sheep, we assessed the transcriptomic signals from bulk lung and tracheobronchial lymph node samples of aoudad and bighorn sheep exposed to Mycoplasma ovipneumoniae in either the presence or absence of leukotoxigenc Pasteurellaceae. Our aim was to determine gene expression patterns related to respiratory pathogenic exposure within nonindigenous aoudad and native bighorn sheep to provide crucial information related to respiratory pathogenesis and identify potentially predictive patterns in individuals as it relates to interspecific contact and mortality events.

sample_organism:
Ammotragus lervia
Ovis canadensis

platform_organism:
Ammotragus lervia
Ovis canadensis

overall_design: RNA-Seq profiling of frozen lung (combined cranioventral and caudodorsal) and tracheobronchial lymph node samples collected at time of mortality.

middle: A

first: Logan

last: Thomas

first: Robert

last: Valeris-Chacin

first: Walter

last: Cook


title: Estrogen Receptor α Protects Against Obesity-Induced Metabolic Dysfunction by Regulating VAT Tregs (oVAT)

city: Atlanta

first: Gregory

middle: K

last: Tharp

state: GA

address: 954 Gatewood Dr

department: Developmental and Cognitive Neuroscience

institute: Yerkes National Primate Research Center

summary: Estrogens are important for metabolic health. Individuals with low levels of circulating estrogens, including men and postmenopausal women, exhibit an elevated risk for developing obesity-associated metabolic syndromes. Chronic low-grade inflammation in the visceral adipose tissue (VAT) is a major contributor to metabolic dysfunction during obesity. Regulatory T cells (Tregs) in the VAT limit tissue inflammation and protect against obesity-associated metabolic disease. In this study, we identify opposing roles of estrogen receptor α (ERα) in regulating VAT Tregs in female mice under steady-state and obese conditions. At steady state, ERα restrained the age-dependent clonal expansion of specific VAT Treg subsets expressing the IL-33 receptor ST2. However, during obesity, ERα-deficiency predisposed females to the loss of ST2+ VAT Tregs, exacerbating VAT inflammation and insulin resistance. These findings indicate that ERα signaling protects against obesity-induced metabolic diseases by preserving metabolically protective ST2+ VAT Treg subsets, and the loss of this protection may contribute to the heightened metabolic risk in estrogen-deficient individuals.

overall_design: ovarian visceral adipose tissue (oVAT) was isolated from 27-week-old Era+/+ or Era-/- female mice fed an NCD or HFD for 17 weeks. Stromal vascular fractions from each group were stained with antibodies targeting appropriate surface markers along with corresponding TotalSeq™ hashtag antibodies for downstream demultiplexing. CD4+ CD25hi Tregs from all groups were sort-purified into one tube containing RPMI 1640 with 10% FBS for 10X genomics 5' single cell RNA/TCR sequencing analysis.

first: Cody

last: Elkins

first: Jianliang

last: Zhang

first: Chengyu

last: Ye

first: Samara

last: Moll

first: M

last: Weitzmann

first: Chaoran

last: Li


title: Transcriptomic Characterization of Liver Tissue Changes in Human and Mice with Acute-on-Chronic Liver Failure and Liver Cirrhosis/Fibrosis

city: Shanghai

first: Yun

last: Song

address: 1111 Xianxia Road, Shanghai 200336, China

institute: shanghai jiao tong university

summary: This study aims to investigate gene expression differences at the transcriptional level in liver tissue from acute-on-chronic liver failure (ACLF) compared to liver cirrhosis (CLD, human) or Fibrosis (mice) and healthy control groups.For human samples, they were categorized into ACLF, CLD, and healthy control (HC) groups. For mouse samples, they were divided into ACLF, Fibrosis, and HC groups.

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: Regarding human samples, liver tissue was collected. For mouse samples, fibrosis was induced by intraperitoneal injection of 10% CCl4 in olive oil at a dose of 0.2 mL/kg, twice a week for 8 weeks. Subsequently, ACLF model mice were established by inducing acute liver injury in the fibrosis mice with an intraperitoneal injection of CCl4 at 0.4 mL/kg, followed by an intraperitoneal injection of 100 μL Klebsiella pneumoniae bacterial solution 24 hours after the acute injury.

first: Panyu

last: Chen

first: Xiao

last: Lin

first: Zhaokai

last: Zeng

first: Wenxi

last: Su

first: Yunyun

last: Ren

first: Chen

last: Wang

first: Kang

last: He

first: Min

last: Shi

first: Yugang


title: Dbf4-Dependent Kinase Finetunes INO80 Function at Chromosome Replication Origins

city: Martinsried

first: Tobias

last: Straub

address: Großhadener Str. 9

department: Biomedical Center, Bioinformatics

institute: LMU Munich

summary: The highly conserved Dbf4-Dependent Kinase (DDK) plays a pivotal role in the nucleus during S phase, where it directly phosphorylates the replicative helicase, the minichromosome maintenance (MCM) complex. This leads to the initiation of chromosome replication. However, aside from the MCM complex, few other targets have been identified to date, leaving DDK an understudied kinase. Here, we describe a two-pronged mass spectrometry-based approach and define the nuclear DDK-dependent phosphoproteome, which consists of approximately 400 phosphorylation events. Within this network, we found that DDK directly phosphorylates the Arp8 subunit of the multi-subunit chromatin remodeler complex INO80. Arp8 phosphorylation stabilises INO80's intramolecular complex integrity, which finetunes its nucleosome spacing activity at replication origins. This adjustment of origin chromatin architecture stimulates replication and is important for the response to replication stress. Our results represent a significant advance in our understanding of the molecular mechanisms underlying the regulation of replication origins.

overall_design: It was tested whether DDK phosphorylation of INO80 might influence the transcriptome genome-wide. Gene expression profiling analysis was performed using RNAseq data obtained from isogenic ARP8 wild-type and arp-8-P (serine 65 to alanine, serine 233 to alanine) strains. Three biological replicates were performed. Another experiment analysed transcription in synchronised cells. Cells were arrested with alpha factor and harvested in G1 and early S phase.

first: Priyanka

last: Bansal

first: Shibojyoti

last: Lahiri

first: Chandni

last: Kumar

first: Lorenzo

last: Galanti

first: Jessica

last: Furtmeier

first: Erika

last: Chacin

first: Lorenz

last: Spechthauser

first: Garp

last: Linder

first: Juan

last: de Dios Barba Tena

first: María

last: Ortíz-Bazán

first: Marisa

last: Müller

first: Petra

last: Vizjak

first: Felix

last: Mueller-Planitz

first: Johannes

last: Stigler

first: Andrés

last: Aguilera

first: Belen

last: Gómez-González

first: Boris

last: Pfander

first: Philipp

last: Korber

first: Axel

last: Imhof

first: Christoph

middle: F

last: Kurat


title: Syntaxin 4 Enrichment in β-Cells Prevents Conversion to Autoimmune Diabetes in Non-Obese Diabetic (NOD) Mice

city: Duarte

first: Debbie

middle: C.

last: Thurmond

state: California

address: 1500 E Duarte Rd

institute: City of Hope

summary: Syntaxin 4 (STX4), a plasma membrane–localized SNARE protein, regulates human islet β-cell insulin secretion and preservation of β-cell mass. We found that human type 1 diabetes (T1D) and NOD mouse islets show reduced β-cell STX4 expression, consistent with decreased STX4 expression, as a potential driver of T1D phenotypes. To test this hypothesis, we generated inducible β-cell–specific STX4-expressing NOD mice (NOD-iβSTX4). Of NOD-iβSTX4 mice, 73% had sustained normoglycemia vs. <20% of control NOD (NOD-Ctrl) mice by 25 weeks of age. At 12 weeks of age, before diabetes conversion, NOD-iβSTX4 mice demonstrated superior whole-body glucose tolerance and β-cell glucose responsiveness than NOD-Ctrl mice. Higher β-cell mass and reduced β-cell apoptosis were also detected in NOD-iβSTX4 pancreata compared with pancreata of NOD-Ctrl mice. Single-cell RNA sequencing revealed that islets from NOD-iβSTX4 had markedly reduced interferon-γ signaling and tumor necrosis factor-α signaling via nuclear factor-κB in islet β-cells, including reduced expression of the chemokine CCL5; CD4+ regulatory T cells were also enriched in NOD-iβSTX4 islets. These results provide a deeper mechanistic understanding of STX4 function in β-cell protection and warrant further investigation of STX4 enrichment as a strategy to reverse or prevent T1D in humans or protect β-cell grafts.

overall_design: Islets were isolated from female NOD-Ctrl or NOD-iβSTX4 transgenic mice and dispersed into single cells with TrypLE (Invitrogen, Carlsbad, CA). Cell numbers and viability were measured using a TC20 Automated Cell Counter (Bio-Rad); only samples showing at least 70% viability were used. Cells were then loaded onto a chromium controller (10x Genomics, Pleasanton, CA) to generate single-cell Gel Bead-In Emulsions (GEMs) captured in droplets at a targeted cell recovery of 3,000 cells. GEM reverse transcriptions were performed in a Veriti 96-Well Thermal Cycler (Thermo Fisher Scientific). The Chromium Single Cell 3' Reagent Kit V2 (10x Genomics) was used to process samples into single-cell RNA sequencing (scRNA-seq) libraries according to the manufacturer’s protocol. The libraries were sequenced with the paired-end setting of 28 cycles of read 1, 101 cycles of read 2, and 8 cycles of the index read on the Illumina NovaSeq 6000 platform at the Translational Genomics Research Institute (TGen) (Phoenix, AZ).

first: Eunjin

last: Oh

middle: M

last: McCown

first: Miwon

last: Ahn

first: Pablo

last: Garcia

first: Sergio

last: Branciamore

first: Shanshan

last: Tang

first: De-Fu

last: Zeng

first: Bart

middle: O

last: Roep


title: CBP-IDRs regulate acetylation and gene expression

city: Sheffield

first: Daniel

middle: Arun

last: Bose

state: South Yorkshire

address: University of Sheffield, Firth Court, Western Bank

department: Biosciences

country: United Kingdom

institute: The University of Sheffield

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

overall_design: Refer to individual Series


title: Estrogen Receptor α Protects Against Obesity-Induced Metabolic Dysfunction by Regulating VAT Tregs

first: Gregory

last: Tharp

overall_design: Spleen and/or ovarian visceral adipose tissue (oVAT) was isolated from 27-week-old Era+/+ female mice fed an NCD or Era-/- female mice fed an NCD or HFD for 17 weeks. Stromal vascular fractions from each group were stained with antibodies targeting appropriate surface markers along with corresponding TotalSeq™ hashtag antibodies for downstream demultiplexing. CD4+ CD25hi Tregs from all groups were sort-purified into one tube containing RPMI 1640 with 10% FBS for 10X genomics 5' single cell RNA/TCR sequencing analysis.

first: Cody

last: Elkins

first: Chengyu

last: Ye

first: Samara

last: Moll

first: Jianliang

last: Zhang

first: M. Neale

last: Weitzmann

first: Chaoran

last: Li


title: Sex-associated changes to synovial macrophages in the aging joint

city: Chicago

first: Deborah

middle: R

last: Winter

state: IL

address: 240 E. Huron Street, M300

institute: Northwestern University

summary: Single-cell analysis of aging synovial macrophage heterogeneity between sexes

overall_design: CITE-seq on CD45+CD11b+Ly6g-SiglecF-Cd64+ cells isolated from hind joints of young and old, male and female mice.


title: A simple liquid 3D cell culture paradigm models oxidative mitochondrial metabolism of epithelial breast cancer cells with relevance for lung metastases

city: Frederick

first: Yongmei

last: Zhao

state: MD

address: Post Office Box B

department: Advanced Biomedical Computational Science

institute: Frederick National Labroatory for Cancer Research

summary: Three-dimensional (3D) cell culture systems have emerged as powerful tools to model tumor biology ex vivo. However, the diverse array of 3D culture methods available presents challenges in selecting the most appropriate model for specific research questions. This study provides a comparative analysis of breast cancer cells (SUM149, IBC-3, MDA-MB-468) in the mammosphere culture (SphC) model or an “emboli” culture (EmC) model, which enrich for cancer stem cells and epithelial features, respectively. The EmC model, designed originally for inflammatory breast cancer, is characterized by media viscosity and mechanical rocking of the culture vessel. Notably, cells in EmC showed a distinct and durable reduction in cell proliferation while demonstrating increased capacity to establish experimental lung metastases. Quantitative analysis of electron microscopy images suggested that cells in EmC acquire nuclear and mitochondrial features that resemble those of tumor tissue. Proteomics, single-cell transcriptomics, and metabolic flux analyses showed that cells in EmC and SphC favor mitochondrial oxidative metabolism (OXPHOS) and glycolysis, respectively. EmC rendered cells hypersensitive to OXPHOS inhibition, yet more resistant to oxidative stress. Several genes associated with lung metastasis, including ID1, were specifically enriched in EmC. Given the increasingly recognized role of OXPHOS in cancer cell survival during dissemination and as established metastases, we propose that the EmC paradigm is a suitable ex vivo model to study signaling pathways relevant for tumor tissue and to assess drug sensitivities and resistance mechanisms of metastatic breast cancer cells ex vivo

overall_design: SUM149 and IBC-3 cells were cultured in 2D, "emboli" culture (EmC) or mammosphere culture (SphC) for 3 days.

first: Balamurugan

last: Kuppusamy

first: Esta

last: Sterneck


title: Expression data from Knockdown of SKA2 in SNU638 cell line

status: Public on Feb 11 2026

city: Shenzhen

first: Hong

middle: Lei

last: Chen

state: Guangdong

address: Room 3025, Shen Nan Middle Road, Futian District

department: Gastrointestinal Endoscopy Center

institute: The Eighth Affiliated Hospital of Sun Yat-sen University

summary: Gastric cancer (GC) has a rapid metastatic rate and is associated with high mortality worldwide. During tumorigenesis, the oncogenic genes mutation or expression, following specific sets of genes are up-regulated or down-regulated. Some of them, for example, control metabolism reprogramming to promote tumor growth and malignant progression. We used microarrays to detail the global programme of gene expression regulated by SKA2, which is overexpressed in gastric cancer.

overall_design: RNA-seq was carried out on the BGISEQ-500 platform. We sought to obtain gene expression profiles regulated by SKA2 in gastric cancer cell. SNU638 was infected with packaged lentivirus supernatant and selected resistant clones in stably expressing cell lines by puromycin.

first: peng

last: zhang

first: Jianfeng

last: Zhong

first: Depei

last: Jiang

first: Lekun

last: Fang

first: Huizhen

last: Xiong

first: Honglei


title: LMO1 expression in neuroblastoma cells reprograms tumor-associated macrophages to promote metastasis.

city: Rochester

first: Cheng

state: MN

address: 200 1st street SW

institute: Mayo Clinic

summary: Our earlier study has showed that the transcriptional coactivator LMO1 synergizes with the MYCN oncogene to enhance NB tumorigenesis and metastasis. To better understand how these two oncogenes cooperate during NB development, we performed single-cell RNA sequencing analysis on primary tumors from transgenic zebrafish with overexpression of MYCN, either alone or in combination with LMO1. Interestingly, we found significantly enriched signaling pathways involved in biogenesis and metabolism in NB cells with overexpression of LMO1 and MYCN. In addition, the macrophage populations from the two tumor types were distinctly clustered.

overall_design: Primary neuroblastoma tumors from MYCN (n = 2) and MYCN;LMO1 (n = 3) zebrafish lines were isolated, dissociated and submitted individually for a single-cell RNA-sequencing. cDNA libraries from single cells were prepared using the SMART-seq strategy and subjected to Illumina Hi-Seq sequencing at the Harvard Medical School Biopolymers Facility. A total of 16,630 cells were sequenced, and 9,082 high-quality transcriptomes were obtained after quality control and filtering from the 5 tumor samples.

first: Ke-En

last: Tan

first: Zuag

middle: P

last: Her

first: Kok

last: Yeo

first: Taylor

last: Weiskittel

first: Cassie

last: Howe

first: Shyang

middle: H

first: Thomas

middle: E

last: Rubino Jr

first: Hu

first: Shizhen

last: Zhu


title: SLC33A1 exports oxidized glutathione to maintain endoplasmic reticulum redox homeostasis [ERIP_RNASeq]

first: Shanshan

last: Liu

summary: The endoplasmic reticulum (ER) is the primary site of synthesis of secretory and membrane proteins, suggesting that specific mRNAs may be enriched at the ER surface. To characterize ER-associated transcripts, ER fractions were isolated using ER immunoprecipitation (ER-IP) and RNA was extracted from ER-bound material and whole-cell lysates. RNA sequencing was performed to compare transcript composition between ER-associated and total cellular RNA. ER-IP RNA sequencing revealed enrichment of transcripts encoding proteins localized to the plasma membrane, ER, Golgi apparatus, lysosome, and extracellular space. This dataset provides transcriptomic profiling of ER-associated RNA and corresponding whole-cell controls.

overall_design: ER-associated RNA was isolated by ER immunoprecipitation in the presence of RNase inhibitor. RNA was extracted from ER-IP material and from whole-cell lysates collected prior to ER purification. Libraries were prepared and sequenced to compare ER-associated transcripts with total cellular RNA. Biological replicates were analyzed for each condition. Sequencing reads were pseudoaligned using Salmon and differential enrichment was analyzed using limma-voom.

first: Alon

last: Millet

first: Kivanc

last: Birsoy


title: Bulk RNA-seq datasets supporting analysis of the MYC–USP10–SOX4 pathway in thymocytes and T-ALL

city: Changsha

first: Mengdi

last: Zhang

state: Hunan

address: 139 Middle Renmin Road, Furong District

department: National Clinical Research Center for Metabolic Diseases, Metabolic Syndrome Research Center, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology

institute: The Second Xiangya Hospital of Central South University

summary: This study presents bulk RNA-seq datasets generated from thymocytes of C57BL/6J mice to elucidate the transcriptional impact of thymus-specific loss of the deubiquitinase USP10. Total RNA was isolated from age-matched wild-type (WT) and USP10 conditional-knockout (USP10-cKO) thymus tissues, poly(A)+ fractions were enriched, and paired-end 150 bp libraries were sequenced on an Illumina NovaSeq 6000 platform. The resulting expression profiles allow direct comparison of global gene-expression programs between normal thymocyte development and USP10-deficient conditions, providing a resource for identifying USP10-regulated pathways, discerning stage-specific transcriptional alterations, and advancing our understanding of how ubiquitin signaling modulates early T-cell differentiation.

overall_design: RNA-seq profiling of thymocytes from thymus-specific USP10-knockout and wild-type C57BL/6J mice

first: Bin

last: Zhao


title: The chromatin remodeling factor Arp9 modulates the drug-resistance of Aspergillus flavus

city: 福建省

first: mei

middle: dong

last: Ma

address: Shangxiadian Road, Jianxin Town, Cangshan District, Fuzhou City

institute: Fujian Agriculture and Forestry University

summary: Transcriptome analysis, combined with RT-qPCR validation and high-performance liquid chromatography (HPLC) assay, determined that the absence of Arp9 down-regulated the expression levels of genes Erg3 and Erg6 in the ergosterol synthesis pathway, resulted in reducing the amount of ergosterol synthesized, which rendered A. flavus more sensitive to AMB. This study further revealed that ΔArp9 strain resistance to VOR was modulated by up-regulating VOR's drug target Erg11A and the drug efflux pumps Mdr1 and AtrF.

overall_design: In order to study the gene expression differences between Arp9 and WT, we constructed an Arp9 gene deletion strain

first: Dongmei

first: Zhenhong

last: Zhuang


title: Transcriptional profile in  SK-LM_S1 cells mediated by abrogation of  MAPK7 and VCAN gene expression [Part 1]

city: Madrid

first: Yosra

last: Berrouayel

address: Arturo Duperier, 4

country: Spain

institute: Universidad Autónoma de Madrid

summary: The ERK5 signaling pathway has emerged as a novel key player in soft tissue sarcoma biology, mediating tumour growth and progression. Here we show how the expression of VCAN, a member of the chondroitin sulphate proteoglycan family, is modulated by the ERK5 pathway at the transcriptional level and mediates biological processes such as migration, adhesion, proliferation and tumourigenesis in vivo.  This conclusion is based on genetic (shRNA, overexpression) and pharmacological approaches using  the human soft tissue sarcoma  cell lline Sk-LM-S1 a. In particular, VCAN knockdown mimics ERK5 knockdown in vitro and in vivo, whereas VCAN overexpression restores the phenotypes observed after ERK5 knockdown. In addition, transcriptomic studies show that VCAN is a central mediator in the ERK5-associated transcriptional landscape, supporting its role in diverse biological processes. Taken together, these data support VCAN as a new key target in the ERK5 pathway.

overall_design: Following effective knockdown of VCAN and MAPK7 gene expression in SK-LM-S1 cells using specific shRNA, samples were collected and transcriptomic profile analyzed by RNA-seq.

last: Berrouayel Dahour

first: Francisco J

last: Cimas

first: Luis

last: del Peso

first: Ricardo

last: Sanchez-Prieto


title: RIPseq of AtMKIP1-YFP and AtBE3-YFP in Arabidopsis thaliana

city: Potsdam

first: Yang

last: Gao

state: Brandenburg

address: Am Mühlenberg 1

department: Organelle Biology, Biotechnology and Molecular Ecophysiology

institute: Max Planck Institute of Molecular Plant Physiology

summary: Chloroplast group IIA introns derive from bacterial ribozymes. Their splicing likely requires Maturase K (MatK), which has been largely inaccessible to functional analyses being itself a chloroplast intron-encoded protein. We show that MatK physically interacts with a conserved, essential plastid-localized homolog of starch branching enzymes (BEs), dubbed MATURASE K INTERACTING PROTEIN1 (MKIP1). We demonstrate that MKIP1 proteins have lost BE activity and acquired an insertion enabling direct interaction with the N-terminal region of MatK. Arabidopsis MKIP1 specifically co-precipitates all known intron targets of MatK. Induced MKIP1 silencing results in pale newly emerging leaves, in which the splicing of these intron targets is strongly reduced. Our data suggest that MKIP1 functionally diverged from canonical BEs to facilitate splicing in conjunction with MatK. We propose that the N-terminus of MatK, in turn, has evolved from an RNA-binding domain into a platform for protein interaction, helping its transition towards a general splicing factor.

overall_design: To identify RNA regions specifically associated with AtMKIP1 or its complex in vivo, we performed RNA co-immunoprecipitation (co-IP) followed by RNA sequencing (RIP-seq) on 10-days old Arabidopsis thaliana seedlings (Col-0 ecotype) stably expressing PUBQ10::AtMKIP1-YFP in the mkip1 mutant background. An Arabidopsis thaliana line stably expressing PUBQ10::AtBE3-YFP (in the wild-type background) served as control. The input RNA and immunoprecipitated RNA associated with either bait (AtMKIP1-YFP or AtBE3-YFP) in Arabidopsis seedlings were subjected to RNA sequencing. Three replicates, each consisting of ~10 g (fresh weight) of pooled 10-day old seedlings, were analyzed per line.

first: Yuanyuan

last: Liang

first: Reimo

last: Zoschke

first: Barbara

last: Pfister


title: Gene expression levels of Acidithiobacillus ferrooxidans with varying intracellular c-di-GMP concentrations during bioleaching

city: BeiJing

first: Xi

last: Han

address: 5 Yiheyuan Road, Haidian District, Beijing, China   Postal Code: 100871

institute: Peking University

summary: Bioleaching, a sustainable and environmentally friendly emerging technology, relies on Acidithiobacillus ferrooxidans as a model microorganism for extracting metals from ores. This study investigated how intracellular cyclic diguanylate (c-di-GMP) concentrations regulate biofilm composition and bioleaching performance in A. ferrooxidans. By constructing strains with varying c-di-GMP levels, it was found that moderate c-di-GMP concentrations enhance bioleaching efficiency by upregulating genes associated with extracellular electron transfer (e.g., omcB and cyc2) in biofilms, a mechanism linked to optimized iron oxidation pathways. In contrast, high c-di-GMP levels improve arsenic resistance by promoting exopolysaccharide (EPS) synthesis in biofilms, likely through activation of pel-like operons (e.g., pelD), which strengthen biofilm structural integrity under toxic conditions. These findings reveal a dual regulatory role of c-di-GMP: prioritizing leaching efficiency via electron transport in low-arsenic environments and enhancing stress resistance through EPS production in high-arsenic scenarios. This study provides a theoretical foundation for tailoring A. ferrooxidans to diverse industrial bioleaching environments, leveraging its metabolic versatility and biofilm adaptability. The integration of synthetic biology approaches (e.g., genetic engineering of c-di-GMP pathways) further highlights potential applications for optimizing bioleaching strains.

overall_design: Cell transcriptome data of Acidithiobacillus ferrooxidans strains with varying intracellular cyclic diguanylate (c-di-GMP) concentrations during bioleaching under arsenic stress.


title: Decaying and expanding Erk gradients process memory of skeletal size during zebrafish fin regeneration

city: Madison

first: Jianhong

last: Ou

state: Wisconsin

address: 330 N Orchard Street

institute: Morgridge Institute For Research

summary: Regeneration of amputated salamander limbs or fish fins restores pre-injury size, illustrating positional memory. Although appreciated for centuries, the identity of position-dependent cues and how they control tissue growth are not resolved. Here, we quantify Erk signaling events in populations of osteoblasts during zebrafish fin regeneration. We find osteoblast Erk activity depends on Fgf receptor signaling and organizes into millimeter-long gradients spanning the distal tip to the amputation site. Erk activity scales with amount of tissue amputated, predicts likelihood of osteoblast cycling, and predicts size of regenerated skeletal structures. Mathematical modeling suggests gradients are established by transient deposition of long-lived ligands that are transported by tissue growth. This is supported by the observed scaling of expression of the essential epidermal ligand fgf20a with extents of amputation. Our work provides evidence that localized, scaled expression of pro-regenerative ligands instructs long-range signaling and cycling to control size in regenerating appendages.

overall_design: To isolate RNA from the amputation plane, a region spanning one bone segment above and below the amputation plane was collected from fish at 0, 3.5, 7, 14, and 21 dpa. For each time point, tissue samples from 10 animals were pooled for each of 3 biological replicates. Bulk RNAseq libraries were prepared to identify gene expression profiles at the distal tip of regenerates.

first: Ashley

last: Rich

first: Ziqi

last: Lu

first: Alessandro

last: De Simone

first: Lucas

last: Garcia

first: Jacqueline

last: Janssen

first: Kazunori

last: Ando

first: Massimo

last: Vergassola

first: Kenneth D

last: Poss

first: Stefano

last: Di Talia


title: Single-cell RNA-Seq profiling to characterize mammary tumor infiltrated immune cells with iron supplement during anti-PD-1 immunotherapy

status: Public on Feb 10 2026

city: Indianapolis

first: Qingfei

last: Wang

state: IN

address: Walther Hall-R3 C243

department: Division of Hematology/Oncology, Department of Medicine

institute: Indiana University School of Medicine

summary: In previous study, we demonstrated that iron supplementation augmented the antitumor effect of PD-1 based immunotherapy in triple-negative breast cancer models. To gain a more profound understanding into whether and how iron plus PD-1 antibody combination influences tumor immune microenvironment to exert better therapeutic activity, in this study, we performed single cell RNA-sequencing with PIP-seq to profile and compare tumor infiltrated CD45+ cells derived from control, iron or PD-1 antibody alone, and combination treated E0771 tumors.

overall_design: Tumor infiltrated CD45+ cells derived from control, iron or PD-1 antibody alone, and combination treated E0771 tumors were flow sorted and analyzed by single cell RNA-sequencing using PIP-seq pipelines. Cells from three or four tumors of each treatment group were pooled for PIP-seq.

first: Mateusz

last: Opyrchal


title: Spatial transcriptomics data of the wild-type and App NL-G-F mouse posterior cortex

city: London

first: Samuel

middle: J

last: Barnes

address: Hammersmith Hospital Campus, Du Cane Road

institute: Imperial College London

summary: Our in vivo imaging data suggest that GABAergic microcircuitry is dysfunctional in the App NL-G-F mouse.   To determine the relative contribution of different GABAergic subclasses to abnormal synaptic processing,  we tested for cell-type-specific molecular processes associated with early-stage amyloidosis.   To do this, we used the CosMx (Nanostring/Bruker) spatial transcriptomic system to investigate   cellular changes in posterior cortical regions (visual and retrosplenial cortices) identified as expressing  dysregulated resting-state activity in 3-4 months and 6-8 months App NL-G-F mice. Our results suggest  that parvalbumin interneurons show some of the earliest transcriptomic changes in posterior cortical regions,   with dysregulated activity in App NL-G-F mice, which are linked to a downregulation of GABAergic synaptic transmission.   Both parvalbumin and somatostatin interneurons show the highest number of transcripts that covary with local plaque load,   which are associated with synaptic processes.

overall_design: CosMx technology [CosMx Mouse Neuroscience Panel (950-plex); Bruker/Nanostring, USA]   was applied to the posterior cortex and adjacent regions of AppNL-G-F mice and wild-type controls   at 3-4 months and 6-8 months of age. [Platform: GPL36279 NanoString CosMx SMI (Mus musculus)]

first: Leire

last: Melgosa-Ecenarro

first: Carola

middle: I

last: Radulescu

first: Nazanin

last: Doostdar

first: Anna

last: Mallach


title: Innate lymphoid cells in unaffected colon, colorectal cancer and peritoneal metastasis

city: Huddinge

first: Anne

last: Marchalot

address: Alfred Nobel Allé 8, Center for Infectious Medicine

country: Sweden

institute: Karolinska Institutet

summary: 10X Next GEM Single Cell 5’ Kit v2 scRNAseq of maximum 15 000 sorted CD127+ ILCs (CD45+, CD3-, CD19-, Lin- and CD127+), NK cells (CD45+, CD3-, CD19-, Lin-, CD94+/- and CD56+) and non-conventional (nc)ILCs (CD45+, CD3-, CD19-, Lin-, CD94+/-, CD56- and CD7+) per sample from 11 patients. Total of 4 paired healthy colon and colorectal cancer tumours, 2 paired healthy colon, colorectal cancer tumours and peritoneal metastasis and 5 unpaired peritoneal metastasis.

overall_design:
scRNA-seq profiling of ILC and NK cells from primary colorectal tumors, peritoneal metastasis and unafected colon

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

first: Jenny

last: Mjösberg


title: Prussian blue nanoparticles targeting multiple PANoptosome-mediated PANoptosis for myocardial ischemia-reperfusion injury therapy

city: shanghai

first: ling

middle: ling

last: xu

address: tianlin street

institute: shanghai jiaotong university

summary: The extensive crosstalk between pyroptosis, apoptosis, and necroptosis suggests that inhibiting one of them can lead to compensating for the other, thereby reducing therapeutic efficacy. Here, we identify Prussian blue (PB) nanoparticle as an effective PANoptosis inhibitor that binds to key proteins (RIPK1, ZBP1, and AIM2) to regulate multiple PANoptosomes, thereby comprehensively inhibiting pyroptosis, apoptosis, and necroptosis and blocking their crosstalk in myocardial ischemia-reperfusion injury (MIRI) therapy. This PANoptosis inhibitor significantly alleviated MIRI-induced cardiac functional impairment and adverse ventricular remodeling, promoted extracellular matrix repair and neovascularization, and prevented cardiomyocyte hypertrophy. Furthermore, it modulated mitochondrial metabolism and immune-inflammatory homeostasis, helping to block the crosstalk within PANoptosis. Specifically, single-nuclear transcriptome sequencing of human heart samples, molecular dynamics simulations, transcriptome sequencing analysis, medical imaging technology, and molecular biological methods comprehensively elucidated the role of PB as a PANoptosis inhibitor in MIRI therapy. This study provides a reference paradigm for exploring the role of PANoptosis in other diseases and a framework for studying nanobiological interactions to uncover broader nanomaterial mechanisms.

overall_design: RNA-seq profiles of mouse myocardial tissues in the same treatment groups (control group, MIRI group, PB group, PB@PM group).

first: Lingling

last: Xu


title: Micro-RNA networks in T-cell prolymphocytic leukemia reflect T-cell activation and shape DNA damage response and survival pathways

status: Public on Feb 09 2026

city: Leipzig

first: Dennis

last: Jungherz

address: Johannisallee 32a

department: Hematology

institute: University of Leipzig Medical Center

summary: T-cell prolymphocytic leukemia (T-PLL) is a poor-prognostic mature T-cell malignancy. It typically presents with exponentially rising lymphocyte counts, splenomegaly, and bone marrow infiltration. Effective treatment options are scarce and a better understanding of TPLL's pathogenesis is desirable. Activation of the TCL1 proto-oncogene and loss-of-function perturbations of the tumor suppressor ATM are TPLL's genomic hallmarks. The leukemic cell reveals a phenotype of active T-cell receptor (TCR) signaling and aberrant DNA damage responses. Regulatory networks based on the profile of microRNA (miR) have not been described for T-PLL. In a combined approach of small-RNA and transcriptome sequencing in 46 clinically and moleculary well-characterized T-PLL, we identified a global T-PLL-specific miR expression profile that involves 34 significantly deregulated miR species. This pattern strikingly resembled miR-ome signatures of TCR-activated T cells. By integrating these T-PLL miR profiles with transcriptome data, we uncovered regulatory networks associated with cell survival signaling and DNA damage response pathways. Despite a miR-ome that discerned leukemic from normal T cells, there were also robust subsets of T-PLL defined by a small set of specific miR. Most prominently, miR-141 and the miR- 200c-cluster separated cases into two major subgroups. Furthermore, increased expression of miR-223-3p as well as reduced expression of miR-21 and the miR-29 cluster were associated with more activated Tcell phenotypes and more aggressive disease presentations. Based on the implicated pathobiological role of these miR deregulations, targeting strategies around their effectors appear worth pursuing. We also established a combinatorial miR-based overall survival score for T-PLL (miROS-T-PLL), that might improve current clinical stratifications.

overall_design: polyA-RNA data of healthy donors and T-PLL patients

first: Till

last: Braun

first: Linus

last: Wahnschaffe

first: Markus

last: Glaß

first: Janine

last: Altmüller

first: Stefan

last: Hüttelmaier

first: Alexandra

last: Schrader

first: Marco

last: Herling


title: Alterations in energy production in a Drosophila model for the X-linked dystonia-parkinsonism-related Taf1 deficiency

city: Luebeck

first: Melissa

last: Vos

address: Ratzeburger Allee 160, building 67

department: Institute of Neurogenetics

institute: University of Luebeck, UKSH

summary: Background: X-linked dystonia-parkinsonism (XDP), an adult-onset neurodegenerative disorder, is caused by an SVA insertion in the TAF1 gene, containing a hexanucleotide, the length of which is correlated to the severity of the disease. The SVA insertion moderately disrupts gene expression; however, the underlying disease mechanism remains enigmatic. Methods: Here, we characterized a fly model for Taf1 deficiency and performed a pilot RNA sequencing analysis. Subsequently, we validated these findings in Taf1-deficient flies and in XDP patient-derived fibroblasts.  Results: We identified an upregulation of genes involved in lipid-dependent energy production as a compensatory mechanism to maintain proper ATP levels. However, studies in XDP patient-derived fibroblasts with minor TAF1 reduction did not confirm these findings. Conclusion: β-oxidation is elevated in flies with severe TAF1 reduction but not detected in XDP-patient fibroblasts, suggesting that this compensatory mechanism may only manifest above a critical TAF1 dosage threshold, absent in patient basal conditions. This finding thus suggests that dosage-dependent metabolic responses occur following TAF1 loss.

overall_design: A heterozygous Taf1 mutant line and its control was used to isolate RNA. RNAseq was performed to get a preliminary output alterations in KEGG pathways

first: Philip

last: Seibler

first: Christine

last: Klein


title: Cell-autonomous control coupled with tissue context regulates the cessation of migration at the site of organ development

city: Berlin

first: Johanna

middle: Berenike

last: Kroll

address: Hannoversche Str.28

department: Berlin Institute for medical Systems Biology

institute: Max Delbrück Center for Molecular Medicine

summary: Organ development relies on interactions among different cell types that form three-dimensional structures to carry out specific tasks. This process often involves active migration of progenitor cells toward specific positions within the embryo, where the cells then become immotile and form stable connections among each other and with neighboring cell types. In this work, we study the process of motility loss using zebrafish primordial germ cells as an in vivo model. We show that changes in embryonic tissues as well as cell-autonomous events regulate germ cells’ behavior as they arrive at their target region. Importantly, we find that reduction in germ cell motility is correlated with the decay of RNA encoding for Dead end 1 (Dnd1), a conserved vertebrate RNA-binding protein that is essential for PGC migration. Indeed, decreasing or increasing the level of Dnd1 results in a premature or delayed stop to motility, respectively. These findings represent a novel RNA decay-based mechanism for timing the duration of cell migration in vivo.

overall_design: To generate spatially-resolved RNA-seq data for 24 hpf (hours post fertilization) old embryos, we cryosectioned samples, extracted RNA from the individual sections, and amplified and barcoded mRNA using the CEL-seq protocol (Hashimshony et al., Cell Reports, 2012) with a few modifications. Libraries were sequenced on Illumina NextSeq500.

first: Zahra

last: Labbaf

first: Moritz

last: Ophaus

first: Michal

last: Reichman-Fried

middle: B

first: Jan Philipp

last: Junker

first: Erez

last: Raz


title: ACSS2-Mediated Lysine Crotonylation Attenuates Senescence and Enhances the Therapeutic Efficacy of Adipose-derived Stem Cells in Inflammatory Bowel Disease [RNA-Seq]

city: Guangzhou

first: Ming

last: Yuan

address: 26 Yuancun Erheng Rd

institute: The sixth affiliated hostpital, sun yat-sen university

summary: Background Inflammatory bowel disease (IBD) remains a significant clinical challenge with limited curative options. Adipose-derived mesenchymal stem cells (ADSCs) hold therapeutic promise, but their anti-inflammatory efficacy is often compromised by cellular senescence. This study investigates the role of lysine crotonylation (Kcr) in ADSCs senescence and explores its therapeutic potential. Methods We analyzed Pan-Kcr levels in senescent ADSCs and evaluated the effects of sodium crotonate (NaCr), a crotonyl-CoA precursor, on senescence, proliferation, and anti-inflammatory function. A murine colitis model was used to assess therapeutic efficacy. Molecular mechanisms focusing on ACSS2-mediated Kcr regulation and H3K9 crotonylation (H3K9cr) at the ACSS2 promoter. Results Senescent ADSCs exhibited a marked decline in Pan-Kcr levels. NaCr treatment ameliorated senescence, enhanced proliferation, and improved anti-inflammatory capacity. ACSS2, a key regulator of Kcr, was downregulated in senescent ADSCs. Moreover, the anti-senescence effect of NaCr depended on ACSS2-mediated crotonylation. NaCr promoted H3K9cr modification at the ACSS2 promoter, forming a positive feedback loop that elevated Kcr levels. Mechanistically, ACSS2-mediated Kcr suppressed the NF-κB pathway to delay ADSCs senescence. Conclusion Our findings reveal an epigenetic pathway (ACSS2-Kcr-H3K9cr) regulating ADSCs senescence and propose Kcr modulation as a novel strategy to enhance ADSCs-based therapy for IBD.

overall_design: RNA-seq profiling of ADSCs at  passage 3 and passage 7

first: Senmao

last: Li

first: Shaopeng

last: Chen

first: Minghui

last: Zhu

first: Runfeng

last: Yu

first: Junfeng

last: Huang

first: Guanzhan

last: Liang

first: Chi

last: Zhang

first: Xiaowen

last: He

first: Ping

last: Lan

first: Xianrui

last: Wu


title: Respiratory syncytial virus infection induces heterologous protection against SARS-CoV-2 via induction of trained immunity and SARS-CoV-2 reactive mucosal T cells

city: Galveston

first: Haiping

last: Hao

state: Texas

address: 301 University Blvd

institute: UTMB NGS Core

summary: The respiratory viruses can concurrently or sequentially infect a host and influence the trajectory of each other. The underlying immune mechanisms are not well understood. Here, we investigated whether respiratory syncytial virus (RSV) infection affects host vulnerability to subsequent SARS-CoV-2 infection in both BALB/c and the K18 hACE-2 transgenic mouse models. We found that RSV infection- induced heterologous protection against subsequent SARS-CoV-2 infection was dose and time dependent. RNA-seq and immunological analyses revealed that RSV infection triggered antigen presenting cell (APC)s and SARS-CoV-2 reactive mucosal T cell activation in the lung at day 9, which declined at 1 month. RSV infection induced the expansion and the upregulation of cellular metabolic pathways of gd T cells. Furthermore, RSV infection in TCRd-/- mice, which are deficient of gd T cells triggered a lower SARS-CoV-2 reactive mucosal T cell response. Following SARS-CoV-2 infection, TCRd-/- mice with prior RSV infection had increased viral loads and higher levels of virus-induced inflammatory responses in the lung compared to the WT group. In summary, our results suggest that RSV infection provides heterologous protection against subsequent SARS-CoV-2 infection via induction gd T cell- mediated trained immunity in the lung and SARS-CoV-2 reactive mucosal T cell responses.

overall_design: 7- to 8-week-old  C57BL/(B)6 mice were infected intranasally (i.n) with 5 × 106  of RSV. At day 9 post RSV infection, mice were challenged with 1 × 104 PFU of the SARS-CoV-2 CMA4 strain. infected mice were euthanized at day 2 for tissue collection.

first: Awadalkareem

last: Adam

first: Tian

last: Wang


title: The Notch ligand Jagged1 regulates extracellular matrix production and organization in triple-negative breast cancer

city: Turku

first: Marjaana

last: Parikainen

address: Tykistökatu 6

country: Finland

institute: Åbo Akademi University

summary: The extracellular matrix (ECM) in the tumor microenvironment plays an essential role in the progression of cancer. Here, we show that expression of the Notch ligand Jagged1 correlates with poor patient survival in aggressive breast cancer and that Jagged1 promotes in vivo tumor growth and invasion of triple-negative breast cancer cells. Using transcriptomics, proteomics, and imaging approaches of cancer cell/fibroblast co-cultures, both in vitro and in vivo, we demonstrate that Jagged1 drives fibroblast activation, increased collagen deposition, and aligned organization of ECM fibers. Jagged1 increases transforming growth factor beta (TGFβ) related signaling in fibroblast co-cultures and the Jagged1-induced ECM alignment can be prevented by a TGFβ inhibitor. Thus, Jagged1 regulates ECM remodeling upstream of TGFβ. With the emergence of safe therapeutics targeting specific Notch ligands and receptors, Jagged1 modulation may offer a path to therapeutically target invasive breast cancer.

overall_design: RNA-seq profiling of wildtype MDA-MB-231 breast cancer cells and their derivative cell lines (Jag1KO, Jag1KO+rescue, Jag1KO+ctrl, siCtrl, and siJag1) with altered expression of JAG1, grown for 7 days as 3D Matrigel cultures. 3 biological replicates of each sample.

first: Ujjwal

last: Suwal

first: Pekka

last: Rappu

first: Jyrki

last: Heino

first: Cecilia

last: Sahlgren


title: ACSS2-Mediated Lysine Crotonylation Attenuates Senescence and Enhances the Therapeutic Efficacy of Adipose-derived Stem Cells in Inflammatory Bowel Disease [ChIP-Seq]

first: Ming

last: Yuan

overall_design: ChIP-seq of H3K9cr in ADSCs at  passage 3 and passage 7

first: Senmao

last: Li

first: Shaopeng

last: Chen


title: Transcriptional and cellular maturation of the chick spinal cord in the context of distinct neuromuscular circuits

city: Basel

first: Patrick

last: Tschopp

state: Basel-Stadt

address: Vesalgasse 1

department: Umweltwissenschaften

country: Switzerland

institute: Universität Basel

summary: The chicken spinal cord is a classic model system to study the early specification of neuronal cell types along its anterior-posterior axis. Here, we follow the ensuing maturation dynamics at limb levels with single cell resolution and contrast neuronal populations innervating appendages of distinct form and function. We use gene co-expression modules to identify rare cell populations with specific biological functions, and show that appendages with different motor outputs – wings and legs – rely on largely similar spinal cord cell type repertoires. Challenging the system with experimental alterations to the peripheral limb musculature reveals limited transcriptional changes, but spatially restricted plasticity in spinal cord motor neuron numbers. Collectively, our results provide a resource to investigate the molecular and cellular basis of neuronal maturation in the avian spinal cord and highlight the plastic nature of embryonic cells to adapt to changes in the limb periphery at both developmental and evolutionary timescales.

overall_design: 10X scRNA-seq of Day 5 (brachial), Day 7 (brachial), and Day 10 (brachial, lumbar, and brachial with induced polydactyly) chick spinal cord.

first: Fabio

last: Sacher

first: Bianka

last: Berki

first: Antoine

last: Fages

first: Maëva

last: Luxey


title: Effect of depletion of MALAT1 on gene expression during LPS stimulation on THP-1 derived differentiated macrophages

city: Chiba

first: Ichiro

last: Manabe

address: 1-8-1 Inohana, Chuo

country: Japan

institute: Chiba University

summary: Long non-coding RNAs (lncRNAs) are known for their diverse roles in regulating gene expression, cellular functions, and metabolic pathways. Among them, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been extensively studied in cancer and inflammation. Here, we report a newly discovered interaction between MALAT1 and HADHB—a key enzyme in mitochondrial fatty acid oxidation (FAO)—which reveals additional regulatory roles for MALAT1 in human macrophages. Our findings show that MALAT1 binds to hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex subunit beta (HADHB), significantly enhancing its thiolase activity and its expression during the inflammation.By targeting HADHB, MALAT1 influences both inflammatory and metabolic pathways, providing insights into its potential as a therapeutic target for modulating macrophage activity and metabolic balance in chronic inflammatory diseases. This study not only identifies HADHB as a new target of MALAT1 but also underscores the conserved functional roles of lncRNAs across species, particularly in immune and metabolic regulation.

overall_design: To explore the function of MALAT1 in the different time points stimulated by LPS, we performed human THP-1 derived macrophages in which the MALAT1 is been knocked down by siRNA. We then performed gene expression profiling analysis using  data obtained from RNA-seq of two different cells at four time points. Comparative gene expression profiling analysis of RNA-seq data for THP-1 derived macrophages transfected by negative control (siControl)  and its KD derivatives (siMALAT1). Each sample has three replicates.

first: Yuxiang

last: Liu

first: Katsuhito

last: Fujiu


title: Decoding the total RNAs bound to human HADHB in the THP-1 derived macrophages

overall_design: To explore the RNAs bound to human HADHB, RNA immunoprecipitation sequencing (RIP-seq) for human HADHB was performed in THP-1 derived macrophages stimulated by LPS for 24H.

first: Yukiteru

last: Nakayama


title: FANCD2 restrains fork progression and prevents fragility at early origins upon re-replication

status: Public on Feb 08 2026

city: Seville

first: Andrés

last: Aguilera

address: Av. Américo Vespucio 24

department: Genome BIology

institute: CABIMER, Universidad de Sevilla

summary: DNA replication is tightly regulated to ensure a single round of chromosome duplication per cell division. DNA licensing restricts origin firing to once-per-cell-cycle while aberrant licensing promotes re-replication and genome instability. Here, we investigate the mechanisms that protect genome integrity following re-replication induced by depletion of the licensing inhibitor Geminin. We find that re-replicating cells require FANCD2 to prevent genome instability. FANCD2 is rapidly recruited to chromatin upon Geminin loss, where it limits unrestrained fork progression and prevents single strand DNA gap accumulation and fork breakage. Genome-wide analyses reveal that upon re-replication, FANCD2 localizes to early origins within highly transcribed regions prone to accumulate R-loops and enriched in early replicating fragile sites. Importantly, reducing transcription and R-loops alleviates re-replication-induced genome fragility, whereas PARP inhibition exacerbates it. Our study uncovers a role for FANCD2 in safeguarding genome integrity during re-replication, offering avenues for selective targeting of cancer cells.

overall_design: ChIP-seq of FANCD2 in K562 cells (lymphobalst; myelogenous leukemia) with siRNA-induced silencing of Geminin (siGMNN) and control cells (non targeting siRNAs; siC).

first: Badra-Fajardo

last: Nibal

first: Karydi

last: Elena

first: Bayona-Feliu

last: Aleix

first: Gómez-González

last: Belén

first: Preza

last: Ourania

first: Arbi

last: Marina

first: Kalogeropoulou

last: Argyro

first: Rantala

last: Juha K.

first: Taraviras

last: Stavros

first: Aguilera

last: Andrés

first: Lygerou

last: Zoi


title: Spatial transcriptomics profile of mammary gland tumours in MMTV-PyMT mouse model of breast cancer [MERFISH]

city: San Juan de Alicante

first: Angela

last: Nieto

state: Alicante

address: Av. Ramón y Cajal s/n

department: Developmental Neurobiology

institute: Instituto de Neurociencias (CSIC-UMH)

summary: Disseminated cancer cells rarely succeed in forming macrometastases, yet they continue to be the most life-threatening cause of patient mortality. The determinants driving metastatic competence, however, are still poorly understood. Using data from human breast cancer patients and genetic mouse models, we uncover a non-linear relationship between the expression of the EMT transcription factor Prrx1 in the primary tumor and metastatic outcome. Multi-omics analyses in mouse tumors reveal that Prrx1 functions as a dual regulator, promoting invasive behavior while simultaneously inducing dormancy. Cells with intermediate Prrx1 levels exhibit the highest metastatic fitness, whereas extreme levels (negative or too high) lead to less metastasis, typical of a hormetic behavior, and respectively due to insufficient invasiveness or to dormancy. These findings provide mechanistic insight into the regulation of dormancy and its link to metastatic potential. Additionally, we propose that combined signatures of invasion and proliferation allow robust prognosis prediction in breast cancer patients. Our study further highlights Prrx1-driven heterogeneity, established in the primary tumor, as a key determinant of metastatic competence.

overall_design: We designed a MERSCOPE panel targeting 265 genes using the Vizgen Gene Panel Design Portal. Formalin-fixed paraffin-embedded (FFPE) samples from three distinct MMTV-PyMT tumors were processed according to Vizgen MERSCOPE protocols. The resulting data were utilized to analyze transcriptional heterogeneity at the spatial level within the tumors.

first: Nitin

last: Narwade

first: Raúl

last: Jiménez-Castaño

first: Khalil

middle: K

last: Youssef


title: Adaptive immune responses to vaccination reflect social status at first exposure in rhesus macaques

status: Public on Feb 06 2026

city: Chicago

first: Joao

last: Barroso-Batista

address: The University of Chicago, KCBD room 9220E, 900 E 57th Street

institute: The University of Chicago

summary: Social gradients are consistently associated with variation in health outcomes, including infectious disease. However, distinguishing between social gradients in antigen exposure versus susceptibility remains challenging. Here, we use a nonhuman primate model for chronic social stress to investigate how social status influences the influenza vaccine-induced adaptive immune response. We manipulated the social status of female rhesus macaques to test the response to influenza antigens in naïve individuals and after secondary exposure. Higher social status at the time of first exposure, but not at the time of secondary exposure, predicted stronger antibody responses to both exposures. Social status also drove gene expression differences for adaptive immune pathways, and genes that predict the magnitude of the antibody response overlap with those linked to social status. Thus, social gradients shape the adaptive immune response in a temporally dependent manner, with particular sensitivity at the time of initial antigen exposure.

overall_design: RNA-seq profiling of PBMCsfrom rhesus macaques before (day 0) and 1, 3 or 7 days following influenza vaccination

first: C. Ryan

last: Campbell

first: Luis B.

last: Barreiro

first: Jenny

last: Tung


title: In situ spatial transcriptomics reveal novel markers of the limbal stem cell niche and ocular surface epithelia

city: Kensington

first: Orazio

last: Vittorio

address: High St

department: School of Biomedical Sciences, Faculty of Medicine

country: Australia

institute: UNSW Sydney

summary: The mammalian cornea is endowed with stem cells (SCs) that have lifelong regenerative activity for its stratified epithelium. The niche for these cells is the limbus, and damage to this microstructure or its SCs results in a blinding disease known as limbal stem cell deficiency (LSCD). Despite the numerous studies that employ single-cell RNA sequencing, the identity of these cells remains an enigma principally because their spatial positioning is lost upon dissociation from their repository, and their gene expression is altered upon exposure to physical and chemical stressors during procurement. Herein, these adversities were avoided by conducting spatial transcriptomic screening directly on corneal, limbal and conjunctival tissues. Differentially expressed genes in the limbus included Krt16 and Nkiras1 among 6 others, which play a role in maintaining stemness, epithelial organization, immune surveillance, and tumor suppression. Krt16 was dynamically expressed in the developing limbus, correlated with slow-cycling label-retaining limbal epithelia and was induced during corneal injury; observations consistent with marking functional SCs. Additionally, we established Nkiras1 as a novel maker of neutrophils in the limbal SC niche, and Alox12e as a specific marker of conjunctival epithelia. Because current gold standard treatments for LSCD include SC transplantation, our data will inform future studies in delivering a more reliable standard therapy which incorporates an identifiable SC population to improve clinical outcomes.

overall_design: C57BL/6 male and female wild-type mice (n = 81) were obtained from Australian BioResources (Moss Vale, Sydney, Australia). They were housed under pathogen-free conditions in temperature-controlled rooms and given ad libitum access to standard chow and water. Eyes (n=3) were fixed in 4% paraformaldehyde (PFA) overnight. The superior nasal (SN) quadrant was dissected and paraffin-embedded. Sections (5µm) were mounted onto glass slides within a 35.3mm x 14.1mm area, dried at 58°C for 3 hrs, then subjected to the GeoMx DSP workflow (Bruker Spatial Biology, San Jose, CA). Prior to selecting ROIs, serial sections were stained with hematoxylin or double immunostained for K8 and K12 to identify tissue boundaries. ROIs included corneal, transitional (containing some limbus and cornea), limbal and bulbar conjunctival epithelia.

first: Lamia

last: Nureen

first: Antonietta

last: Salerno

first: Nick

last: Di Girolamo


title: Nutritional Genomics Uncovers Vitamin B3 Therapy as Curative for NAXD Disease

city: San Francisco

first: Ayushi

last: Agrawal

state: CA

address: 1650 Owens St

institute: Gladstone Institutes

summary: Vitamins are essential metabolites that must be obtained from external sources. All 13 vitamins were identified in the early 1900s, a rich era of biochemistry. More recently, they are consumed indiscriminately. We introduce a new nutritional genomics framework that begins with a treatment and identifies all potential disease candidates. Using a genome-wide CRISPR screen at varying vitamin B3 levels, we nominated dozens of diseases for B3-based therapy. The top candidate was NAXD, a proofreading enzyme involved in correcting an aberrant form of NADH (NADHX). Mutations in NAXD cause severe neurodevelopmental disease, with no proven therapies. We created a new mouse model of disease, observing NADHX accumulation and NAD+ depletion in affected organs, leading to impaired serine biosynthesis. Low B3 diets worsened the disease, while B3 supplementation was curative, extending lifespan by more than 20-fold. This work introduces a new approach to nutritional genomics and precision vitamin therapies.

overall_design: Nuclei were isolated from frozen hemi brains of P5 mice across different genotypes and experimental treatments. All mouse pups were treated with either vehicle or 750 mg/kg Nicotinamide Riboside starting from postnatal day 0 until collection on postnatal day 5. Mice were perfused with PBS, and the left hemi-brains (excluding the olfactory bulb) were collected from both Control and NAXD KO mice (n = 4 per genotype per treatment group). We then employed a single-nucleus RNA sequencing approach on these isolated nuclei using the 10x Genomics GEM-X Flex Kit protocol, where samples first undergo fixation before Gene Expression library preparation. This single-nucleus RNA-seq experiment using the GEM-X Flex protocol is probe-based rather than using 3' capture. We randomized the samples being assigned to each mouse probe barcode and assigned to each GEM reaction.

first: Ankur

last: Garg

first: Adam

last: Turner

first: Skyler

last: Blume

first: Michela

last: Traglia

first: Reuben

last: Thomas

first: Ryan

last: Corces

first: Isha

last: Jain


title: EPB41L4A-AS1 long noncoding RNA acts in both cis- and trans-acting transcriptional regulation and controls nucleolar biology

city: Rehovot

first: Igor

last: Ulitsky

address: Hertzl St.

country: Israel

institute: Weizmann Institute of Science

summary: Mammalian genomes are pervasively transcribed into long noncoding RNAs (lncRNAs), whose functions and modes of action remain poorly understood. EPB41L4A-AS1 is an evolutionary conserved and broadly and highly expressed lncRNA that produces the H/ACA snoRNA SNORA13 from one of its introns. We studied the consequences of EPB41L4A-AS1 perturbation in breast cancer cells and found that it acts both in cis to enhance expression of the proximal EPB41L4A gene, and in trans by broadly regulating gene expression, including expression of snoRNAs, transcription of genes involved in nucleolar biology and the distribution of nucleolar proteins. These effects are phenocopied by loss of SUB1, an interactor of EPB41L4A-AS1 and are observed following transient perturbations of EPB41L4A-AS1 that do not affect steady-state SNORA13 levels. Exogenous expression of the full-length EPB41L4A-AS1 locus but not SNORA13 expression can rescue the trans-acting transcriptional effects of its perturbation. The EPB41L4A-AS1 gene is thus a versatile locus producing RNA molecules acting on multiple levels and important for key cellular functions.

overall_design: RNA-seq, CUT&RUN and SLAM-seq from MCF-7 breast cancer cells after perturbing the expression of EPB41L4A-AS1, SUB1 or GAS5.

first: Alan

last: Monziani


title: A transcriptomic microglia taxonomy across mouse and human pathologies

city: Freiburg

first: Chintan

last: Chhatbar

address: Breisacher strasse 64

department: Department of Neuropathology

institute: Uniklinikum Freiburg

summary: Microglia are the key immune cells involved in virtually all diseases of the central nervous system (CNS). Numerous previous single-cell sequencing approaches to the study of microglia have revealed extensive diversity in this cell type in the human and mouse brain in different conditions. Importantly, a unifying, comprehensive, disease- and species spanning transcriptomic immune cell-focused atlas of the perturbed CNS, including true single-cell spatial transcriptomic information on neighborhood relationships, is lacking. Here, we generated a novel large-scale single-cell RNA-sequencing-derived taxonomy through the analysis of > 1 million CNS cells enriched for myeloid cells across > 30 different pathologies and conditions. Disease-associated human microglia, together with CNS-associated macrophages and monocytes, were differentiated iteratively into 27 superclusters and 192 clusters, showing substantial overlap with their counterparts in the corresponding murine pathologies. This top-down approach, in combination with targeted and genome-wide subcellular spatial transcriptomics, enabled us to examine and compare the spatial interactome of the identified superclusters and clusters within and across pathologies and species. Using cell-specific mutants, we further characterized the underlying transcriptional programs of activation-associated microglial clusters, identifying distinct dependencies on type I and II interferons and colony stimulating factor 1 receptor pathways. Our data provide new insights into the spatial dynamics of the endogenous CNS immune system during development, health and disease in human and mouse.

overall_design: CNS nuclei were isolated from frozen specimen, stained with anti-NeuN and anti-Olig2, FACS purified (DAPI+NeuN-Olig2-), and analyzed with single nucleus RNA-seq.

first: Marco

last: Prinz


title: PAN2 Maintains mRNA PolyA Tail Homeostasis and Regulates Translation during Spermiogenesis in Mouse

city: Hangzhou

first: Heng-yu

last: Fan

state: Zhejiang

address: Yuhangtang Road

institute: Life Sciences  Institute

summary: Elongation and shortening of the polyA tail are the most common type of post-transcriptional mRNA regulation in eukaryotic cells. Two protein complexes, PAN2-PAN3 and CCR4-NOT, are major cytoplasmic deadenylases that trim the mRNA polyA tails. While PAN2-PAN3 removes the distal portion of the long polyA tails, CCR4-NOT removes adenosine closer to the 3'-UTR. Some subunits in the CCR4-NOT complex have been shown to play synergistic biochemical functions during mouse germ cell development. However, the in vivo functions of the upstream deadenylase PAN2-PAN3 remain unclear, particularly in mammals. In this study, we found that germline-specific deletion of Pan2 leads to male infertility. Pan2 knockout did not affect the prophase of meiosis I, but led to abnormal spermiogenesis and apoptosis of male germ-cells. By Palso-seq and Ribo-lite, we found that the deletion of Pan2 increased the number of long-tail mRNAs in spermiogenesis and disrupted the translation efficiency of genes that should be highly translated at this stage. These findings highlight the crucial physiological functions of PAN2 in gametogenesis and expand our understanding of the posttranscriptional regulation of mRNAs in specific physiological processes.

overall_design: MII stage spermatocytes and round spermatids form Pan2flox/-;Stra8-Cre mice were subjected to RNA-seq using the Smart-seq2 method with minor modifications.

first: Xuan

last: Wu


title: Dedifferentiation-Driven Oncogenic Stemness Promotes Tumor-Sustaining Adaptability in the Intestinal Epithelium

city: Hoboken

first: ansu

last: perekatt

state: NJ

address: 507 River street

department: CCB

institute: Stevens Institute of Technology

summary: Intestinal tumors can arise either from mutations sustained in Lgr5⁺ stem cells (bottom-up) or through dedifferentiation of lineage-committed epithelial cells (top-down). Using a Smad4 loss-of-function and β-catenin gain-of-function mutant mouse model, we show that dedifferentiation-derived stem cells sustain tumorigenesis more effectively than mutant Lgr5⁺ cells in the endogenous crypts. Bulk and single-cell RNA sequencing revealed transcriptional reprogramming and the emergence of oncogenic villus-derived stem-like cells. Complementary in vivo and organoid studies suggest that dedifferentiation-derived oncogenic stem cells possess superior tumor-initiating and sustaining capacity

overall_design: Intestinal epithelial cells expressing red fluorescent protein, or the the stem cell marker CD44, was FACS isolated from wild type crypt, and the  Smad4 loss-of-function and β-catenin gain-of-function mutant crypt and villus epithelium and analyzed by single cell RNA-sequencing. Unlabeled cells from the wild type villus epithelium was also subjected to sc-RNA-sequencing.

first: Kylee

last: Zgeib

first: Thompson

last: Hui

first: Atharva

last: Inamdar

first: Ansu

last: Perekatt

first: Simon

last: Garcia

first: Binfeng

last: Lu

first: Crysta

last: Lim

first: Shima

last: Nejati

first: Amartya

last: Singh

first: Zahra

last: Hashemi

first: Dahlia

last: Matouba

first: Christina

last: Li


overall_design: Intestinal epithelial cells expressing red fluorescent protein, or the the stem cell marker CD44, was FACS isolated from wild type crypt, and the Smad4 loss-of-function and β-catenin gain-of-function mutant crypt and villus epithelium and analyzed by single cell RNA-sequencing. Unlabeled cells from the wild type villus epithelium was also subjected to sc-RNA-sequencing

first: Crystal

last: Sigh


title: Crip2 preserves hematopoietic stem and progenitor cell production through inhibition of Notch signals

city: Trieste

first: UDAY

last: RANGASWAMY

state: Trieste

address: via bonomea 265

department: NEUROSCIENCE

country: Italy

institute: SISSA

summary: To decipher the mechanisms underlying the cripDM phenotype, single cell RNA sequencing was performed on sorted, kdrl:mCherry+ cells at 30 hpf. The analysis revealed an upregulation of genes essential for vascular development.

overall_design: 10X single-cell RNA sequencing from sorted mCherry+ endothelial cells from whole zebrafish embryos at 30 hours post fertilization comparing wild-type and crip mutant samples.

first: Angelika

middle: G

last: Aleman

first: Uday

last: Rangaswamy

first: Remo

last: Sanges

first: Kimara

middle: L

last: Targoff


title: Mapping convergent regulators of melanoma drug resistance by PerturbFate

city: New York

first: Zihan

last: Xu

state: NY

address: 1230 York Ave

institute: The Rockefeller University

summary: High-throughput genomic studies have uncovered associations between diverse genetic alterations and disease phenotypes; however, elucidating how perturbations in functionally disparate genes give rise to convergent cellular states remains challenging. Here, we present PerturbFate, a high-throughput, cost-effective, combinatorial-indexing single-cell platform that enables systematic interrogation of massively parallel CRISPR interference (CRISPRi) perturbations across the full spectrum of gene regulation, from chromatin remodeling and nascent transcription to steady-state transcriptomic phenotypes. Using PerturbFate, we profiled over 300,000 cultured melanoma cells to characterize multi-modal phenotypic and gene regulatory responses to perturbations in more than 140 Vemurafenib resistance-associated genes. We uncovered a shared dedifferentiated cell state marked by convergent cooperative transcription factor (TF) activities across diverse genetic perturbations. We further dissected phenotypic responses to perturbations in Mediator Complex components, linking module-specific biochemical properties to convergent transcriptional activations. Together, we reveal common regulatory nodes that drive similar phenotypic outcomes across distinct genetic perturbations. We also delineate how perturbations in functionally unrelated genes reshape cell state. PerturbFate thus establishes a versatile platform for identifying key molecular regulators by anchoring multi-modal regulatory dynamics to disease-relevant phenotypes.

overall_design: Single-cell and parallel bulk CRISPR screen including 143 gRNA pairs targeting 143 genes and no-target with either DMSO or Vemurafenib treatment

first: Ziyu

first: Aileen

last: Ugurbil

first: Abdulraouf

last: Abdulraouf

first: Andrew

last: Liao

first: Jianxiang

last: Zhang

first: Wei

last: Zhou

first: Junyue

last: Cao