title: Bulk RNA-seq of mouse metastatic mammary cancer cells TUBO

summary: A key problem in cancer biology is understanding the phenotypic characteristics of the aggressive cell states present in macrometastases and their molecular underpinnings. Here we report on the cellular constituents of  breast cancer metastases,  revealing that these malignant cells display a gene-expression profile associated to embryonic development of tubular organs.

overall_design: TUBO cells are cultured in petri dishes and then harvested for RNA-seq

first: Robin

last: Caire

first: Giusy

last: Battilana

first: Francesca

last: Zanconato

first: Oriana

last: Romano


title: Bulk RNA-seq of mouse 4T1 cells with ETV4 KO [FGF]

status: Public on Mar 27 2026

city: Padova

first: Silvio

last: Bicciato

address: via U. Bassi 59/b

department: Molecular Medicine

country: Italy

institute: University of Padova

type: Expression profiling by high throughput sequencing

overall_design: Control or ETV4 KO cells are cultured in 3D Collagen I gels, with 2% Serum and with or without FGF ligands, and then harvested for RNA-seq

first: Michelangelo

last: Cordenonsi

first: Stefano

last: Piccolo


title: Evolutionary transcriptomic and cellular specializations within the mammalian striatum

city: Los Angeles

first: Genevieve

last: Konopka

state: CA

address: 650 Charles Young Drive South, 73-214 CHS

department: Neurobiology

country: USA

institute: UCLA David Geffen School of Medicine

summary: In this study we generated and analyzed single-nucleus RNA sequencing (snRNA-seq) of human, chimpanzee, rhesus macaque (this study and GSE167920), marmoset (GSE151761 and GSE165578), bat caudate (CN) and putamen (Pu) separately, ferret caudate (GSE151761), and mouse caudoputamen (C-Pu)(GSE151761) spanning 94 million years of evolution. We identified novel interneuron cell types in bat Pu while uncovering fundamental cellular compositional and transcriptomic differences between primate and non-primate striata.

sample_organism:
Macaca mulatta
Pan troglodytes
Homo sapiens
Phyllostomus discolor

overall_design: Generated single nuclear RNA profiles of human, chimpanzee, rhesus macaque, and bat striatal regions, caudate nucleus and putamen.

first: Gozde

last: Buyukkahraman

first: Emre

last: Caglayan

first: Yaqiang

last: Zhang

first: Stephen

last: Hoerpel

first: Carlos

last: Orozco

first: Amber

last: Main

first: Chet

middle: C

last: Sherwood

first: William

middle: D

last: Hopkins

first: Todd

last: Roberts

first: Sonja

last: Vernes


title: Bulk RNA-seq of mouse 4T1 cells with FGFR2 KO

overall_design: Control or FGFR2 KO cells are cultured in 3D Collagen I gels and then harvested for RNA-seq

first: Robin

last: Caire

first: Giusy

last: Battilana


title: Influence of NIPBL Knockdown-Induced Alterations in Cohesin Loop Extrusion on CTCF Loops, Enhancer-Promoter Connectivity, and PRC Domain Contacts During hESC Differentiation into Pancreatic Lineages

status: Public on Mar 31 2026

city: XIAMEN

first: XIAOWEN

last: LYU

state: FUJIAN

address: No.4221, Xiang'an South Road, Xiang'an District

country: China

institute: XIAMEN UNIVERSITY

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Cell differentiation is orchestrated by precise enhancer-promoter interactions that rely on three-dimensional (3D) chromatin organization, influenced by cohesin dynamics and architectural proteins such as CTCF and NIPBL. In this study, we investigated the effects of knocking down NIPBL, a critical cohesin loading factor, in human embryonic stem cells (hESCs) and their differentiated pancreatic lineages. Our results demonstrate that NIPBL depletion leads to a global loss of cohesin occupancy and altered chromatin architecture, particularly affecting enhancer-promoter loops and CTCF loops. Notably, while CTCF anchors maintain cohesin, enhancer-promoter interactions diminish significantly, highlighting the role of cohesive loading in transcriptional regulation. Additionally, we observed disrupted interactions within Polycomb Repressive Complex (PRC) domains and super enhancers, suggesting that NIPBL is crucial for maintaining the structural integrity of these regulatory elements. The study reveals that cohesin loading and loop extrusion processes are vital for establishing and preserving 3D chromatin interactions essential for gene expression during pancreatic differentiation. These findings underscore the intricate relationships between chromatin organization and gene regulation, with implications for understanding developmental processes and diseases associated with chromatin dysregulation.

overall_design: ChIP-Seq, ATAC-seq, RNA-Seq and HiChIP derived from H9 human embryonic stem cells (hESCs) treated with si-RNAs targeting NIPBL, CTCF and WAPL and chemical inhibitors including 1,6-HD, UNC3866 and TPA as well as their pancreatic differentiation derivatives.

first: Xiaowen

last: Lyu

first: Longtao

last: Yu


title: Time-resolved transcriptomic profiling of surgical wounds identifies stage-specific therapeutic targets for residual ovarian cancer

city: Seoul

first: Mahesh

middle: Chandra

last: Patra

state: 경기도

address: 241 Gangnam-daero

country: South Korea

institute: Arontier Co. Ltd

summary: Background: The optimal timing of adjuvant chemotherapy after cytoreductive surgery in epithelial ovarian cancer remains uncertain, and perioperative wound-healing responses may transiently create a pro-tumorigenic and drug-resistant microenvironment. This study aimed to characterize time-dependent wound-induced transcriptomic alterations and to identify pharmacologic agents capable of reversing these responses. Methods: An ID8 murine ovarian cancer model was used to compare no treatment, anesthesia alone, and anesthesia plus surgical wounding mimicking futile laparotomy. Tumors were collected at baseline, 1 day (T1), 1 week (T2), and 2 weeks (T3) after intervention. RNA sequencing was performed, and wound-specific differentially expressed genes (WsDEGs) were defined by excluding anesthesia- and progression-related signatures. Functional enrichment analyses were conducted, followed by transcriptome-based drug repurposing using the REMEDY platform to identify compounds predicted to reverse wound-induced gene expression profiles. Results: Surgical wounding significantly increased tumor burden at T1. Transcriptomic analyses revealed distinct, time-dependent wound-associated programs. At T1, WsDEGs were enriched in inflammatory signaling, coagulation, angiogenesis, and immune cell migration, with Vorinostat and Homohar-ringtonine identified as top candidates to counteract these signatures. At T2, pathways related to cell survival, adhesion, and morphogenesis predominated, with LY-2090314, Artesunate, and Birinapant emerging as potential modulators. At T3, cell-cycle regulation and lipid metabolic pathways were dominant, and Fulvestrant, Atorvastatin, Imatinib, and ABT-737 were predicted to inhibit these processes. Conclusions: Perioperative sur-gical wounding induces dynamic, stage-specific transcriptomic programs that may promote ovarian cancer progression and alter drug responsiveness. These findings support time-adapted perioperative pharmacologic strategies to optimize postoperative cancer therapy.

overall_design: RNA-seq profiling ID8 murine ovarian cancer cells without treatment, with only anesthesia, and with anesthesia-cum-surgical wounding at baseline, 1 day (T1), 1 week (T2), and 2 weeks (T3).

first: Seongyun

last: Lim

first: Young-Jae

last: Cho

first: Myeong-Seon

last: Kim

first: Jung-Joo

last: Choi

first: Ji-Yoon

last: Ryu

first: Jae Ryoung

last: Hwang

first: Ju-Yeon

first: Mohamed

middle: E

last: Farh

first: Insuk

last: Sohn

first: Jeong-Won

last: Lee

first: Yoo-Young


title: Changes to small RNA expression in macrophages in response to very low-density lipoprotein lipid hydrolysis by lipoprotein lipase and NADPH oxidase inhibition

city: St. John's

first: Lourdes

last: Peña-Castillo

state: Newfoundland and Labrador

address: 9 Arctic Ave

country: Canada

institute: Memorial University of Newfoundland

type: Non-coding RNA profiling by high throughput sequencing

summary: Lipoprotein lipid hydrolysis products generated by lipoprotein lipase (LPL) (herein, HP) can contribute to the conversion of macrophages into foam cells, but the molecular processes are not well understood. We previously reported that HP from total lipoproteins significantly changed the transcriptome of human macrophages, including an increased representation of small nucleolar RNAs. Cellular stress within cardiomyocytes was previously reported to increase the expression of small nucleolar RNAs through an increase of reactive oxygen species (ROS) generation by NADPH oxidase (NOX). Thus, we hypothesized that the HP induced ROS production through NOX activity, resulting in changes to small RNA transcripts. We examined changes to small RNA expression using RNA-seq in the absence or presence of HP, and whether those changes could be reversed by NOX inhibition. We identified eight differentially expressed small RNAs: three with differed expression in response to HP, and five with differed expression in response to NOX inhibition in the presence of HP.

overall_design: Small RNA-seq profiling of HEK-293 cells after 18 hours of incubation without or with HP, in the absence or presence of NOX inhibitors. P = Cells treated with very low-density lipoprotein (VLDL); L = Cells treated with VLDL lipid hydrolysis products generated by LPL; and G = “L” + the NOX1/4 inhibitor GKT136901.

first: Mariam

middle: O

last: Tijani

first: Elizabeth

last: Chia

first: Natalie

last: Cotter

first: Robert

middle: J

last: Brown


title: Bulk RNA-seq of mouse metastatic Breast Cancer cells

first: Silvio

last: Bicciato

overall_design: Control or ETV4 KO cells are cultured as 2D monlayers or in 3D Collagen I gels and then harvested for RNA-seq

first: Robin

last: Caire

first: Giusy

last: Battilana

first: Francesca

last: Zanconato

first: Oriana

last: Romano

first: Michelangelo

last: Cordenonsi

first: Stefano

last: Piccolo


title: scRNA-seq of primary tumors and lung metastases from mouse models of metastatic breast cancer

overall_design: Primary tumors were dissected from 3 months-old MMTV-PyVT female mice, and from 6 months-old MMTV-Neu female mice. For each sample, tumors from 2 donors were pooled and processed together. Metastasis-containing lungs were harvested from 3 months-old MMTV-PyVT female mice, and from 7-8 months-old MMTV-Neu female mice; lungs were processed after confirming the presence of visible macroscopic metastases; extrapulmonary primary bronchi and mediastinal lymph nodes were discarded; for each sample, lungs from two mice were pooled and processed together.

first: Tito

last: Panciera

first: Paolo

last: Contessotto


title: Circulatory ILC2 convert and persist as part of the long-term tissue-resident pool after infection [Infection Timecourse with Vascular Labelling]

status: Public on Mar 30 2026

city: Denver

first: Richard

middle: Lee

last: Reinhardt

state: Colorado

address: 1400 Jackson Street, K817A

department: Biomedical Research

institute: National Jewish Health

summary: Circulating ILC2 can serve as a first line of defense against infection prior to the local expansion of lung-resident ILC2. The fate of these circulating ILC2 and their contribution to the long-term lung-resident ILC2 pool is not understood. Using reporter mice in combination with single cell RNA sequencing (scRNA-seq) and novel applications of Cellular Indexing of Transcriptomes and Epitopes sequencing (CITE-seq), we assessed vascular and parenchymal ILC2 populations during helminth infection and the fate of circulatory ILC2. These studies revealed that circulating ILC2 rapidly convert to a tissue-resident phenotype upon arrival in the lung. Once converted, former circulating ILC2 become largely indistinguishable from lung-resident ILC2 over time. Key gene expression retained by converted ILC2 at the peak of the tissue-resident ILC2 response was related to maintained IL-25-responsiveness and unique cytokine potential. These converted ILC2 accumulate, expand, and persist alongside conventional lung-resident populations even after repeated pulmonary infections. These findings reveal an important contribution of circulating ILC2 to the long-term health and maintenance of the lung-resident ILC2 population.

overall_design: Mice were infected with the helminth Nippostrongylus brasiliensis. On days 5 and 7 of infection, mice were administered PE-conjugated anti-CD45 antibody (clone 30-F11) by intravenous injection in the tail 5 minutes prior to euthanasia. Lung ILC2s were sorted and sequenced. anti-PE was included in the CITE-seq antibodies to allow identification of vascularly labelled cells. Two biological replicates were hashed and pooled per condition. Experiment was repeated on two consecutive days, for a total of 4 biological replicates per condition. Conditions = Day 5 without intravenous injection, D5 with intravenous injection, D7 with intravenous injection. "A" and "B" in sample names correspond to first and second experimental days.

first: Amita

last: Kashyap

middle: L


title: A systematic exploration of the intrinsic mechanisms controling axon growth during development

status: Public on Mar 26 2026

city: Rehovot

first: Oren

last: Schuldiner

address: 234 Herzl Street

department: Molecular Cell Biology

country: Israel

institute: Weizmann Institute of Science

summary: The ability of neurons to extend axons is governed by tightly regulated genetic programs that vary across developmental stages and cell types. Understanding the molecular features that control axon growth potential is critical for uncovering how neural circuits form, mature, and respond to injury or disease. The Drosophila mushroom body (MB) offers a powerful model to dissect axon growth programs, as lineage-related Kenyon cells (KCs) undergo different developmental events under shared spatiotemporal conditions. During metamorphosis, gamma-KCs undergo axon pruning, followed by developmental regrowth at the same time-frame as alpha-beta-KCs initiate axon outgrowth - thus providing a unique opportunity to compare these distinct growth paradigms. To uncover the underlying genetic programs, we performed RNA-sequencing of alpha-beta- and gamma-KCs during their initial outgrowth and developmental regrowth, respectively, revealing dynamic transcriptional changes and identifying 300 shared genes upregulated during both growth states. A targeted loss-of-function screen revealed genes specifically required for either Alpha-beta initial growth, gamma regrowth, or both. Focusing on one such candidate, pmvk, we found that it plays a crucial role in axon regrowth by acting within the mevalonate pathway. Notably, other enzymes in this pathway were also required, suggesting that the entire metabolic pathway is essential for supporting regrowth. Using mutant analyses and rescue exepriements, we demosntrate that pmvk likely controls axon regrwoth via prenylation of Rheb, an effector of the TOR pathway, which we previously found to be required for regrowth. Our developmental transcriptomic atlas not only advances understanding of intrinsic axon growth programs, but also provides candidate genes and a valuable framework for future studies aimed at enhancing axon regeneration in the adult nervous system

overall_design: Transcriptional profiling of alpha-beta neurons during initial axon outgrowth and gamma neurons during axon regrowth

first: Lora

last: Fahdan

first: Noa

last: Wigoda

first: Hagar

last: Meltzer


title: Bulk RNA-seq of human MDA cells with ETV4 KO

overall_design: Control or ETV1/4/5 KO cells are cultured in 3D Collagen I gels and then harvested for RNA-seq


title: Human scRNA-seq of three breast cancer metastases and three normal mammary glands

summary: A key problem in cancer biology is understanding the phenotypic characteristics of the aggressive cell states present in macrometastases and their molecular underpinnings. Here we report on the cellular constituents of human breast cancer metastases,  revealing that these malignant cells are invariably locked in a chimeric cell state. Human BC metastatic cells indeed display a gene-expression profile associated to embryonic development of tubular organs, while also retaining the transcriptional features of their original adult mammary luminal lineage.

overall_design: Discard tissues from three anonymized healthy women undergoing reduction mastoplasty surgery and one surgical metastatic BC sample (BBM5) were collected from Azienda Ospedaliera di Padova, with informed consent according to University of Padua’s institutional guidelines and the Azienda Ospedaliera di Padova Ethics Committee (CESC). Two other metastatic samples (BBM0 and BSM1) were collected from anonymized women with informed consent, as approved by the ethics committee and institutional review board of Regina Elena National Cancer Institute (Rome).

first: Matteo

last: Marchionni

first: Mattia

last: Forcato

first: Sara

last: Donzelli

first: Giovanni

last: Blandino


title: In situ single-cell profiling of lung metastases from the MMTV-PyMT mouse model of metastatic breast cancer

first: Silvio

last: Bicciato

overall_design: CosMxTM technology [CosMxTM Human Universal Cell Characterization RNA Panel (1000-plex); Nanostring, USA] was applied on a section mouse lung, freshly-harvested from a female MMTV-PyMT C57BL/6J mouse at 5.5 months of age, resulting 18 fields of view (FoVs). The following cell surface markers were used for morphology visualization: B2M/CD298, PanCK, CD45, CD3 antibodies and DAPI.


title: The potent biodegrading actinomycete Rhodococcus opacus 1CP: Relating aromatic compound metabolism with whole-genome and transcriptome data

city: Bielefeld

first: Christian

last: Ruckert-Reed

address: Sequenz 1

department: Medical School OWL

country: Germany

institute: Bielefeld University

summary: The genus Rhodococcus comprises numerous strains recognized for pollutant degradation, secondary metabolite production including biosurfactant, lignin breakdown, or utilization of volatile organic compounds. Often gene redundancies and evolution of alternative pathways are attributed to such characteristics. Rhodococcus opacus 1CP initially isolated as a chlorophenol degrading strain was found to be a model organism comprising several such features. In this study, we analyzed the genome and transcriptome and demonstrated that the strain 1CP undergo three different routes of ortho, meta, and side chain attack in degrading aromatic compounds. The wild type strain, single or double knock-out mutant of phenol hydroxylases, well compensated the loss and chooses the classical ortho-route to attack substituted phenols, while the triple knock-out mutant takes the meta-pathway to act on p-cresol indicating that this pathway serves as a reserve in strain 1CP. Growth of 1CP in phenol, p-cresol and styrene induces several gene clusters that are associated in lignin metabolization. Catechol, protocatechuate, and phenylacetic acid are major key intermediates that are funneled into central pathways which enable the strain 1CP to degrade acetophenone, benzoate, phenol, 2-phenylethanol, and styrene. Strain 1CP has an alternative option with the modified ortho-cleavage pathway which enables it to degrade 2-chlorophenol. Interestingly, in almost all cases, redundant genes were identified, but only in minor cases as phenol hydroxylases, they were found to be active and simultaneously involved in metabolic activities. The transcriptome and kinetic data showed that the redundant styrene-oxide isomerase is upregulated and involved in styrene degradation.

overall_design: Whole transcriptomes of Rhodococcus opacus 1CP grown on 2mM of different carbon sources (tetradecane, phenol, styrol, and p-cresol) using 4 biological replicates each, pooled in the case of tetradecane.

first: Selvapravin

last: Kumaran

first: Thomas

last: Heine

first: Janosch

middle: A

last: Gröning

first: Tobias

last: Busche

first: Jörn

last: Kalinowski

last: Rückert-Reed

first: Michael

last: Schlömann

first: Dirk

last: Tischler


title: Hijacking innate immunity to enhance mRNA therapeutics

status: Public on Mar 25 2026

city: Guangzhou

first: Shu

last: Meng

state: Guangdong

address: No.9, XingDaoHuanBei Road, Guangzhou International Bio-island, Haizhu District

department: Department of Basic Science Research

institute: Guangzhou National Laboratory

summary: The therapeutic success of in vitro-transcribed (IVT) mRNA depends on its stability and efficient translation. However, IVT mRNA is highly susceptible to immune-mediated degradation, limiting its efficacy. Here, we co-transfected IVT mCherry mRNA with immune suppressor M or SOCS1 mRNA in human umbilical vein endothelial cells (HUVECs) for 6h and 24h to explore whether hijacking innate immunity could enhance expression and half-life of IVT mRNA. Subsequently, RNA-seq was performed to investigate the transcriptomic changes in HUVECs after transfecting IVT mRNA. We sought to clarify the potential mechanism underlying degradation of IVT mRNA.

overall_design: HUVECs were transfected with IVT mCherry mRNA, IVT mCherry mRNA + Luc, IVT mCherry mRNA + M, and IVT mCherry mRNA + SOCS1, respectively. Then, HUVECS were collected at 6h and 24h after transfection. Control group was also included. We got three replicates for each time point and each group. Total RNA were extracted and subjected to rRNA depletion-based RNA-seq profiling.

first: Tinghong

last: Zhang

first: Jinling

last: Qin

first: Xing

last: Peng


title: An optimized protocol for efficient derivation of pancreatic islets from multiple human pluripotent stem cell lines

city: Stockholm

first: Cheng

last: Zhao

state: Stockholm

address: H9 Klinisk vetenskap,171 77 Stockholm

department: Clinical Science

country: Sweden

institute: Karolinska institute

summary: Future success of cell therapy for type 1 diabetes (T1D) relies on robust protocols for the differentiation of stem cells to pancreatic islets. However, currently established protocols generate stem cell-derived pancreatic islets (SC-islets) which contain non-endocrine cell populations and have immature functionality. Herein we report the development of a new protocol for the generation of potent SC-islets enriched in functional endocrine cells from multiple human pluripotent stem cell (hPSC) lines. We show that laminin-521 efficiently supports monolayer differentiation of 8 testes hPSC lines to endocrine progenitor (EP)  stage. The efficiency was further improved by reducing the pancreatic progenitor (PP) stage. Importantly, we find that aggregation of EP reduces unwanted non-endocrine and proliferative cells. Subsequent suspension cultures generate SC-islets with  strong in vitro glucose responsiveness, similar to human islets. Upon transplantation of 300 SC-islets into the anterior chamber of the eye of a diabetic mouse model, the SC-islets undergo further maturation in vivo and re-establish normal glycemic control. The SC-islets before and after transplantation are to a major extent free of non-endocrine cell populations. In conclusion, our robust differentiation protocol results in endocrine enriched and highly functional SC-islets that should be well suited for transplantation into patients with T1D.

overall_design: In vitro differentiation of human pluripotent stem cells into pancreatic islets followed by thier transplantation into the anterior chamber of the eye of diabetic mice

first: Siqin

last: Wu

first: Galyna

last: Bryzgalova

first: Shivam

last: Chandel

first: Paschalis

last: Efstathopoulos

first: Kelly

last: Blust

first: Anna

last: Voznesenskaya

last: Falk

first: My

last: Hedhammar

first: Per-Olof

last: Berggren

first: Fredrik

last: Lanner


title: Bulk RNA-seq of mouse 4T1 cells with ETV4 KO

first: Silvio

last: Bicciato

overall_design: Control or ETV4 KO cells are cultured in 3D Collagen I gels and then harvested for RNA-seq

first: Robin

last: Caire

first: Giusy

last: Battilana

first: Francesca

last: Zanconato

first: Oriana

last: Romano

first: Michelangelo

last: Cordenonsi

first: Stefano

last: Piccolo


title: Human scRNA-seq of three primary and five metastatic breast cancers

summary: A key problem in cancer biology is understanding the phenotypic characteristics of the aggressive cell states present in macrometastases and their molecular underpinnings. Here we report on the cellular constituents of human breast cancer metastases,  revealing that these malignant cells are invariably locked in a chimeric cell state. Human BC metastatic cells indeed display a gene-expression profile associated to embryonic development of tubular organs, while also retaining the transcriptional features of the primary tumor subtype.

overall_design: Primary breast cancer samples and the brain metastatic samples were obtained from Istituto Nazionale dei Tumori, Milan, and Istituto Neurologico “Carlo Besta”, Milan, respectively, following ethical approval from their Institutional Review Boards and acquisition of informed consent from all patients.

first: Roberta

last: Bordo

first: Ramona

last: Bason

first: Massimiliano

last: Pagani


title: Bulk RNA-seq of human metastatic Breast Cancer cells

overall_design: Control or ETV1/4/5 KO cells are cultured as 2D monlayers or in 3D Collagen I gels and then harvested for RNA-seq


title: Assay for transposase-accessible chromatin using sequencing (ATAC-Seq) of Barley CI 16151 and fast-neutron-derived, immune-compromised mutants infected with the powdery mildew fungus (Blumeria hordei (Bh); isolate 5874)

city: Ames

first: Roger

last: Wise

state: IA

address: Department of Plant Pathology, Entomology, and Microbiology, Iowa State University, 1344 Advanced Teaching & Research Bldg., 2213 Pammel Dr.

department: CICGRU

institute: USDA/ARS

summary: Transcriptional reprogramming is a key component of disease resistance. MLA (mildew locus a), is an immune receptor that interacts with several transcription factors (TFs), and thus, represents a model to explore regulatory architecture during defense. To characterize chromatin accessibility of barley during powdery mildew infection, a series of isogenic mutant genotypes and timepoints were subjected to ATAC sequencing. We designed our study around two diverse genes in host immunity, mildew locus a (Mla6), a nucleotide binding leucine-rich repeat (NLR) immune receptor, and the Blufensin1 (Bln1) basal defense regulator, which influence immunity in a resistance (R)-gene dependent and R-gene independent manner, respectively. In addition to the CI 16151 resistant progenitor (Mla6, Bln1), three mutants were utilized: the susceptible mla6-m18982, the resistant bln1-m19089, and the susceptible double mutant (mla6+bln1)-m19028 (Chapman et al., 2021; Velásquez-Zapata et al., 2024). Four infection timepoints (0, 16, 20, 32 HAI) were taken to sample across key pathogen life cycle events such as appressorial penetration and haustorial development. Validation of the ATAC-Seq dataset was performed using the correlation with gene expression profiles from RNA-Seq data; by checking the presence of epistatic events at the chromatin level, phenomenon that was recently described using RNA-Seq (Velásquez-Zapata et al., 2024).

overall_design: An Assay for Transposase-Accessible Chromatin was coupled with next-generation sequencing to identify chromatin-accessible regions, thereby mapping transcription factor binding sites associated with the immune receptor MLA (mildew locus a). The wild-type progenitor, CI 16151 (Mla6, Bln1) and three fast-neutron derived mutants [m18982 (mla6, Bln1); m19089 (Mla6, bln1); m19028 (mla6, bln1)] were blocked by biological replicate and plant genotype and inoculated with Blumeria hordei (Bh) isolate 5874 (AVRa6). Tissue was collected at four biologically relevant timepoints (0, 16, 20, and 32 HAI). The entire experiment was replicated four times. Libraries were sequenced on an Illumina NovaSeq 6000 using paired-end 150 bp reads.

first: Valeria

last: Velasquez-Zapata

first: Gregory

last: Fuerst

middle: P


title: Highlights of Tuft Cells in Mouse and Human Salivary Glands

city: Chicago

first: George

last: Chlipala

state: IL

address: 900 S. Ashland Ave

department: Research Informatics Core

institute: University of Illinois Chicago

summary: Tuft cells (TCs) are rare chemosensory epithelial cells that regulate mucosal homeostasis in several organs, but their role in salivary glands (SGs) remains unclear. This study investigated TC features in both mouse and human SGs. In mouse samples, transmission electron microscopy (TEM), histological analysis, bulk RNA-sequencing and proteomic analyses were performed on submandibular glands (SMGs) from female and male C57BL/6J (wild-type) and C57BL/6J-Pou2f3-/- mice, which lack TCs. Moreover, human minor SG biopsies were evaluated by immunostaining and Poisson regression to identify clinical, serological, and histopathological features correlated with TC abundance. TEM analysis confirmed conserved TC ultrastructure—apical microvilli, a tubulovesicular system, and cytospinules—in both female and male mouse SMGs. Moreover, TC loss was associated with sex-specific transcriptional remodeling (1742 differentially expressed genes in females versus 175 in males), morphological alterations and sex-specific saliva proteomic remodeling. In human minor SG biopsies, TC counts were correlated with salivary flow, serological and histopathology features. In summary, these findings suggest that TCs are regulators of epithelial integrity and potential biomarkers of SG dysfunction.

overall_design: This study compared tuft cells (TCs) across mouse and human salivary glands. In mice, female and male C57BL/6J wild-type and Pou2f3−/− (TC-deficient) submandibular glands were analyzed to test effects of genotype and sex on TC structure/localization (TEM, POU2F3/KRT8 staining), gland architecture (histology), transcriptome (bulk RNA-seq), and salivary function/composition (saliva flow and proteomics). In humans, minor salivary gland biopsies from Sjögren’s disease and non-Sjögren sicca cohorts were immunostained to quantify TC abundance and modeled against salivary flow, autoantibodies, and histopathology features.

first: Michael

last: Rusiniak

first: Lara

last: Shimagami

first: Victor

middle: Z

last: Drummond

first: Mariana

middle: S

last: Santos

first: Fernanda

last: Castro

first: Chao

last: Xue

first: Ming

last: Zhang

first: Jun

last: Qu

first: Mark

last: Maienschein-Cline

first: Tarcilia

last: Silva

first: Silvia

middle: F

last: Sousa

first: Harim

last: Tavares dos Santos


title: In situ single-cell profiling of a brain metastasis from a HER2+ Breast Cancer Patient and 8 primary tumors from TNBC patients.

first: Silvio

last: Bicciato

summary: A key problem in cancer biology is understanding the phenotypic characteristics of the aggressive cell states present in macrometastases and their molecular underpinnings. Here we report on the cellular constituents of  breast cancer metastases,  revealing that these malignant cells display a gene-expression profile associated to embryonic development of tubular organs. Similar properties are found in malignant cells from pro-metastatic primary tumors but not in primary tumors that never metastatize.

overall_design: CosMxTM technology [CosMxTM Human Universal Cell Characterization RNA Panel (1000-plex); Nanostring, USA] was applied on a  5 um FFPE section from archival surgical specimens derived from BC patients in our institution. The following cell surface markers were used for morphology visualization: B2M/CD298, PanCK, CD45, CD3 (metastasis) or CD68 (primary tumors) antibodies and DAPI.

first: Tito

last: Panciera

first: Francesca

last: Zanconato

first: Michelangelo

last: Cordenonsi

first: Stefano

last: Piccolo


title: Molecular characterisation of the metastatic cell state in Breast Cancer

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

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: Refer to individual Series


title: Effect of palmitate treatment on transcriptome in Pompe disease patient fibroblasts

status: Public on Mar 23 2026

city: Paris

first: Ganna

last: Panasyuk

address: 156-160 Rue Vaugirard, Faculté de Médecine Paris Descartes,, 4th Floor - Lab-408/Office-404,, 4th Floor - Lab-408/Office-404,

country: France

institute: Inserm U1151/CNRS UMR 8253, Necker Enfants Malades Institute (INEM)

summary: Lysosomal storage disorders (LSDs) are rare inherited diseases caused by mutations in lysosomal proteins, leading to substrate accumulation and lysosomal dysfunction. Whether this build-up compromises lysosomal membrane integrity remains an open question. In this study, we aimed to investigate the presence of lysosomal membrane damage in LSD cells and to identify mechanisms that could reveal potential therapeutic strategies for amelioration of cellular physiology. Methods: Primary skin fibroblasts from Pompe disease patients were used to evaluate lysosomal integrity and function. Pharmacologic and metabolite treatments were applied in loss-of-function and rescue analyses, and transcriptomics analysis was done under these conditions. Results: In Pompe disease, caused by mutations in the acid alpha-glucosidase gene, glycogen accumulation, palmitate treatment improved lysosomal function in fibroblasts from patients, with no significant effect at transcriptional level. Conclusions: These findings open to novel therapeutic opportunities for improvement of lysosomal function through development of treatments that target fatty acid metabolism.

overall_design: Skin fibroblasts of a Pompe disease patient were treated for 24 hours with BSA-palmitate (200 µM) compared to treatment by fatty acid-free BSA (BSA), followed by PE-100 Poly-A enriched RNA-seq  (n=2-3 replicates).

first: Edouard

last: Le Guillou

first: Arianna

last: Segaloni

first: Alexis

last: Gadault

first: Nathaniel

last: Henneman

first: Min

last: Su

first: Ivan

last: Nemazanyy

first: Catia

last: Oliveira Dias

first: Nesrine

last: Hifdi

first: Valérie

last: Nivet-Antoine

first: Michael

last: Laemmerhofer

first: Karim

last: Hnia

first: Catherine

last: Caillaud


title: Milk Fat Globule EGF and Factor V/VIII Domain Containing (MFGE8) as a Novel Player in Equine Endometrial Fibrosis

city: Neustadt am Rübenberge

first: Claudia

last: Klein

state: Lower Saxony

address: Höltystraße 10

department: Biotechnology

institute: Friedrich-Loeffler-Institut

summary: Effects of TGF β1 and MFGE8 on equine endometrial fibroblasts in vitro were investigated by single cell sequencing. Single cell sequencing revealed a certain degree of heterogeneity among cultured fibroblasts. TGF β1 exposure of fibroblasts confirmed its profibrotic effects by altered expression of transcripts associated with extracellular matrix remodeling, the upregulation of growth factors, e.g. platelet-derived growth factor B, while downregulating interferon alpha, beta, and gamma signaling. MFGE8 treatment effects were subtler, including decreased profibrotic leukemia inhibitory factor expression and an upregulation of interferon alpha and beta signaling in a subset of cells. In a fibroblast subpopulation, upregulation of phosphatase and tensin homolog signaling, indicated an antifibrotic effect of MFGE8.

overall_design: Equine endometrial fibroblasts (n=4) were seeded onto collagen-coated hydrogels 12-well plates. From 48 hours to 72 hours (treatment phase), cells were incubated using cell culture medium containing 0.1% BSA and and received either (1) no further supplementation (control) (2) were supplemented with 10 ng/ml human recombinant TGF-β1 or (3) were supplemented with 10 ng/ml mouse recombinant MFGE8. Following 24 hours of incubation, cells were harvested and processed for single cell sequencing using the Chromium Next GEM Single Cell 3’Reagent Kits v3.1, Dual Index (10x Genomics, CA, USA). Resulting libraries were subjected to paired-end (100 bp) sequencing as multiplexed pools on a NovaSeq 6000 using an S4 Reagent Kit v1.5 4XP (290 pM, 200 cycles; Illumina, CA, USA).

first: Elena

last: zu Klampen

first: Gregor

last: Neufeld


title: APOE4 expression causes distinct effects on meningeal immunity, brain lipid composition, and cognition in male and female mice

city: Jacksonville

first: Sandro

last: Da Mesquita

state: FL

address: 4500 San Pablo Road

institute: Mayo Clinic

summary: This experiment was designed to understand the distinct effects of sex and APOE genotype on the transcriptome of meningeal dural vascular and resident immune cells. After transcardiac perfusion with a buffered saline solution containing heparin and actinomycin D, meningeal dural whole mounts were immediately dissected from the skulls of 12-month-old male and female mice expressing APOE3 or APOE4 and digested into a single-cell suspension. After enrichment for CD31+ cells via positive selection using MACS, the cells were counted and approximately 5000 cells per sample were used to obtain single-cell gene expression libraries using 10x Genomics equipment and reagents, namely the Chromium Single Cell 3' Reagent Kits. The generated libraries were sequenced in 2 lanes of a NovaSeq 6000 S4 PE100 flow cell.

overall_design: scRNAseq of MACS-enriched (CD31+), mouse, meningeal dura expressing APOE3 or APOE4, given a control or PLX5622 diet, in males and females


title: A blood-brain barrier-like vascular gate limits immunotherapy efficacy in neuroendocrine cancers

city: Chengdu, China

first: Ailing

last: Zhong

state: Sichuan

address: No.17 Renmin road section3

department: State Key Laboratory of Biotherapy, West China Hospital, Sichuan University.

institute: Sichuan University

summary: Small cell lung cancer (SCLC), a highly aggressive neuroendocrine malignancy, is among the most immune-desert tumor types and exhibits poor response to immunotherapy. However, the mechanisms underlying this immune resistance remain unclear. Here, we identify a unique immune-excluding vascular (IEV) barrier in SCLC, distinct from non-small cell lung cancer (NSCLC) and other cancers, composed of tightly connected endothelial cells, a thickened basement membrane, and dense pericyte coverage. Functionally, this barrier restricts immune cell infiltration, contributing to SCLC’s immunotherapy resistance. Mechanistically, we show that ASCL1, the master transcription factor of SCLC, is essential for IEV barrier formation. ASCL1 drives expression of insulin-like growth factor-binding protein 5 (IGFBP5), and depletion of IGFBP5 in tumor cells reduces IGF1 signaling in endothelial cells. Endothelial-specific disruption of IGF1R impairs barrier integrity. Importantly, targeting this axis either through IGFBP5 knockout or treatment with the IGF1R inhibitor OSI-906 enhances CD8+ T cell infiltration and synergizes with anti-PD1 therapy in SCLC. Furthermore, we demonstrate that this ASCL1-IGFBP5-IGF1R axis and the IEV barrier are conserved across multiple neuroendocrine cancers (NECs). Our findings reveal a previously unrecognized vascular barrier in NECs and propose novel therapeutic strategies to overcome immune exclusion and enhance immunotherapy efficacy in these recalcitrant cancers.

overall_design: SCLC tumor organoids with Igfbp5 knockout were orthotopically or subcutaneously transplanted into mice, and the resulting tumors were used to examine the effects of tumor cell-intrinsic Igfbp5 loss on vascular endothelial cell phenotypes. Tumor-bearing mice were further subjected to anti-PD-1 treatment to assess changes in immune cell infiltration and treatment response. In addition, mice bearing SCLC tumors were treated with OSI-906 in combination with immunotherapy, and tumor tissues were collected for single-cell RNA sequencing to investigate how blockade of the IGFBP5–IGF1/IGF1R axis remodels endothelial and immune cell states.

first: Yiyun

last: Wang


title: Promoter mutagenesis and a massively parallel reporter screen of the MAPT locus identifies cis-regulatory elements and genetic variation effects

city: Huntsville

first: Jesse

middle: Nicholas

last: Cochran

state: AL

address: 601 Genome Way

institute: HudsonAlpha Institute for Biotechnology

first: Nicholas

first: Rebecca

middle: M

last: Hauser


title: HER2 heterogeneous breast cancer models reveal novel therapeutic targets and subclonal dynamics during evolution to resistance to HER2-targeted therapies

status: Public on Mar 20 2026

city: Boston

first: Kornelia

last: Polyak

address: 450 Brookline Ave. S1070

institute: Dana-Farber Cancer Institute

summary: Intratumor heterogeneity for HER2 expression and amplification, observed in up to 40% of HER2-positive breast cancer is a driver of resistance to HER2-targeted therapies. The advancement of treatment for HER2 heterogeneous tumors has been hindered by the lack of preclinical models that accurately replicate the human disease. Here we describe human HER2 heterogeneous breast cancer cell models composed of ERBB2 amplified (HER2hi) and non-amplified (HER2lo) cell populations derived from the same tumor. Utilizing these models and cellular barcoding technology, we provide evidence for subclonal cooperation between HER2hi and HER2lo subpopulations and that HER2lo cells drive resistance to HER2-targeting antibody-drug conjugates (ADC) such as T-DXd but are sensitive to HER2 kinase inhibitors. CRISPR screens in heterogeneous co-cultures identified sensitizers of HER2lo cells to T-DXd including the USP9X deubiquitinating enzyme. USP9X inhibition enhances the lysosomal targeting of HER2 to potentiate ADC payload release, diminishing tumor recurrence after T-DXd treatment. Our results elucidate the functional relevance of HER2 heterogeneity and propose improved therapies for these tumors.

overall_design:
(1) RNAseq: HER2 heterogeneous and HER2-targeted therapies resistant cells
HCC1954, 21NT, and 21PT cells were sorted into HER2hi and HER2lo populations according to their HER2 expression levels. Also, resistant cells for T-DXd, T-DM1, neratinib and tucatinib were generated from the same parental cell lines.
RNA from growing cells was extracted.

(2) scRNA-seq of two human HER2+ breast cancer primary tumors
Primary tumors were digested and stored frozen before performing 10X library preparation for scRNA-seq (20,000 read pairs/cell for 5' Gene Expression Dual Index library)

first: Marie-Anne

last: Goyette


title: NAC promotes co-translational protein folding at the ribosomal tunnel exit

city: Heidelberg

first: Manuel

last: Günnigmann

address: Im Neuenheimer Feld 282

institute: ZMBH

summary: The nascent polypeptide-associated complex (NAC) is crucial for protein biogenesis, coordinating enzymatic modifications and membrane targeting of nascent chains at the ribosomal tunnel exit. However, its role in co-translational folding remains unclear. Here, we report the genome-wide profiling of NAC interactions with nascent chains in human cells, demonstrating that it correlates with emerging segments of folded domains of cytonuclear proteins. Single-molecule and structural analyses revealed that NAC’s b-barrel domain dynamically interacts with the ribosome and emerging chains at the tunnel exit, presumably facilitating initial compaction and early folding, and that NAC binding promotes native folding of proteins. Additionally, we uncovered compartment-specific nascent chain interactions of NAC, supporting it’s role in targeting proteins to the endoplasmic reticulum and in mitochondrial membrane protein biogenesis. Together, these findings establish NAC as a bona fide co-translational chaperone that facilitates early protein folding at the ribosomal tunnel exit, expanding its functional repertoire in protein biogenesis.

overall_design: Selective ribosome profiling (SeRP) of the human nascent polypeptide-associated complex (NAC). NAC subunits (NACA and BTF3) were purified either from a cell lysate or from sucrose cushion purified ribosomes. In addition, soluble ribosome profiling (SolubleRP) was performed in human cells to analyze ribosome engagement with membranes. All experiments were performed in two biological replicates. Ribosome profiling experiments were performed on HEK293T cells containing an NACβ auxin inducible degradation system. Briefly, a GS linker-miniIAA7-GFP11 sequence was inserted at residue 176 of endogenous BTF3 via CRISPR/Cas9-mediated homology-directed repair in cells stably expressing AtAFB2. Cells were seeded on 10 cm dishes 48 hours prior to harvest to ensure an 70-80% confluency at the time of collection. Cells were treated with 100 μg/mL indole-3-acetic acid sodium (Santa Cruz, sc-215171) for 9 hours prior to harvesting. Untreated cells were used as a control. All experiments were performed in two biological replicates.

first: Jaime

last: Santos

first: Radoslaw

last: Gora

first: Marija

last: Iljina

first: Masa

last: Predin

first: Ilgin Eser

last: Kotan

first: Pratiman

last: De

first: Dhawal

last: Choudhary

first: Juwon

last: Jang

first: Frank

last: Tippmann

first: Nenad

last: Ban

first: Sander

last: Tans

first: Shu-ou

last: Shan

first: Günter

last: Kramer

first: Bernd

last: Bukau


title: p53 safeguards chemical reprogramming of human somatic cells towards pluripotency.

city: Beijing

first: Jingxiao

last: Cao

state: Beijing

address: No.5 Yiheyuan Road, Yanyuan Street, Haidian District, Beijing

department: Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, China.

institute: Peking University


title: p53 safeguards chemical reprogramming of human somatic cells towards pluripotency [scRNA-seq]

summary: Cell fate manipulation is powerful for generating desired cell types through reprogramming, such as induced pluripotent stem cells (iPSCs), with broad biological applications. However, reprogramming can be risky due to dramatic changes in cell identity, necessitating strict regulation to ensure safety and efficacy. p53 is essential for maintaining genome stability to prevent abnormalities induced by changes of cell states, which however, functionally counters Yamanaka factors for efficient reprogramming. Thus, delicately balancing p53 activity for efficient reprogramming with highly quality has proven challenging. Here, we demonstrate that efficient human chemical reprogramming is safeguarded by p53, in distinction from Yamanaka factors-mediated reprogramming. Suppressing p53 activity unexpectedly and substantially hinders the generation of chemically induced pluripotent stem cells (CiPSCs). Notably, p53 precisely regulates the mesenchymalization occurred at the early reprogramming stage where cell plasticity is re-established and curbs excessive epithelial-mesenchymal transition (EMT). Furthermore, the retinoid acid receptor agonist, TTNPB, leverages p53’s anti-metastatic functions to facilitate CiPSC generation by activating BTG2. Our results demonstrate that p53 activity distinguishes chemical reprogramming from Yamanaka factors-mediated reprogramming, and offer a promising strategy that delicately balances p53 with reprogramming for both safe and efficient cell fate manipulation.

overall_design: To characterize samples during  human chemical reprogramming by scRNA-Seq.


title: p53 safeguards chemical reprogramming of human somatic cells towards pluripotency [bulk RNA-seq]

overall_design:
To characterize samples during  human chemical reprogramming by RNA-seq.
C, 6, N, A, J are abbreviations for five small chemical molecules. Their full names are CHIR, 616452, TTNPB, Akt, and JNKIN8, respectively.

(bulkRNA_4)  To characterize samples during human chemical reprogramming by RNA-seq.


title: p53 safeguards chemical reprogramming of human somatic cells towards pluripotency [CRISPR]

overall_design: For the functional verification of p53 downstream genes, somatic cells were transfected with lentiviral vectors containing Cas9-sgRNA libarary targeting p53 targeted genes and subjected to chemical reprogramming. Genes depleted in CiPSCs represented the p53 downstream genes that required for chemical reprogramming.


title: Microfluidic technology for low-input mapping of genome-wide lncRNA-chromatin interactions using tissue samples

status: Public on Mar 22 2026

city: Blacksburg

first: Chang

last: Lu

state: VA

address: 235 Goodwin Hall, 635 Prices Fork Road, Virginia Tech

department: Chemical Engineering

institute: Virginia Tech

summary: Long noncoding RNAs (lncRNAs) regulate gene expression through binding to DNA, various RNAs, and proteins, playing potentially important but poorly understood roles in development and diseases. Existing approaches for profiling lncRNA–chromatin interactions at the genome scale require large quantities of input material (e.g., 100 million cells per assay). Applying these technologies to tissue samples has been challenging especially when examination of a specific cell type is desired. Here we demonstrate a low-input microfluidic technology based on Chromatin Isolation by RNA purification (ChIRP) process for mapping lncRNA–chromatin interactions using as few as 50,000 cells. We validate our technology on two lncRNAs of different sizes in human and mouse cell lines and brain tissue. We apply our technology muChIRP-seq to neuronal nuclei from postmortem human brain tissues and integrate our data with histone and RNA-seq data to understand the role of lncRNA in the epigenomic and transcriptomic landscape of schizophrenia. MuChIRP-seq enables the mapping of lncRNA–chromatin interactions in tissue samples and in a cell-type-specific fashion, unlocking new opportunities to study lncRNA-mediated gene regulations.

overall_design: To test the capabilities of muChIRP-seq, bulk ChIRP-seq (Chu et al. Molecular Cell 44 (2011) 667-678) was performed for the lncRNA TERC in HeLa cells and was compared to data collected with muChIRP-seq using 1 million, 500K, 250K, 100K, and 50K cells of input. To further test the method, muChIRP-seq data was collected for the lncRNA Gomafu in NE-4C for 500K, 250K, 100K, and 50K cells of input and in HeLa for 100K cells of input. To test performance in cell-type specific tissue, muChIRP-seq was performed for the lncRNA TERC in FACS-sorted NeuN+ and NeuN- nuclei from mouse cortex tissue from 80-week old mice. As a proof-of-concept study, muChIRP-seq for the lncRNAs TERC and Gomafu was performed on NeuN+ nuclei from prefrontal cortex (PFC) tissue of 7 schizophrenia patients (SCZ) and their matched controls (CNTRL).

first: Jenna

last: Catalano


title: RNAseq analysis of Tox3 dependent gene expression in the mouse cerebellum

status: Public on Mar 19 2026

city: SAN FRANCISCO

first: Xiaoxin

last: Chen

state: California

address: 555 mission bay blvd. south, RM382A

department: Cardiovascular Research Institute

institute: University of California, San Francisco

summary: Organ development relies on precise transcriptional control, yet how lineage-defining factors like Atoh1/Math1 drive robust gene expression despite weak intrinsic transactivation activity remains unclear. Here, we present a comprehensive atlas profiling 1,904 transcription regulators across organs, uncovering TOX3 as a potential co-activator of Atoh1 in cerebellar granule neuron progenitors. Tox3-deficient mice display severe ataxia and cerebellar hypoplasia, driven by depletion of granule neuron progenitors, diminished Atoh1 expression, and impaired primary cilia. Single-nucleus RNA-seq analyses reveals compromised maintenance of the progenitor pool. TOX3 is also highly expressed in subsets of medulloblastoma, and its deletion reduces cerebellar neoplasia and prolongs survival in a mouse model. Mechanistically, Tox3 and Atoh1 co-occupy and synergistically activate E-boxes in shared target genes by up to 120-fold, including an ultra-conserved E-box downstream of Atoh1. These findings establish Tox3 as a critical Atoh1 co-activator in cerebellar development, tumorigenesis and evolution, and provides a resource for exploring novel transcriptional regulators in progenitor maintenance and organogenesis.

overall_design: RNA-seq profiling of control and Tox3 neuronal conditional knockout mice cerebellum at day1 after birth.

first: Chen

last: Xiaoxin

first: Huang

middle: N

last: Guo


title: Spatial transcriptomics identifies IL-32 as a lipid droplet-associated cytokine linked to tubular injury in human diabetic kidney disease

status: Public on Mar 24 2026

city: Calgary

first: Justin

last: Chun

state: Alberta

address: 3330 Hospital Drive NW

institute: University of Calgary

summary: Diabetic kidney disease (DKD) is a severe complication of diabetes mellitus and the leading cause of chronic kidney disease worldwide. Among the many drivers of tubular injury, lipid accumulation and inflammation are emerging as major contributors to kidney disease progression, but the molecular link between lipid metabolism and inflammatory signaling remains to be determined. Kidney biopsies from patients with DKD across pathologic classes were labelled for lipid droplets and analyzed by Nile Red spectroscopy. Digital spatial profiling and single-cell spatial transcriptomics were performed on samples from 14 patients representing different DKD classes. RNA scope and immunofluorescence microscopy were used for data validation and characterization. Lipid droplets (LD) were increasingly abundant in advanced stages of DKD, primarily accumulating in the proximal tubules. Single-cell spatial transcriptomics identified several genes—DUSP5, AZU1, COL9A1, HSPB1, and IGFBP7—as highly upregulated in DKD. Remarkably, IL32, which encodes a LD-associated cytokine, was highly enriched in injured proximal tubules. Immunofluorescence confirmed IL-32 localization to LDs predominantly within KIM1 positive tubules in moderate to advanced DKD. Furthermore, injured IL-32 expressing tubules were in close proximity to infiltrating neutrophils and macrophages, immune effectors of non-resolving inflammation and kidney disease progression. IL-32 is a LD-associated cytokine upregulated during tubular injury that represents a potential link between lipid dysregulation, inflammation and progression in human DKD.

overall_design: 14 human patient kidney biopsy samples ranging in DKD classification from non-disease controls to Class IV DKD. The NanoString CosMx spatial molecular imager was used to assay a 1000-plex CosMx Human RNA panel with the addition of kidney-specific genes: APOL1, AQP1, AQP2, CLDN10, EMCN, HAVCR1, LRP2, NOS1, NPHS1, PALMD, PIEZO2, PLVAP, PROM1, PROX1, REN, SCN2A, SH3GL3, SLC12A1, SLC12A3, SLC14A2, SLC26A4, SLC26A7, SLC4A9, SLC5A12, SLC5A2, SLC7A13, SLC8A1, SYN1, UNC5D. Morphology visualization from upfront staining was performed using CD298, B2M, PanCK, CD45, and/or CD68 and DAPI.

first: Kieran

last: Meadows

first: Hyunjae

last: Chung

first: Son

last: Vo

first: Aysa

last: Imanzadeh

first: Heewon

last: Seo

first: Sisay

middle: G

last: Belay

first: Asha

last: Swamy

first: Wulin

last: Teo

first: Kevin

last: Chapman

first: Graciela

last: Andonegui

first: Hallgrimur

last: Benediktsson

first: Peter

middle: K

last: Stys

first: Thang

last: Pham

first: Daniel

last: Muruve


title: CITEgeist: Cellular Indexing of Transcriptomes and Epitopes for Guided Exploration of Intrinsic Spatial Trends

city: Pittsburgh

first: Alexander

middle: Chih-Chieh

last: Chang

state: PA

address: 5051 Centre Ave

institute: University of Pittsburgh

summary: Spatial transcriptomics provides insights into tissue architecture by linking gene expression with spatial localization. Current deconvolution methods rely heavily on single-cell RNA sequencing (scRNA-seq) references, which are costly and often unavailable, especially if the tissue under evaluation is limited as in a core biopsy specimen. We present a novel tool, CITEgeist, that deconvolutes spatial transcriptomics data using antibody capture from the same slide as the reference, directly leveraging cell surface protein measurements from the same tissue section. This approach circumvents the limitations of scRNA-seq as a reference, offering a cost-effective and biologically grounded alternative. Our method employs mathematical optimization to estimate cell type proportions and gene expression profiles, incorporating sparsity constraints for robustness and interpretability. Benchmarks against state-of-the-art deconvolution methods show improved accuracy in cell type resolution, particularly in dense tumor microenvironments, while maintaining computational efficiency. This antibody-based tool advances spatial transcriptomics by providing a scalable, accurate, and reference-independent solution for deconvolution in complex tissues. We validate this tool by using a combined approach of simulated data and clinical samples by applying CITEgeist to translational pre-treatment and post-treatment ER+ breast tumors from an ongoing clinical trial, emphasizing the applicability and robustness of CITEgeist.

overall_design: 12 breast cancer samples from 6 patients (pre-endocrine therapy biopsy samples and matched post-primary-endocrine therapy surgical samples) were used for analysis

middle: C

first: Brent

middle: T

last: Schlegel

first: Neil

last: Carleton

first: Priscilla

last: McAuliffe

first: Steffi

last: Oesterreich

first: Russell

last: Schwartz

first: Adrian

middle: V

last: Lee


title: SP1 antagonizes H3K27me3 to shape chromatin landscapes for RNA polymerase II recruitment during gastrulation [RNA-seq]

city: chongqing,china

first: xipeng

last: shen

address: yixueyuan road NO.1

department: basic medicine

institute: CQMU

summary: Following implantation, the epiblast undergoes gastrulation to form the three germ layers, a process requiring precise temporal control of developmental gene expression. However, the mechanisms governing RNA polymerase II (Pol II) engagement at developmental gene promoters during this critical stage remain poorly understood. Here, we present a genome-wide analysis of Pol II occupancy in mouse post-implantation embryos, revealing that nearly half of bivalent promoters are bound by Pol II in a lineage-specific and temporally ordered manner. This recruitment follows a stepwise chromatin remodeling cascade, with initial deposition of H3K27me3, followed by H3K4me3 acquisition and Pol II engagement. Through genetic perturbation, we show that KMT2B promotes Pol II loading via H3K4me3 deposition, whereas the Polycomb component EED restricts this process by maintaining H3K27me3. Notably, we identify the transcription factor SP1 as a critical facilitator of Pol II recruitment at bivalent loci. SP1 binding coincides with reduced H3K27me3 levels and enhanced Pol II occupancy, and its loss leads to chromatin re-silencing and transcriptional failure. Together, our findings establish a chromatin-based regulatory framework in which SP1 and histone modifications cooperatively license the transcriptional activation of developmental genes during germ layer formation.

overall_design: To evaluate the gene expression level in different germ layers in E6.5 and E7.5 embryos, Smart-seq2 was perform in normal development embryos as well as in gene knockout E6.5 epiblast including Jarid2, Kmt2b, Eed and Sp1 with control.

first: Xipeng

last: Shen

first: Yuting

last: Wen

first: Yunlong

last: Xiang


title: Phenotypically similar but functionally distinct NK cell populations within the human maternal-fetal interface

status: Public on Mar 18 2026

city: Brest

first: Marie

last: Frutoso

address: 9 rue Félix le Dantec

institute: LBAI, UMR1227

summary: Natural Killer cell function within tissues extends beyond exerting cytotoxicity, encompassing a range of functions that are just starting to become fully elucidated. In the context of human placentation, NK cells play a key role in enabling initial placentation, which is associated with the acquisition of tolerance-like properties. If and to which extent NK cells maintain these tolerance-like properties over the course of human pregnancy is still poorly understood. We have employed a single-cell sequencing approach using the BD RhapsodyTM system to study the transcriptomic profile of Natural Killer (NK) cells in the decidual-placental interface (DPI) and the decidua (in comparison to NK cells from the maternal circulating blood and the cord blood). We found that NK cells from both location had similar transcriptional profile with the presence of resident NK cells. Yet, when stimulated in vitro, CD103+CD69+ tissue-resident NK cells exhibited distinct effector function from one another. Together, our findings reveal the presence of distinct functional resident NK cell populations in two anatomically adjacent tissues at healthy full-term pregnancies.

overall_design: Immune cell  characterization utilizing targeted single cell RNA sequencing paired with oligo tagged antibodies using the BD Rhapsody/ AbSeq system. In details, cells from maternal blood, cordblood, DPI and decidua from healthy donors and patients who experienced chorioamnionitis were stained with a cytometry panel and one specific oligo-protein-tag for multiplexing (BD Biosciences SMK). Live, CD45+ immune cells were sorted (using the BD Symphony S6 cell sorter equipped with a 70um nozzle for batches 1 and 2 and the FACSAria III equiped with a 100um nozzle). For batches 1 and 2, Live CD45+ cells were enriched for ILC (CD45+CD19-CD14-CD3-CD127+CD34-), NK cells (CD45+CD19-CD14-CD3-CD127-NKp46+) and myeloid cells (CD45+CD3-CD19-NKp46-HLA-DR+).  For batch 3 CD45+ were sorted without enrichment of specific cell type. After sorting, cells from all donors and tissues were pooled and stained with 56 oligo-proteins. Stained cells were then loaded on the BD Rhapsody cartridges (between 35 - 45,000 cells were loaded per cartridges). Cells from the 1st batch (comprising 2 donors and the 4 tissue types) were split into 4 cartridges and sequenced once. Cells from the 2nd batch (comprising 2 donors and the 4 tissue types) were split into 3 cartridges and sequenced once. Cells from the 3rd batch (comprising 4 donors with DPI only) were split into 4 cartridges and each cartridge was sequenced twice.

first: Martin

last: Prlic

first: Caitlin S

last: DeJong


title: HER2-Specific Synthetic Antigen Receptor (SAR) T Cell Therapy Synergizes with Radiotherapy to Provide Improved Anti-Tumor Efficacy in Non-Small Cell Lung Cancer (NSCLC)

city: Hamilton

first: Theodoros

last: Tsakiridis

address: 699 Concession St

institute: McMaster University

summary: In non-small cell lung cancer (NSCLC), radiotherapy not only mediates cytotoxicity but also activates radioresistance drivers like HER2. We investigated radiotherapy combined with HER2-targeted T cell therapy in an NSCLC model. The antitumor efficacy of radiotherapy and engineered T cells expressing a DAP12-associated synthetic antigen receptor (SAR) targeting HER2 was evaluated in HER2-expressing A549 xenografts. HER2 modulation, transcriptional regulation, and tumor T cell infiltration were assessed using immunoblotting, realtime quantitative polymerase chain reaction, flow cytometry, RNA-seq, and immunohistochemistry. High-dose HER2-SAR T cell infusion abolished A549 tumor growth but induced graft-vs-host disease. Low-dose T cell infusion was well-tolerated and provided partial tumor inhibition. Induction radiotherapy (7 d before T cell infusion) synergistically improved tumor control and survival. Radiotherapy transiently upregulated HER2 expression (4 to 24 h), though administering HER2-SAR T cells within this window did not enhance antitumor efficacy. Radiation did not enhance T cell-mediated cytotoxicity in vitro. However, in tumors, radiotherapy increased intratumoral proliferation and accumulation of HER2-SAR T cells and enhanced the extrinsic apoptotic pathway, including induction of Fas transcript and protein levels and cleaved caspase-3 (CC3). RNA-seq of irradiated tumors revealed lasting transcriptional reprogramming with increased immune activation and decreased proliferation and oncogenic signaling. Induction radiotherapy enhances HER2-SAR T cell infiltration and provides synergistic tumor suppression, likely through additional activation of immune-mediated apoptosis. These findings support further assessment of HER2-SAR T cell therapy in HER2-expressing NSCLC.

overall_design: Total RNA was isolated from enhanced firefly luciferase (Luc)-expressing A549 tumors grown in NRG mice. Tumors from three biological replicates were treated with either 0Gy (control) or 5Gy (treatment) radiotherapy and harvested either 24h or 7 days post-treatment. In total, 12 samples were analyzed: 3x24h post-0Gy, 3x24h post-5Gy, 3x7d post-0Gy and 3x7d post-5Gy.

first: Olga-Demetra

last: Biziotis

first: Christopher

last: Silvestri

first: Allyson

middle: E

last: Moore

first: Russta

last: Fayyazi

first: Simon

last: Wang

first: Elham

last: Ahmadi

last: Del Rosso

first: Amr

last: Ali

first: Evangelia

last: Baker

first: Craig

middle: W

last: Aarts

first: Bojana

last: Bojovic

first: Joanne

last: Hammill

first: Gregory

middle: R

last: Steinberg

first: Jonathan

last: Bramson


title: Ancestral Bisphenol A Exposure Induces Sexually Dimorphic Nonalcoholic Fatty Liver Disease Through Transgenerational Transmission of Sperm Gene Body CpG Island Methylation

city: Columbia

first: Ramji

last: Bhandari

state: MO

address: 1200 University Ave

department: Division of Biological Sciences

institute: University of Missouri

type: Methylation profiling by high throughput sequencing

summary: Environmentally induced heritable disease phenotypes involve intergenerational transmission of germline epigenetic alterations (epimutations), yet how epimutations establish a sex-biased metabolic disease in descendants remains unclear. Here, we demonstrate using bisphenol A as an environmental stressor and medaka as an organismal model that environmentally induced heritable sexually dimorphic nonalcoholic fatty liver disease (NAFLD) involves intergenerational transmission of stable sperm DNA methylation memories. Environmental stress was pronounced in females which included severe macrovesicular steatosis with 5,376 differentially expressed genes (DEGs), enrichment for human NAFLD signatures, dysregulated clinically validated biomarkers, and suppressed mitochondrial electron transport chain genes, whereas males showed attenuated microvesicular steatosis with only 306 DEGs. Promoter hypermethylation accompanied silenced key hepatic master regulators, HNF4A in female livers and SREBF1 in male livers. Whole‑genome bisulfite sequencing revealed twice as many differentially methylated regions (DMRs) in females versus males, enriched in exons, 3′ UTRs, and gene-body CpG-islands versus promoters, indicating non‑promoter‑centric regulation. Critically, intergenerational sperm analysis revealed 61 gene-body CpG-island DMRs persisting across F0 sperm, F1 sperm, and F2 livers, with mTOR signaling emerging uniquely in F2 liver consistent with nutrient-sensing dysregulation and lipogenesis, while Notch signaling was exclusively enriched in F2 females, aligning with fibrogenic progression. These findings establish gene-body CpG-island methylation as a principal conduit for sex‑specific transgenerational epigenetic inheritance linking environmental stressor to liver disease.

overall_design: Whole-genome bisulfite sequencing (WGBS) was performed on the sperm from three biological replicates of both BPA and control lineages of Medaka fish from the F0 and F1 generations. Additionally, WGBS was conducted on the liver tissue of three biological replicates of male and female Medaka fish from the F2 generation for both BPA and control lineages.

first: Sourav

last: Chakraborty

first: Santosh

last: Anand


title: Chromatin occupancy by Tox3 in mouse cerebellum

first: Xiaoxin

last: Chen

overall_design: ChIP-seq of TOX3 in control and Tox3 neuronal conditional knockout mice cerebella at postnatal day 1.

first: Chen

last: Xiaoxin

first: Huang

last: Guo


title: APOBEC3B regulates HPV replication by inducing R-loop formation and genomic instability [RNA-Seq]

status: Public on Mar 17 2026

city: Chicago

first: Conor

last: Templeton

address: 300 E Superior Street

institute: Northwestern University

summary: APOBECs are cytidine deaminases whose levels are increased in cells with high-risk HPV genomes and are responsible for most mutations in HPV associated cancers. APOBEC3B is a nuclear member of this family and is shown to be a positive regulator of HPV replication as well as expression. The proviral effects of A3B found in HPV positive cells contrast with its role as a restriction factor for many other viruses. Studies demonstrated that A3B can bind and regulate the formation of R-loops, which are trimeric nucleic acid structures consisting of an RNA paired with its complementary DNA strand, displacing one of the DNA strands. The present study demonstrates that A3B binds stably to both cellular and viral chromatin at sequences containing high R-loop levels, including the HPV URR and early polyadenylation sites. Importantly, A3B was found to play a critical role in the replication of HPV genomes and in regulating viral expression. Reduction of R-loop levels through overexpression of the R-loop specific RNase, RNase H1, impaired A3B binding to viral genomes as well as at multiple cellular sites. When A3B was depleted, total R-loop levels decreased by ~50%, leading to impaired viral transcription and an increase in the expression of immune genes, such as OASL, IL6, and IRF1. Mapping R-loop formation in A3B depleted cells revealed that A3B regulated a subset of R-loops that form on the transcriptional start (TSS) and termination sites (TTS) of cellular genes, including at the HPV URR.  Furthermore, A3B depletion resulted in over a 50% reduction of DNA breaks along with altered expression of DNA damage repair proteins. This study demonstrates that A3B is an inducer of R-loop formation and genomic instability in HPV positive cells, thereby regulating cellular and viral gene expression along with HPV replication.

overall_design: RNA-Seq profiling of shAPOBEC3B (shA3B01 is sample3 and sample4, and shA3B11 is sample5 and sample6) knockdowns of CIN612 cells compared to a shScramble control (sample1 and sample2).

first: Conor W.

first: Jasmine S.

last: Gulik

first: Laimonis A.

last: Laimins


title: Single-nucleus RNA-seq analysis of Tox3 dependent gene expression in the mouse cerebellum

overall_design: single-nucleus RNA-seq profiling of control and Tox3 neuronal conditional knockout mice cerebella at postnatal day 1.


title: Prolactin, cortisol, and extracellular osmolality regulate cftr, ostf1, and sgk1 in tilapia ionocytes

city: Saratoga Springs

first: Jason

last: Breves

state: New York

address: 815 N. Broadway

department: Biology

institute: Skidmore College

summary: Objective: Euryhaline fishes can inhabit salinities ranging from fresh water (FW) to seawater (SW), in part because their endocrine system aligns the ion-transporting capacities of branchial ionocytes with the external environment. Ionocytes also directly sense extracellular osmolality and adjust their functions accordingly; therefore, this study investigated the interplay between osmotic conditions and osmoregulatory hormones in Mozambique tilapia (Oreochromis mossambicus) to further elucidate the basis of euryhalinity. We sought to determine whether prolactin (Prl) supports FW acclimation by counteracting osmotic and hormonal signals that initiate branchial responses to SW environments. Methods: We first combined hypophysectomy, hormone replacement, RNA-Seq, and qPCR to identify cystic fibrosis transmembrane conductance regulator (cftr), osmotic stress transcription factor 1 (ostf1), and serum- and glucocorticoid-inducible kinase 1 (sgk1) as Prl-repressed genes. We then leveraged a series of in vivo and in vitro experimental paradigms to characterize their regulation by environmental salinity, Prl, cortisol, and extracellular osmolality. Results: Our findings indicate that 1) Prl’s capacity to antagonize cortisol-stimulated cftr expression depends on extracellular osmotic conditions; 2) Prl and cortisol play opposing roles in regulating branchial ostf1 expression; 3) Sgk1 is expressed in ‘SW-type’ ionocytes, where interactions among Prl, cortisol, and osmotic conditions influence its expression; and 4) Prl promotes the expression of Na+/Cl- cotransporter 2 and Clc family Cl− channel 2c, as shown previously. Conclusions: The combined actions of osmotic stimuli, Prl, and cortisol shape the branchial expression of cftr, ostf1, and sgk1. While hyperosmotic extracellular conditions and cortisol promote the activation of these genes during SW acclimation, Prl supports FW adaptation by simultaneously suppressing these genes and promoting processes underlying active ion uptake. Thus, euryhaline tilapia adjust the ion-transporting activity of their branchial ionocytes to meet environmental demands by integrating multiple regulatory cues.

overall_design: RNA-Seq analysis of gill filaments collected from hypophysectomized male tilapia (80-110 g) following IP-injection with ovine prolactin (5 ug/g body weight) or saline vehicle. Hypophysectomy was performed by the transorbital technique (see Nishioka, 1994 and Breves et al., 2010).

first: Ming-Wen

last: Hu

first: Mayu

last: Inokuchi

first: Lucia

middle: A

last: Seale

first: Andre


title: A transcription regulator atlas identifies TOX3 as an Atoh1 co-activator in cerebellar development and tumorigenesis

summary: Organ development and function are orchestrated by intricate transcriptional circuits. Here, we present a comprehensive atlas profiling 1,904 transcription regulators in the brain, cerebellum, heart, kidney, liver, ovary, and testis of fetal, neonatal and adult mice. Using this dataset, we uncover TOX High Mobility Group Box Family Member 3 (TOX3) as a potential co-activator of Atoh1 in cerebellar granule neuron progenitors. Tox3-deficient mice display severe ataxia and cerebellar hypoplasia, driven by depletion of granule neuron progenitors, diminished Atoh1 expression, and impaired primary cilia. Single-nucleus RNA-seq analyses reveals compromised maintenance of the progenitor pool. TOX3 is also highly expressed in subsets of medulloblastoma, and its deletion reduces cerebellar neoplasia and prolongs survival in a mouse model. Mechanistically, how lineage-defining factors such as Atoh1 drive robust gene expression despite weak intrinsic transactivation activity remains unclear. We show that Tox3 physically associates with Atoh1 and co-occupies shared regulatory elements, converting an otherwise weak single-copy Atoh1-reponsive E-box into a highly active enhancer that drives transcriptional activation by up to 120-fold, including at an ultra-conserved E-box downstream of Atoh1 itself. Cross-species single-cell comparisons further show an association between Tox3 expression and cerebellum expansion during vertebrate evolution. Together, this work supports Tox3 as a critical Atoh1 co-activator in cerebellar development, tumorigenesis and evolution, while providing an atlas and screening strategy as a valuable resource for exploring novel transcriptional regulators in organogenesis and tissue physiology.

overall_design: Refer to individual Series

first: Guo

last: Huang


title: Impact of Candida albicans NDT80 and UME6 on biofilm formation and fluconazole susceptibility

status: Public on Mar 16 2026

city: Athens

first: Katharina

last: Goerlich

state: GA

address: 120E Green St

department: Microbiology

institute: University of Georgia

summary:
The fungus Candida albicans is part of the human microbiome and an opportunistic
pathogen. Virulence traits include its ability to produce biofilm, a surface-associated
growth form that persists on mucosal surfaces and implanted medical devices. C.
albicans clinical isolates vary considerably in ability to produce biofilm and the
constituent filamentous cell types. Here we focus on two transcription factors that
promote filamentation and biofilm formation, Ndt80 and Ume6. We address two
questions. First, how variable is the impact of Ndt80 among C. albicans strains?
Second, what is the genetic interaction between NDT80 and UME6? We find that
Ndt80 is required for filamentation and biofilm formation in five clinical isolates in
addition to the reference strain SC5314, where Ndt80 function has been well
established. RNA-sequencing (RNA-seq) data indicate that UME6 RNA levels are
reduced in an ndt80Δ/Δ mutant, possibly a result of altered RME1 and WOR1
expression, both of which control UME6. Increased expression of UME6 in ndt80Δ/Δ
mutants of three strain backgrounds restores filamentation and biofilm formation, though
RNA-seq assays indicate that it does not suppress the overall ndt80Δ/Δ gene
expression defect. Ndt80 has a second role in promoting tolerance to the antifungal
drug fluconazole, an inhibitor of ergosterol synthesis. Increased expression of UME6 in
ndt80Δ/Δ mutants enhances their susceptibility to fluconazole. Therefore, our results
show an unexpected relationship between Ume6 expression and azole drug sensitivity.
To our knowledge Ume6 has previously been known to function only in filamentation
and biofilm formation.

overall_design: RNA-seq profiling of WT C. albicans cells and their mutant derivatives (ndt80△/△, ndt80△/△UME6OE, and UME6OE). Cells were greown for 4h at 37 degrees in RPMI.

first: Aaron

middle: P

last: Mitchell


title: Alternative splicing-triggered mRNA decay informs splice-switching targets for neurodevelopmental disorders

first: Xiaochang

last: Zhang

department: Department of Human Genetics

institute: University of Chicago

summary: Alternative splicing-triggered nonsense-mediated mRNA decay (AS-NMD) critically regulates gene expression, but the extent to which neuronal genes are regulated by AS-NMD remains understudied. Here, we identified more than 3,000 developmentally regulated AS-NMD exons in mouse and human brains, and validated them in cultured neurons. AS-NMD suppresses synaptic genes during brain development and differentially regulates more than 200 causal genes for neurodevelopmental disorders (NDDs). We detected an AS-NMD exon in GRIA2 and identified splice-switching antisense oligonucleotides that suppressed GRIA2 NMD and increased its functional isoforms. In summary, this study uncovers genes repressed by AS-NMD in the brain and nominates amenable splice-switching targets for treating dominant NDDs such as autism spectrum disorders and developmental epileptic encephalopathy.

overall_design: (1) Neuroa2 Upf1 siRNA and control. (2) Primary neurons from E16.5 CD1 mouse, CHX and DMSO. (3). Human iPSCs induced neurons (day 4), CHX and DMSO treatments


title: PPAR-γ Suppresses Macrophage Senescence and Allergic Airway Inflammation through Controlling Lipid Metabolic Pathways

city: Baltimore

first: Peisong

last: Gao

state: MARYLAND

address: 5501 Hopkins Bayview Circle

institute: Johns Hopkins Asthma & Allergy Center

summary:
Background: Cellular senescence has emerged as a key contributor to the pathogenesis of chronic lung diseases. Peroxisome proliferator-activated receptor gamma (PPAR-γ), a nuclear transcription factor, regulates senescence across multiple cell types. However, the role of PPAR-γ in allergic airway inflammation, particularly through regulation of macrophage senescence, remains poorly defined.
Methods: Cellular senescence was evaluated in an allergic asthma mouse model using single-cell RNA sequencing (scRNA-seq). Senescent cells were selectively eliminated with dasatinib and quercetin (D&Q) to assess their contribution to disease pathogenesis. Macrophage-lineage-specific PPAR-γ conditional knockout model (PpargΔCD11c) were generated to define the role of macrophage PPAR-γ in senescence and allergic airway inflammation. PPAR-γ activity was further examined in isolated alveolar macrophages and in vivo using rosiglitazone, including macrophage-targeted delivery via phosphatidylserine-modified liposomes (PSL-ROSI).
Findings: scRNA-seq analysis revealed enhanced senescence signatures in mononuclear phagocytes (MNPs), characterized by increased SenMayo scores and elevated Cdkn2a (p16) expression.  Clearance of senescent cells significantly reduced airway inflammation and Th2 cytokine levels (IL-4, IL-5). Correlation analysis identified PPAR-γ as a key transcriptional regulator inversely associated with cellular senescence. Macrophage-lineage–specific deletion of PPAR-γ (PpargΔCD11c) exacerbated airway inflammation and increased cellular senescence. In vitro, rosiglitazone reduced allergen-induced senescence and suppressed proinflammatory mediators (IL-6, ICAM-1, CCL4, CCL5, TIMP-1, TNF-α) in alveolar macrophages. In vivo, rosiglitazone and inhaled PSL-ROSI attenuated cockroach allergen-induced airway inflammation, with PSL-ROSI effectively bypassing the airway mucus barrier to deliver rosiglitazone to lung macrophages. Integrated chromatin binding and transcriptomic analyses demonstrated that PPAR-γ promotes macrophage lipid metabolic programs (e.g., CD36, Fabp4).
Interpretation: These findings identify macrophage senescence as a pathogenic driver of allergic airway inflammation and establish PPAR-γ as a critical regulator of macrophage senescence and homeostasis, highlighting its potential as a therapeutic target for asthma.

overall_design: mice were sensitized by intra-tracheal (i.t.) inhalation of 20 μg cockroach extract in 50 μL of PBS once on day 1, 3, and 5 and challenged with the same dosage of CRE for 3 successive days (day 11–13). Control mice received the same volume of PBS.

first: Wenjing

last: Gu

first: Rongjun

last: Wan

first: Zhifeng

first: Wenshen

last: Wang

first: Shaobing

last: Xie

first: Chuangli

last: Hao

first: Guangshu

last: Liu

first: Mei


title: RNA-seq of human articular chondrocytes after exposure to BMP7-derived peptide p[63-82].

city: maastricht

first: Marjolein

last: Caron

department: Orthopedic Surgery

country: Netherlands

institute: Maastricht University

summary: Osteoarthritis is a degenerative joint disease that can currently only be treated by alleviating pain or, ultimately, by a total joint replacement. The bone morphogenetic protein 7-derived peptide p[63-82] offers a potentially novel molecular treatment option for osteoarthritis. Mapping peptide-induced transcriptomic changes in human articular chondrocytes is expected to help reveal how p[63-82] confers its chondrocyte phenotype modulating bioactivity. To this end,  human articular chondrocytes were isolated from the articular cartilage of patients with late-stage osteoarthritis undergoing total knee arthroplasty (METC approved). Cells were stimulated with 100 nM p[63-82] peptide for 24 hours (or vehicle), after which RNA was isolated, and RNAseq was performed. We found a total of 1976 differentially expressed genes. The p[63-82] peptide induces profound transcriptomic changes in primary human articular chondrocytes. One of the dominant transcriptomic alterations was the differential expression of several collagen-related genes. Many of these collagen-related genes have established roles in cartilage homeostasis. The here-acquired transcriptomic insights provide clues into the therapeutic mechanisms of action of the p[63-82] peptide in human articular chondrocytes.

first: Jessica

last: Steijns

first: Tim

last: Welting


title: Promoter mutagenesis and a massively parallel reporter screen of the MAPT locus identifies cis-regulatory elements and genetic variation effects [Variation and Saturation Mutagenesis MPRA]

city: Huntsville

first: Jesse

last: Cochran

institute: HudsonAlpha Institute for Biotechnology

summary: Tau neurofibrillary tangles are a hallmark of several neurodegenerative diseases called tauopathies, including frontotemporal dementia and Alzheimer's Disease. Ongoing clinical trials for tauopathies seek to reduce Tau in the brain through immunotherapy, antisense oligonucleotides, and siRNA. MAPT codes for Tau, therefore understanding how the MAPT gene is regulated and the effect of genetic variation at its regulatory elements is likely to have high relevance for tauopathies. We screened a ~3 Mb region including the MAPT locus using 2 different massively parallel reporter assay (MPRA) strategies in KOLF2.1J h-NGN2 neurons and HEK293FT cells, identifying previously unannotated cis-regulatory elements (CREs). Using CRISPR interference (CRISPRi) in mixed neuron cultures, we identified a new CRE for MAPT, as well as 2 CREs for another nearby gene of interest, KANSL1. Known genetic variation from the Alzheimer's Disease sequencing project was tested in a separate MPRA at the top CREs near the MAPT gene, identifying variants with altered regulatory effects including those at previously identified CREs for MAPT. Using a saturation mutagenesis screen of a 2,000 bp region encompassing the MAPT promoter, we assessed regulatory effects of each possible single nucleotide variant in this region. We identified several neuron-specific regulatory variant effects at this region, including a high confidence binding site for the transcription factors EGR2, ZBTB14 and TCLF5 at a region of high MPRA activity and genetic conservation.

overall_design: LentiMPRA in KOLF2.1h-NGN2 Neurons (transduced on day 14, collected on day 18) and HEK293FT cells testing known genetic variation at proximal CREs for MAPT as well as a saturation mutagenesis of the MAPT promoter

first: Rebecca

last: Hauser

first: Nicholas


title: Phloem proteomics to identify small Open Reading Frame (sORF)-encoded peptides with a putative role in the control of flowering time in Arabidopsis

city: Burjassot, Valencia

first: Irene

last: Moreno Sanguino

address: Cam. del Cementerio, 1

department: Plant Biology

country: Spain

institute: Univeristy of Valencia, Faculty of Pharmacy

summary: Phloem sap proteomic studies have previously revealed that phloem sap composition varies during development and upon floral induction. Specific proteins, lipids, messenger RNAs (mRNAs) and peptides have been shown to accumulate in different developmental stages. Peptides are of special interest since they have the potential to act as regulatory molecules controlling plant responses to environmental changes, such as salinity and water stress, plant-microbe interactions, and developmental changes. In this context, we have characterised Arabidopsis phloem exudates to identify proteins and peptides with potential to control flowering time, acting as signals fine tuning plant development. In this work, we present the proteomic profiles of the phloem sap samples during floral transition along with the identification of interesting proteins and peptides that could have a role in the control of flowering. Among those, we have described the abundance pattern of the sORF1511 peptide in the phloem sap, which varies upon floral induction. We show that sORF1511 overexpression affects bolting time and alters the expression of several genes involved in the control of flowering time.

overall_design: RNA-seq profiling from 12 das seedlings of Col-0 (WT) and the sORF1511-ox line #7 (overexpressor of sORF1511), each condition comprising two biological replicates, with each replicate consisting of five pooled seedlings.

first: Lucía

last: Argente Collàs

first: Göran

last: Samuelsson

first: Gunnar

last: Wingsle

first: Reyes

last: Benlloch


title: Clec3b⁺ fibroblasts are the primary effectors of portal fibrosis following activation via a KLF4/periostin axis

city: Changchun

first: Lin

last: Lei

address: 5333 Xi’an Road, Changchun, Jilin, China

department: State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, College of Veterinary Medicine

institute: Jilin University

summary: Portal fibrosis, a determinant of progression in virtually all chronic liver diseases, prototypically develops in biliary diseases. Using single-cell RNA sequencing and genetic cell fate tracing in mouse models, we identified Clec3b⁺ fibroblasts as a distinct subset of portal fibroblasts, which rapidly expand after biliary injury and give rise to the bulk portal myofibroblasts. Mechanistic analyses revealed that Clec3b⁺ portal fibroblasts activation is governed by a Krüppel-like factor 4 (KLF4)/periostin (POSTN) axis, i.e., KLF4 directly binds the Postn promoter and represses its transcription in quiescent fibroblasts, whereas after injury, KLF4 is downregulated, which allows POSTN, acting via αvβ5 integrin, to drive portal fibroblast activation and portal fibrosis. Our findings identify Clec3b+ portal fibroblasts as the primary effectors of portal fibrosis and demonstrate that the KLF4/POSTN signaling axis regulates their activation, offering potential therapeutic targets for inhibiting fibrosis in biliary diseases.

overall_design:
We conducted a comprehensive scRNA-seq analysis of the bilio-vascular trees from the mice  subjected to bile duct ligation (BDL)-induced cholestasis, and compared the profiles with those of control mice. We identified 15 major hepatic cell clusters comprising myeloid cells, lymphoid cells, endothelial cells, epithelial cells, and mesenchymal cells, and explored the extent of cell diversity within fibrotic mesenchymal cell populations.

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The table below lists GEO accessions reused/reanalyzed for this study.
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last: LEI

first: Chenchen

last: ZHAO

first: Wenwen

last: GAO

first: Guowen

last: LIU

first: Xinwei

last: LI


title: APOBEC3B regulates HPV replication by inducing R-loop formation and genomic instability [ChIP-Seq]

first: Conor

last: Templeton

overall_design: Enrichment of R-loop formation (S9.6 binding) was compared between Scramble control (Samples 2 and 3) and A3B-depleted CIN 612 cells (Samples 5 and 6). Sample 1 is an input control from the Scramble control CIN 612 cells, and Sample 4 is an input control from A3B-depleted CIN 612 cells.

first: Templeton

last: Conor

first: Gulik

last: Jasmine

first: Laimins

last: Laimonis


title: Sex determines the Natural Killer cell-mediated immunity against Pancreatic Cancer.

city: Halle (Saale)

first: Danny

last: Misiak

address: Kurt-Mothes-Str. 3a

department: Molecular Cell Biology

institute: Martin Luther University Halle-Wittenberg

summary: Pancreatic ductal adenocarcinoma ranks among the most aggressive malignancies and exhibits a higher prevalence and poorer prognosis in male patients. Natural killer cells play a critical role in tumor immunosurveillance by directly recognizing and eliminating tumor cells.  It is well established that females generally mount stronger immune responses than males. The present study aims to answer the question of whether sex has an influence on the NK cell-mediated anti-tumor function in PDAC. To validate our in vitro findings in a physiological context, we employed a syngeneic allograft mouse model.

overall_design: We investigate the in vitro killing efficacy of primary male and female mouse Nk cells on an established PDAC cell line via flow cytometry, RNA sequencing, and live cell imaging. To validate our in vitro findings in a physiological context, we employed a syngeneic allograft mouse model.

first: Arlt

last: Elise

first: Bley

last: Nadine

first: Misiak

last: Danny


title: Histone modifications and SP1 balance Pol II recruitment at bivalent promoters during gastrulation

first: xipeng

last: shen

overall_design: We firstly tested the sensitivity of antibodies to capture total RNA Pol II using low-input Hela cell  using STAR chromatin immunoprecipitation–sequencing (STAR ChIP-seq). To investigate the dynamics of RNA Pol II in mouse post-implantation embryos, we separated mouse E6.5 embryos into epiblast (Epi), visceral endoderm (VE), and extra-embryonic ectoderm (ExE), and E7.5 embryos into ectoderm (Ect), mesoderm (Mes), endoderm (End), and ExE and generated ChIP-seq data for Pol II and Ser2p. To investigate the factors involved in regulating Pol II occupancy at bivalent genes, we utilized CRISPR-Cas9 technology combined with electroporation of fertilized eggs to obtain gene knockout embryos including Jarid2, Kmt2b, Eed and Sp1. ChIP-seq of transcription factors Pol II, Ser2p and SP1 as well as histone modifications H3K4me3 and H3K27me3 were performed.

first: Xipeng

last: Shen

first: Yuting

last: Wen

first: Yunlong

last: Xiang


last: Zhao

state: Jilin Province

address: 5333 Xi’an Road

department: College of Veterinary Medicine

overall_design: To investigate the potential mechanisms by which KLF4 influences the transition of Clec3b-tdT⁺ portal fibroblasts into myofibroblasts, Clec3b-tdT⁺ cells were isolated from the livers of normal Clec3bCreERT2;R26tdT mice via fluorescence-activated cell sorting (FACS). These cells were then transduced with either a Klf4-overexpressing lentivirus (Lenti-Klf4) or a control lentivirus (Lenti-Ctrl). Following transduction, total RNA was extracted from the cells under both conditions, and RNA-seq was performed to analyze the gene expression profiles of Clec3b-tdT⁺ cells in response to Klf4 overexpression compared to the control.

first: Lin

last: Lei

last: Gao

first: Menglin

last: Liu

first: Guoyue

last: Lv

first: Zhongqi

last: Fan

first: Chantal

last: Housset

first: Fouad

last: Lafdil

first: Axelle

last: Cadoret

first: Sara

last: Lemoinne

first: Yongkang

last: Cheng

first: Jinxia

last: Li

first: Fanrong

last: Kong

first: Xiliang

last: Du

first: Yuxiang

last: Song


title: Gene expression profiling of lung organoids at CSD5, CSD14, and ND14 stages.

status: Public on Mar 15 2026

city: Kepala Batas

first: Syahidatulamali

last: Che Shaffi

address: Bandar Putra Bertam

country: Malaysia

institute: Universiti Sains Malaysia

summary:
Lung organoid culture in both normal and COPD-derived from cigarette smoke exposure of COPD mice model.
We used microarrays to analyse the molecular mechanisms and pathways involved in regulating the regenerative potential of lung stem cells in organoid culture development, both normal and COPD derived 3D-organoid models.

overall_design: Lung organoid were harvested in different time point and groups. Cigarette Smoke Day 5 (CSD5), Cigarette Smoke Day 14 (CSD14) and Naive Day 14 (ND14) for RNA extraction and hybridization on Affymetrix microarrays. We sought to understanding the molecular mechanisms behind AT2 cell dysfunction and their contribution to COPD.

last: Shaffi

first: Badrul

last: Hisham


title: The long noncoding RNA C1QTNF1-AS1 interacts with RSRC2 to ensure mitotic fidelity

status: Public on Mar 13 2026

city: London

first: Eleni

last: Maniati

address: John Vane Science Centre, Charterhouse Square

department: Barts Cancer Institute

country: United Kingdom

institute: Queen Mary University of London

summary: Chromosome congression, a process of chromosome alignment at the spindle equator, is a key step in cell division. While much work has addressed the role of protein networks in controlling cell division, we have very little understanding how long noncoding RNAs (lncRNAs) and RNA binding proteins (RBPs) contribute to the fidelity of cell division. To investigate the role of  lncRNA C1QTNF1-AS1 and its interacting protein partner RSRC2 in cell division, we depleted C1QTNF1-AS1 and RSRC2 with LNA gapmers and siRNAs, respectively, in HCT116 cells and analysed their impact on gene expression and splicing alterations.

overall_design: Three LNA gapmers were used to deplete C1QTNF1-AS1 alongside negative control LNA A (LNA A), with four independent experimental replicates performed per each LNA. RSRC2 depletion was examined using targeting or control siRNA in four independent experimental replicates in HCT116 cells. C1QTNF1-AS1 LNA 4 was renamed to LNA 2, and  C1QTNF1-AS1 LNA 5 was renamed to LNA 3.

first: Kaliya

last: Georgieva

first: Alice. O

last: Coomer

first: Giulia

last: Guiducci

first: Anisha

last: Thind

first: Jun

last: Wang

first: Lovorka

last: Stojic


title: Clec3b⁺ fibroblasts are the primary effectors of portal fibrosis following activation via a KLF4/periostin axis [ChIP-Seq]

first: Chenchen

last: Zhao

overall_design: To investigate the potential mechanisms by which KLF4 influences the transition of Clec3b-tdT⁺ portal fibroblasts into myofibroblasts, Clec3b-tdT⁺ cells were isolated from the livers of Clec3bCreERT2;R26tdT mice using fluorescence-activated cell sorting (FACS). ChIP-seq was then performed on these Clec3b-tdT⁺ cells following lentivirus-mediated overexpression of Klf4.

first: Lin

last: Lei

first: Wenwen

last: Gao

first: Menglin

last: Liu

first: Guoyue

last: Lv

first: Zhongqi

last: Fan

first: Chantal

last: Housset

first: Fouad

last: Lafdil

last: Cadoret

first: Guowen

first: Xinwei