title: miRNA Accumulation Correlates with Increased Phloem Cell Proliferation in Tomato hawaiian skirt Mutants

status: Public on Sep 08 2025

city: Tsukuba

first: Fabien

last: Lombardo

address: 1-1, Tennodai 1-Chōme

institute: The University of Tsukuba

summary: The cambium is the meristem responsible for production of plant vascular tissues, the xylem and phloem, during plant radial growth. The tomato hws mutant exhibits miRNA accumulation and produces a markedly enlarged phloem, suggesting a role for miRNAs in regulating vascular development. This study aims to identify the accumulated miRNAs associated with the vascular phenotype in hws mutants Key miRNAs, including miR319 and miR164, were identified as highly accumulated in the mutant pedicels, with predicted targets linked to meristematic activity.

overall_design: The distal parts of pedicels, from above the abscission zone to below the calyx, of 10-DAA WT and hws-1 fruits were collected. Five pedicel segments were bulked into one sample. Total RNA was extracted  and three biological replicates for each line were sequenced using a Illumina NovaSeq X Plus platform at a depth of one million-read per sample. Raw sequence data was analyzed with the sRNAminer pipeline with default settings.

first: Tarek

last: El mestari

first: Thomas

last: Kirat

first: Muhammad

middle: I

last: Jondah

first: Julie

last: Marsaudon

first: Norbert

last: Bollier

first: Chiaki

last: Matsukura


title: Regulation of the NSL complex by TAF4A is critical for genome stability and quiescence of skeletal muscle stem cells

status: Public on Sep 02 2025

city: Bad Nauheim

first: Carsten

last: Kuenne

address: Ludwigstrasse 43

department: Bioinformatics

country: Germany

institute: Max Planck Institute for Heart and Lung Research

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Acetylation of lamin A/C by the NSL complex, containing MOF and KANSL2, is instrumental for maintaining nuclear architecture and genome stability, but the mechanisms controlling expression of NSL complex components in different cell types are poorly characterized. Here, we describe that TAF4A, primarily known as a subunit of the general transcription factor TFIID, is critical for cell type-specific regulation of Kansl2 in MuSCs. Inactivation of Taf4a in MuSCs reduces expression of Kansl2 and alters post-translational modification of lamin A/C, thereby decreasing the stiffness of MuSC nuclei and disrupting the nuclear architecture. Using CUT&RUN technique, we found that TAF4A together with the heterotrimeric transcription factor NF-Y controls Kansl2 expression. In addition to destabilization of the nuclear architecture, reduced expression of Kansl2 in Taf4a-mutant MuSCs changes expression of numerous genes involved in chromatin regulation. The subsequent loss of heterochromatin and MuSC activation, in combination with pronounced genomic instability, activates MuSCs and impairs MuSC proliferation, which depletes the stem cell pool and abolishes skeletal muscle regeneration. We conclude that TAF4A-NF-Y-dependent transcription regulation safeguards heterochromatin and genome stability of MuSCs via the NSL complex.

overall_design: We examined chromatin structure using ATAC-seq in control and Taf4a mutant MuSCs

first: Angelina

middle: M

last: Georgieva

first: Stefan

last: Günther


title: INO80/SWR Remodelers Regulate Pol II Transcription through BRD2 and Chromatin Landscape (TT-seq)

status: Public on Sep 01 2025

city: Beijing

first: Xiong

last: Ji

address: Haidian District, Beijing Summer Palace Road No. 5

department: School of Life Sciences

country: China

institute: Peking University

summary: INO80/SWR remodelers, including INO80, P400/TIP60, and SRCAP, have been viewed to regulate H2A.Z dynamics, but how they control specific gene expression remains unclear. Here, we reveal distinct phenotypes arising from short- and long-term perturbations following the depletion of INO80/SWR remodelers. We identified the direct target genes of INO80, P400, and SRCAP remodelers. Mechanistically, we found that INO80/SWR remodelers interact and facilitate the chromatin occupancy of the H2A.Zac reader protein BRD2, which is crucial for Pol II initiation through TFIID. Additionally, while the degradation of P400 or SRCAP led to a reduction in H2A.Zac, INO80 depletion did not affect H2A.Zac occupancy but decreased the occupancy of P400 and SRCAP. Collectively, our findings suggest that INO80/SWR remodelers primarily regulate the chromatin landscape and influences BRD2 chromatin binding, thereby shedding light on their mechanisms in Pol II transcription regulation during development and disease.

overall_design: We performed ChIP-Seq, Cut&Tag, ATAC-Seq, ChAR-Seq and RNA-Seq to investigate the functions of INO80/SWR remodelers.

first: Meitong

last: Liu

first: Qiqin

last: Xu


title: Treatment of prostate cancer with oncolytic virus OH2 [scRNA-seq_RM-1]

city: Wuhan

first: Jinzhou

state: Hubei

address: Jiefang Avenue

institute: Tongji Hospital

type: Expression profiling by high throughput sequencing

summary: Prostate cancer is a major challenge due to limited treatment options in advanced stages. Immunotherapy has shown promising prospects in various cancers, but it faces obstacles in prostate cancer due to its immunosuppressive microenvironment and low response rate to current therapies. Oncolytic virus therapy provides a new immunotherapy approach by stimulating anti-tumor immune responses. This study investigated the histological changes of the novel herpes simplex virus type II (HSV-II) oncolytic virus OH2 in prostate cancer tumors.

overall_design: Prostate cancer subcutaneous transplanted tumors (RM-1, 3 vs. 3) were treated with oncolytic virus OH2 intervention

first: Ye

last: An

first: Guichen

last: Ye

first: Zhiyu

last: Xia

first: Shaogang

last: Wang

first: Qidong


title: Regulation of the NSL complex by TAF4A is critical for genome stability and quiescence of skeletal muscle stem cells [RNA-seq of MuSCs from control and Taf4asKOmice]

overall_design: Transcriptome profiling of MuSCs from control and Taf4asKOmice


title: Treatment of prostate cancer with oncolytic virus OH2 [bulkRNA-seq_22-Rv1]

overall_design: Prostate cancer cell lines (22-Rv1, 3 vs. 3) were treated with oncolytic virus OH2 intervention


title: Dysregulation of Vitamin D and Its Signaling in Hashimoto's Thyroiditis in Korean Population

city: Goyang

first: Dong-Woo

last: Lim

address: Dongguk-ro 32

country: South Korea

institute: Dongguk university

summary: Hahimoto’s thyroiditis (HT) is the most common thyroid disease leads to hypothyroid in developed countries. Recent studies highlighted the Vitamin D as the potential risk factor or the therapeutic agents for the HT due to its role in modulating immune responses, while the concrete evidence has not been presented. Patients eligible for the surgery of papillary thyroid cancer (PTC) with or without HT were recruited for the study. We analyzed serum thyroid biomarkers including serum vitamin D, anti-TG, anti-TPO for HT patients. Using the RNA-seq the gene expression profile of thyroid tissue, potential correlation between HT and vitamin D or its signaling was investigated.  HT cohort showed common clinical characteristics known for the HT in serum biomarkers and enrichment analysis of BP terms and KEGG pathways. Serum vitamin D level was significantly lower in HT patients. However, vitamin D receptor (VDR) expression and genes involved in vitamin D-associated BP terms were significantly upregulated in HT. Real-time PCR and Immunofluorescence staining confirmed enhanced VDR expression throughout the thyroid tissue of HT cohort.   This study demonstrated dysregulated vitamin D signaling in thyroid tissue of HT cohort. Further study need to be performed to elucidate etiology, susceptibility, and development of HT in relation with vitamin D signaling.

overall_design: RNA-seq profiling of isolated thyroid tissue from papillary thyroid cancer (PTC) patients eligible for surgery with or without HT etiology.

first: Seok-Mo

last: Kim


title: Treatment of prostate cancer with oncolytic virus OH2 [bulkRNA-seq_C4-2]

overall_design: Prostate cancer cell lines (C4-2, 3 vs. 3) were treated with oncolytic virus OH2 intervention


title: ChIP-seq of resting and anti-CD3/CD28-stimuated Jurkat cells

city: Guangzhou

first: Mulin Jun

last: Li

state: Guangdong

address: No. 9 Jinsui Road, Guangzhou

institute: Guangzhou Women and Children's Medical Center

summary: To finely dissect the dynamic changes in the epigenome and chromatin state during T cell activation, we utilized the Jurkat cell line as a model and performed ChIP-seq on both resting and anti-CD3/CD28-stimulated Jurkat cells, targeting various histone modifications (H3K27ac, H3K4me1, H3K4me3, H3K27me3), RNA PolII, and CTCF.

overall_design:
We performed ChIP-seq on both resting and anti-CD3/CD28-stimulated Jurkat cells for distinct histone modifications and TFs. Anti-CD28 and anti-CD3 antibodies were utilized to activate T cells as previously described (Simeonov et al. Nature, 2017). Briefly, the culture plate was coated with 10 µg/ml of anti-CD28 (TONBO Biosciences, 40-0289) for 12 hours at 4°C prior to cell inoculation. Jurkat or CD4+ T cells were then seeded with 10 µg/ml of anti-CD3 (40-0038). The cells were harvested 24 hours later for subsequent experimental analysis.

**Please note that the records have been updated as below on Sep 22, 2025:
[1] both raw and processed data for GSM8522707-GSM8522720 have been replaced
[2] additional sample records have been included

first: Zhao

first: Wei

last: Dong


title: Coordinated control of genome-nuclear lamina interactions by Topoisomerase 2B and Lamin B receptor (pA-DamID)

status: Public on Sep 15 2025

city: Milano

first: Stefano

middle: Giustino

last: Manzo

state: MI

address: Via Celoria 26, Dipartimento Bioscienze, Torre A, Piano 4

department: Biosciences

country: Italy

institute: University of Milan

summary: Lamina-associated domains (LADs) are megabase-sized genomic regions anchored to the nuclear lamina (NL). Factors controlling the interactions of the genome with the NL have largely remained elusive. Here, we identified DNA topoisomerase 2 beta (TOP2B) as a regulator of these interactions. TOP2B binds predominantly to inter-LAD (iLAD) chromatin and its depletion results in a partial loss of genomic partitioning between LADs and iLADs, suggesting that this enzyme might protect specific iLADs from interacting with the NL. TOP2B depletion affects LAD interactions with lamin B receptor (LBR) more than with lamins. LBR depletion phenocopies the effects of TOP2B depletion, despite the different positioning of the two proteins in the genome. This suggests a complementary mechanism for organising the genome at the NL. Indeed, co-depletion of TOP2B and LBR causes partial LAD/iLAD inversion, reflecting changes typical of oncogene-induced senescence. We propose that a coordinated axis controlled by TOP2B in iLADs and LBR in LADs maintains the partitioning of the genome between the NL and the nuclear interior.

overall_design: pA-DamID experiment were performed on RPE1(SunTag and iCUT), K

middle: G

first: Tom

last: van Schaik

first: Marcel

last: de Haas

first: Jeremie

last: Breda

first: Mikhail

last: Magnitov

first: Elzo

last: de Wit

first: Anna

last: Manjon

first: Rene

middle: H

last: Medema

first: Adam

middle: J

last: Buckle

first: Catherine

last: Naughton

first: Nick

last: Gilbert

first: Bas

last: van Steensel


title: CD28 region-capture HiC of resting and anti-CD3/CD28-stimuated Jurkat cells

summary: To meticulously explore how local chromatin architecture influences T cell activation, we conducted high-resolution regional capture Hi-C by designing tiling capture probes that span the CD28, CTLA4, and ICOS genes along with their distal regulatory sequences (chr2:204300000-205000000, GRCh37) in both resting and stimulated Jurkat cells.

overall_design: We performed CD28 region-capture HiC on both resting and anti-CD3/CD28-stimulated Jurkat cells. Anti-CD28 and anti-CD3 antibodies were utilized to activate T cells as previously described (Simeonov et al. Nature, 2017). Briefly, the culture plate was coated with 10 µg/ml of anti-CD28 (TONBO Biosciences, 40-0289) for 12 hours at 4°C prior to cell inoculation. Jurkat or CD4+ T cells were then seeded with 10 µg/ml of anti-CD3 (40-0038). The cells were harvested 24 hours later for subsequent experimental analysis.

last: Wang


title: ATAC-seq of resting and anti-CD3/CD28-stimuated Jurkat cells

summary: The majority of genetic risk variants associated with autoimmune diseases are located in chromatin regions that are accessible during T cell stimulation. To systematically investigate the dynamic changes in chromatin accessibility during T cell activation, we utilized the Jurkat cell line as a model and performed ATAC-seq on both resting and anti-CD3/CD28-stimulated Jurkat cells.

overall_design: We performed ATAC-seq on both resting and anti-CD3/CD28-stimulated Jurkat cells.Anti-CD28 and anti-CD3 antibodies were utilized to activate T cells as previously described (Simeonov et al. Nature, 2017). Briefly, the culture plate was coated with 10 µg/ml of anti-CD28 (TONBO Biosciences, 40-0289) for 12 hours at 4°C prior to cell inoculation. Jurkat or CD4+ T cells were then seeded with 10 µg/ml of anti-CD3 (40-0038). The cells were harvested 24 hours later for subsequent experimental analysis. The ATAC-seq library was prepared with the TruePrep DNA Library Prep Kit V2 for Illumina (Vazyme, TD501) and the TruePrep Index Kit V2 for Illumina (Vazyme, TD202), following the kit’s instructions.


title: RNA-seq of resting and anti-CD3/CD28-stimuated Jurkat cells

summary: To investigate the dynamics of gene expression during T cell activation and identify essential genes responsive to stimulation, we conducted RNA sequencing on both resting and stimulated Jurkat cells.

overall_design: We performed RNA-seq on both resting and anti-CD3/CD28-stimulated Jurkat cells, with each sample including two replicates. Anti-CD28 and anti-CD3 antibodies were utilized to activate T cells as previously described (Simeonov et al. Nature, 2017). Briefly, the culture plate was coated with 10 µg/ml of anti-CD28 (TONBO Biosciences, 40-0289) for 12 hours at 4°C prior to cell inoculation. Jurkat or CD4+ T cells were then seeded with 10 µg/ml of anti-CD3 (40-0038). The cells were harvested 24 hours later for subsequent experimental analysis. The freshly extracted total RNAs with high qualities were sent to the Novogene (Beijing, China) for constructing libraries and sequencing.


title: 4C-seq of resting and anti-CD3/CD28-stimuated Jurkat cells

summary: To investigate the interacting loci within the region containing rs5837875, we employed the circularized chromosome conformation capture (4C) assay to elucidate the spatial interactions and regulatory networks associated with rs5837875, utilizing this specific region as the bait in Jurkat cells.

overall_design: We performed 4C-seq on both resting and anti-CD3/CD28-stimulated Jurkat cells. Anti-CD28 and anti-CD3 antibodies were utilized to activate T cells as previously described (Simeonov et al. Nature, 2017). Briefly, the culture plate was coated with 10 µg/ml of anti-CD28 (TONBO Biosciences, 40-0289) for 12 hours at 4°C prior to cell inoculation. Jurkat or CD4+ T cells were then seeded with 10 µg/ml of anti-CD3 (40-0038). The cells were harvested 24 hours later for subsequent experimental analysis.


title: Multi-omics of resting and anti-CD3/CD28-stimuated Jurkat cells

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

overall_design: Refer to individual Series


title: INO80 / SWR remodelers regulate Pol II transcription through BRD2 and chromatin landscape (ATAC-Seq)

first: Xiong

last: Ji

summary: INO80 / SWR remodelers, including INO80, P400 / TIP60, and SR CAP, ha v e been vie w ed to regulate H2A.Z dynamics, but how they control specific gene expression remains unclear. Here, we reveal distinct phenotypes arising from short- and long-term perturbations f ollo wing the depletion of INO80 / SWR remodelers. We identified the direct target genes of INO80, P400, and SRCAP remodelers. Mechanistically, we found that INO80 / SWR remodelers interact and facilitate the chromatin occupancy of the H2A.Zac reader protein BRD2, thereby elucidating the regulation of Pol II transcription b y INO80 / SWR remodelers. A dditionally, while the degradation of P400 or SRCAP led to a reduction in H2A.Zac, INO80 depletion did not affect H2A.Zac occupancy but decreased the occupancy of P400 and SRCAP. Collectively, our findings suggest that INO80 / SWR remodelers primarily regulate the chromatin landscape and influences BRD2 chromatin binding, thereby shedding light on their mechanisms in Pol II transcription regulation during de v elopment and disease.

first: Hui

first: Qiqin

last: Xu


title: INO80 / SWR remodelers regulate Pol II transcription through BRD2 and chromatin landscape


title: Characterization of mouse melanocytes reveals ultrastructural and immunological insights into the inner ear function

status: Public on Aug 31 2025

city: Jinan

first: Jing

last: Cai

state: Shandong

address: 4 Duanxing West Road

department: Shandong Provincial ENT Hospital

institute: Shandong University

summary: Melanocytes are important components of the inner ear’s cellular architecture. However, limited morphological research has hindered a complete understanding of inner ear function. This study characterized the morphology of inner ear melanocytes and cells often misidentified as melanocytes. Immunofluorescence, Smart-seq, transmission/field emission scanning electron microscopy, and immunoelectron microscopy were used. Cells with a “black ball” appearance in the vestibule were identified as macrophages. We examined variation in melanocytes or macrophages with age, strain, and cisplatin injury. Kir4.1 expression and the greater noise resistance observed in pigmented mice suggest potential melanocyte functions. Based on melanin distribution in Pou3f4y/- mice, we hypothesize that melanocytes migrate from the modiolus along Reissner's membrane to the stria vascularis, following a base to apex gradient. These findings provide novel ultrastructural and immunological insights into inner ear function.

overall_design: Smart-RNA-seq profiling of Cells with a “black ball” appearance in the vestibule.

first: Lei

first: Yongdong

last: Song

first: Aizhen

last: Zhang

first: Zheng

last: Li

first: Boqin

first: Haibo


title: INO80/SWR Remodelers Regulate Pol II Transcription through BRD2 and Chromatin Landscape (ChIP-Seq)

first: Meitong

last: Liu


title: Transcriptomic of ileocecal junction of DBA/1 mice with spontaneous arthritis (SpAD)

city: Chihuahua

first: Susana

middle: Aideé

last: González-Chávez

state: Chihuahua

address: Circuito Universitario Campus II

department: Facultad de Medicina

country: Mexico

institute: Universidad Autónoma de Chihuahua

summary:
The spontaneous arthritis (SpAD) model in the DBA/1 mouse strain resembles the Spondyloarthritis human disease, including the intestinal inflammation characterized by loss of the integrity of the epithelial barrier and increased permeability. The transcriptome characteristics in this mouse model's gut are very scarce.
Transcriptome analysis was performed using DNA microarrays of ileocolic junction of DBA/1 strain mice with spontaneous arthritis (SpAD).

overall_design: The spontaneous arthritis (SpAD) model was generated in the DBA/1 mouse strain as described for the model. After sacrifice, the ileocolic junction was dissected, and total RNA was extracted and hybridized on Affymetrix microarrays.

first: Susana Aideé

first: César Francisco

last: Pacheco-Tena


title: 4T1 cells treated by Astragalin

city: Chongqing

first: Si-zhen

last: Yang

state: Chongqing

address: Gaotanyan Street, No.30

institute: Army Medical University

summary: 4T1 breast cancer cells were treated by Astragalin, to detect the effects of Astragalin on the cellular fate of 4T1 cells

overall_design: 4T1 cells were treated with AS at 20μM for 24 hrs in vitro

first: Ying

first: Xu

last: Hu

first: Tong-wei

last: Chu


title: Native CFTR codon bias controls translation rate to balance off-pathway aggregation and channel function by conformational imprinting

status: Public on Aug 29 2025

city: Lexington

first: Jae Seok

last: YOON

state: MA

address: 44 Hartwell Avenue

department: CFFT Lab

country: USA

institute: Cystic Fibrosis Foundation

summary: Protein folding in vivo is biologically tuned to minimize off-pathway events and optimize native folding outcomes.  A key factor in this process is biased synonymous codon usage, in which synonymous codons modulate local translation rate while maintaining the native amino acid sequence.  Here, we demonstrate that native codon usage within the first nucleotide-binding domain (NBD1) of the cystic fibrosis transmembrane conductance regulator (CFTR) induces a translational pause during a critical window of synthesis that is important for CFTR folding, processing, and function.  Eliminating this pause by substituting synonymous codons increased the aggregation propensity of immature CFTR and induced conformational and functional changes that persisted during CFTR processing and plasma membrane expression.  Interestingly, the resulting mature CFTR protein at the plasma membrane exhibited enhanced ATP-dependent chloride channel gating.  Thus, during protein synthesis, cotranslational events dictated by codon usage can imprint persistent conformational and functional properties upon CFTR.  Our findings suggest that CFTR codon usage has evolved and adapted to balance a compromise between protein aggregation and a modest loss of channel function.

overall_design: Ribosome profiling of heterologously expressed CFTR variants with different synonymous codons in HEK293 cells

last: Yoon

first: Hongyu

first: Yonjung

last: Kim

first: Hideki

last: Shishido

first: David

middle: N

last: Sheppard

first: Min Goo

last: Lee

first: William

middle: R

last: Skach


title: Therapeutic Strategies for MMAE-Resistant Bladder Cancer Through DPP4 Inhibition

status: Public on Aug 30 2025

city: Kagoshima

first: Gang

address: 8-35-1 Sakuragaoka

department: Urology

country: Japan

institute: Graduate School of Medical and Dental Sciences, Kagoshima University

summary: Monomethyl auristatin E (MMAE) is used as the cytotoxic payload for enfortumab vedotin (EV) in the treatment of locally advanced and metastatic bladder cancer (BC). However, the development of resistance to MMAE in BC is a therapeutic problem. To explore the mechanism of resistance to MMAE in BC, we established MMAE-resistant BC cells (MR-BCs). RNA sequencing analysis showed that the expression of dipeptidyl peptidase 4 (DPP4, also called CD26) increased significantly in MR-BCs compared with parental BC cells. Knock down of DPP4 expression using small interfering RNA inhibited the viability of MR-BCs. In addition, the DPP4 inhibitor sitagliptin suppressed the proliferation, migration, and invasion of BC cells, and cotreatment with MMAE effectively induced cell apoptosis, arrested cells in the G2M phase of the cell cycle, increased reactive oxygen species production by inhibiting the AKT pathway, and significantly inhibited the in vivo growth of MMAE-resistant cells. This study provides insights into the use of DPP4 inhibitors as a treatment strategy for MMAE-resistant BC.

overall_design: We established MMAE-resistant BC cells, MMAE-resistant T24 (MR-T24) and MMAE-resistant J82 (MR-J82). Then, we performed RNA sequencing analysis to compare gene expression levels between MR-T24 and T24, as well as MR-J82 and J82.


title: TGF-β signaling mediates microglial resilience to age-dependent dorsal column myelin alterations

city: Stockholm

first: Keying

last: Zhu

state: -- select state --

address: L8:04, Center for Molecular Medicine, Karolinska University Hospital

country: Sweden

institute: Karolinska Institutet

summary: Microglia survey and regulate central nervous system myelination during development and homeostasis. However, whether microglia-myelin interactions are anatomically regulated remains unexplored. Herein, by exploring the spinal cord, which contains several white matter tracts, we demonstrate age-dependent myelin ultrastructural abnormalities occurring in the dorsal column (DC) but not the ventral column (VC). Transcriptomic analyses comparing aged and young spinal cords reveal major changes in genes regulating myelin, microglial function, and the TGF-β signaling pathway. The TGF-β signaling pathway is upregulated in the spinal cord with aging, and a TGFβ-enriched microenvironment is induced in the DC. Disrupting TGFβ1-TGFBR1/2 axis in microglia, by altering either ligand or receptor expression, leads to increased microglial activation, abnormal phagocytic behavior, and myelin loss in the DC, accompanied by neurological deficits more severe in older mice. snRNA-seq reveals a TGF-β signaling-sensitive microglial subset in the spinal cord, spatially restricted in the DC. These findings demonstrate that TGF-β signaling is indispensable for maintaining microglial resilience to myelin alterations in the DC during the aging process, highlighting a previously unresolved checkpoint mechanism of TGF-β signaling with regional specificity.

overall_design: To understand the transcriptomic changes of microglia in the spinal cord following Tgfbr2 deletion, we sorted 100 microglia from the spinal cords of Cx3cr1CreER:Tgfbr2fl/fl mice from the dorsal column (DC), ventral column (VC), and grey matter (GM) at 18 and 28 days post tamoxifen injection. Tgfbr2fl/fl mice were used as the wildtype control.

first: Robert

middle: A

last: Harris

first: Harald

last: Lund


title: Integrated Single-Cell Lung Cancer Atlas Revealed Distinct Fibroblast Phenotypes between Adenocarcinoma and Squamous Cell Carcinomas

city: Minato-ku

first: Yuta

last: Hirano

state: Tokyo

address: 3-25-8 Nishi-shimbashi

department: Internal Medicine

institute: The Jikei University School of Medicine

summary: The tumor microenvironment (TME) not only influences cancer progression but has also been shown to have a significant impact on patient prognosis. One of the major TME components is cancer-associated fibroblasts (CAFs), of which several subtypes are identified in tumor tissues. Although scRNA-seq technology is a powerful tool to investigate the cellular proportion and composition in tissues, large-scale datasets are required to analyze a small number of cell populations. Here, we constructed an integrated single-cell RNA-seq dataset for non-small cell lung cancer (NSCLC) by compiling publicly-available data and demonstrated differences in TME heterogeneity and cellular composition between lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). Particularly, we identified significant differences in CAF subtypes between LUAD and LUSC. Inflammatory CAFs (iCAFs) were dominantly found in LUAD, while myofibroblastic CAFs (mCAFs) were more common in LUSC. Co-culture analysis with lung fibroblasts confirmed that LUAD cells induced iCAF phenotype and, in contrast, LUSC promoted myofibroblastic differentiation. Correlation analysis with patient prognosis identified mCAF as a poor prognostic factor in both LUAD and LUSC, but iCAF was found to be a poor prognostic factor only in LUSC, and vice versa in LUAD. This work highlights important considerations on CAF subtype dominance in LUAD and LUSC, which may relate to patient prognosis.

overall_design: Normal embryonic lung fibroblast (MRC5) were either mono-cultured or indirect co-cultured with Lung adenocarcinoma (Calu-3) and Lung squamous cell carcinoma (LC1). Total RNA was extracted after 5days culture.

first: Yusuke

last: Yamamoto

first: Yu

last: Fujita


title: Differential gene expression in the knee of DBA/1 mice with spontaneous arthritis (SpAD) compared to healthy BALB/c mice

first: Susana

last: González-Chávez

summary:
The DBA/1 mouse strain produces spontaneous arthritis (SpAD) characterized by an inflammatory process and changes in the joint structures that resemble human spondyloarthritis. Normally, it is the hind paws that are analyzed in this model and information on the alterations in the knee is very scarce.
Transcriptome analysis was performed using DNA microarrays of knees of DBA/1 strain mice with spontaneous arthritis (SpAD) and BALB/c strain mice as a control.

overall_design: The spontaneous arthritis (SpAD) model was generated in DBA/1 mouse strain as described for the model. After sacrifice, the knees of diseased mice and healthy BALB/c mice were dissected. Total RNA was extracted from the knees and hybridized on Affymetrix microarrays.

first: César

middle: F

last: Pacheco-Tena


title: INO80 / SWR remodelers regulate Pol II transcription through BRD2 and chromatin landscape (ChAR-Seq)

first: Xiong

last: Ji

overall_design: We performed ChIP-Seq, Cut&Tag, ATAC-Seq, ChAR-Seq and RNA-Seq to investigate the functions of INO80/SWR remodelers.

first: Hui

last: Wang

first: Qiqin

last: Xu


title: Lysine-specific demethylase 6B promotes STAT1-mediated macrophages activation during atherosclerosis development [MeRIP-Seq]

city: hangzhou

first: huan

last: chen

state: Zhejiang

address: Hangzhou, Zhejiang Province, China

institute: Zhejiang Chinese Medical University

summary: Atherosclerosis (AS) induced coronary heart disease is still the first killer threatening human health due to high morbidity and mortality. How N6-methyladenosine modification (m6A) in macrophage participates in atherosclerosis progression is still completely unclear. In this study, by performing meRIP-seq in macrophages during differentiation and activation processes, we aim to understand the landscape of m6A spectrum in macrophage from different stages. Moreover, we also find a large class of histone methylation modification enzymes were regulated by m6A modification. Western blot, qPCR and ChIP-seq results demonstrate m6A modification regulates Lysine-specific demethylase 6B (Kdm6b)-dependent macrophage activation. In mechanism, Kdm6b interacts and methylates Jak1 inducing its phosphorylation-mediated macrophage activation. Furthermore, RIP-qPCR detection indicates following macrophage differentiation and activation, both m6A writers Mettl3 and Rbm15 participates in m6A modification of Kdm6b mRNA. Finally, by performing atherosclerotic model on macrophage-specific Kdm6b knockout mice on Ldlr-/- background, we demonstrate Kdm6b promotes macrophage activation-mediated atherosclerosis by amplifying inflammation and destabilizing plaque. This study will provide a new understanding of the pathogenesis of AS and is expected to develop a new target for the treatment of AS.

overall_design: m6A sequencing data analysis: Effects of IFNγ on m6A modification sites on RNA molecules in mouse bone marrow-derived macrophages


title: INO80 / SWR remodelers regulate Pol II transcription through BRD2 and chromatin landscape (RNA-Seq)


title: Treatment of prostate cancer with oncolytic virus OH2 [bulkRNA-seq_tumors]

first: Jinzhou

summary: Prostate cancer is a major challenge due to limited treatment options in advanced stages. Immunotherapy has shown promising prospects in various cancers, but it faces obstacles in prostate cancer due to its immunosuppressive microenvironment and low response rate to current therapies. Oncolytic virus therapy provides a new immunotherapy approach by stimulating anti-tumor immune responses. This study investigated the histological changes of the novel herpes simplex virus type II (HSV-II) oncolytic virus OH2 in prostate cancer tumors.

overall_design: Prostate cancer subcutaneous transplanted tumors (RM-1, 5 vs. 5) were treated with oncolytic virus OH2 intervention

first: Ye

last: An

first: Guichen

last: Ye

first: Zhiyu

last: Xia

first: Shaogang

first: Qidong


title: RSS mediated persulfidation cascade regulation mechanism of novel transcription factor SscRAc in extremophile Acidithiobacillus caldus under extreme copper stress

city: Wuxi

first: Xingyu

last: Huo

state: Jiangsu

address: No. 1800, Lihu Avenue

institute: Jiangnan University

summary: Biomining microorganisms are classified as extremophiles due to their chronic exposure to elevated metal ion concentrations, which drives evolutionary adaptations for environmental stress resistance. This study investigates the copper tolerance mechanisms in Acidithiobacillus caldus CCTCC M 2018727, a strain demonstrating exceptional metal resistance through long-term adaptive laboratory evolution (survival at 250 mM Cu²⁺). Comparative analysis revealed a 350.6% increase in intracellular reactive sulfur species (RSS) levels under 250 mM Cu²⁺ stress. Sulfur-related post-translational modification proteomics demonstrated system-wide persulfidation enhancement and identified SscRAc, a novel RSS-sensitive MarR family transcription factor. Genetic deletion of sscRAc increased copper susceptibility and disrupted cellular redox homeostasis. Chromatin immunoprecipitation and qRT-PCR analyses revealed SscRAc’s dual regulatory mechanism: suppressing copper efflux systems while activating RSS metabolic pathways to maintain intracellular equilibrium. LC-MS/MS analysis revealed that both Cys74 and Cys78 in SscRAc interact with RSS and undergo persulfidation, resulting in the dissociation of the protein from the promoter-DNA of target genes. Furthermore, upstream signaling analysis uncovered a reciprocal regulatory relationship between SscRAc and the copper-sensitive transcription factor CsoRAc, establishing a coordinated copper-RSS signaling network. This work identifies SscRAc as a pivotal regulator of copper tolerance in A. caldus and delineates a novel metal stress response pathway connecting copper toxicity with sulfur redox biochemistry.

overall_design: ChIP-seq profiling of SscRAc transcription factor binding sites in Acidithiobacillus caldus strain CCTCC M 2018727. Constructed recombinant plasmid p-sscRAc-Flag expressing 3×Flag-tagged SscRAc, which was transformed into donor strain E. coli SM10. The A. caldus p-sscRAc-Flag strain was subsequently generated via conjugation transfer.

first: Huo

last: Xingyu

first: Tong

last: Yanjun

first: Yang

last: Haililn

first: Feng

last: Shoushuai


title: Brain pericytes and Wnt/β-catenin signaling induce functional blood-brain barrier phenotype in human iPSC-derived model

status: Public on Aug 28 2025

city: Amsterdam

first: Henrique

last: Nogueira Pinto

address: De Boelelaan 1117

country: Netherlands

institute: Amsterdam UMC

summary: The blood-brain barrier (BBB), formed by brain microvascular endothelial cells (BMECs), restricts vascular permeability by establishing tight junctions, reducing vesicular transport, and regulating molecular trafficking via dedicated transporters. In disease, BBB dysfunction leads to barrier disruption and neuroinflammation. Existing human in vitro BBB models recapitulate some but not all of these key BMEC features. Here, we present a method to differentiate human induced pluripotent stem cells (hiPSCs) into BMECs (hiBMECs) by co-culturing hiPSC-derived endothelial cells with brain pericytes (hiBPCs) and activating the Wnt/β-catenin pathway. The resulting hiBMECs exhibit barrier properties, functional efflux transporters, and appropriate inflammatory responses. RNA sequencing revealed a transcriptomic profile in hiBMECs closely matching the adult human BBB. Mechanistically, hiBPCs and Wnt/β-catenin signaling provided complementary cues that converged on ETS1, SMAD3/4, and PPARγ transcriptional networks. These findings reveal a synergistic mechanism by which brain pericytes and Wnt/β-catenin signaling orchestrate human BMEC differentiation and function, providing mechanistic insight into human BBB development and an improved hiPSC-derived BBB model for future drug screening and disease modeling.

overall_design: RNA-seq profiling of hiBMEC, hiEC, hiEC+hiBPC, hiEC+CHIR, hiBPC, hiBPC+hiEC and hiBPC+hiBMEC, with or without inflammatory stimulation with TNFa and IFNg (25 IU/mL, 16h).

first: Nine R

last: Kok

first: Philipp C

last: Hauger

first: Manon

last: Kersten-van Diepen

first: Michael

last: de Kok

first: Nanne J

last: Paauw

first: Susanne MA

last: van der Pol

first: Joline P

last: Nugteren-Boogaard

first: Peter L

last: Hordijk

first: Stephanie D

last: Beekhuis-Hoekstra

first: Susan

last: Gibbs

first: Nienke M

last: de Wit

first: Helga E

last: de Vries


title: Multimodal blood based profiling reveals insights into mechanisms of immunotherapy resistance

city: Cambridge

first: Samuel

last: Wright

address: 415 Main St.

institute: Broad Institute of MIT and Harvard

summary: Many cancer patients treated with immune checkpoint blockade (ICB) do not have durable treatment responses. Circulating biomarkers have the potential to identify patients with primary resistance or early progression on therapy to alter treatment course and avoid unnecessary toxicity. Unbiased multimodal proteomic profiling in blood has been underexplored due to the previously limited scalability of multiplexing technologies or cohorts lacking time-series sampling. To address this, we performed plasma proteomic profiling of >2,900 proteins and high-dimensional mass cytometry of peripheral blood lymphocytes across serial time points in 250 metastatic melanoma patients on ICB treatment. We further obtained 92 patient-matched tumor samples, which were processed for single-cell and/or bulk RNA sequencing. Proteins upregulated post-ICB were associated with inflammatory pathways involving the activation of effector immune functions. Expression of genes corresponding to these proteins was higher in immune cells involved in recruitment and tumor reactivity. Expression of genes corresponding to plasma proteins more abundant in non-responders was highest in suppressive myeloid subsets and malignant cells. We further posit the involvement of these non-responder genes in immunosuppressive and pro-tumor interactions, which we confirmed using publicly available spatial transcriptomic data. We also found that epithelial-specific proteins in the circulation of responders post-ICB correlate with patient toxicity and likely originate from healthy tissues. Together, these data represent one of the deepest peripheral biomarker studies using paired blood and tumor samples in melanoma patients treated with ICB, and begin to elucidate the complex interplay between tumors and the systemic immune response within the host.

overall_design:
Tumor samples were collected from melanoma patients and analyzed using bulk RNA-seq.

***************************************************************
Raw data files are not included as there are privacy concerns regarding public access to raw data files.
***************************************************************

first: S

first: A

last: Mehta

first: N

last: Hacohen

first: G

last: Boland


title: Adipocyte heterogeneity regulated by the Bithorax Complex-Wnt signaling crosstalk in Drosophila

city: New Orleans

first: Jun-yuan

last: Ji

state: LA

address: 1700 Tulane Avenue

department: Department of Biochemistry and Molecular Biology

institute: Tulane University

summary: Adipocytes distributed throughout the body are essential for lipid metabolism and energy homeostasis, with regional differences affecting their functions and disease susceptibility. However, the mechanisms driving this regional heterogeneity remain poorly understood. Here, we show that the interactions between Wnt/Wingless signaling and Bithorax Complex (BX-C) genes – specifically abdominal A (abd-A) and Abdominal B (Abd-B) – drive regional differences in Drosophila larval adipocytes. Abdominal adipocytes, expressing abd-A and Abd-B, differ from thoracic ones, with active Wnt signaling further amplifying these differences. Depleting abd-A and Abd-B, genes in adipocytes reduces fat accumulation, delays larval-pupal transition, and leads to pupal lethality, while also attenuating Wnt signaling-induced lipid mobilization. Moreover, Wnt signaling stimulates abd-A and Abd-B, transcription, creating a feedforward loop that intensifies the interaction between Wnt signaling and BX-C genes. These findings elucidate how the crosstalk between cell-autonomous BX-C gene expression and Wnt signaling defines adipocyte heterogeneity in Drosophila larvae.

overall_design: RNA-seq on fat bodies of control or axn/abd-A/Abd-B depleted animals. Following principal component analysis (PCA), we excluded two outlier samples from subsequent analyses: dcg+4 from the dcg+ group and dcg-AiBi-1 from the dcg-AiBi group.


title: RNA-seq of tomato leaves under JCK1241 treatment and/or Ralstonia solanacearum challenge

city: Busan

first: Young-Su

last: Seo

address: Geumjeong-Gu

department: Microbiology

institute: Pusan National University

summary: This study performed RNA sequencing (RNA-seq) of tomato (Solanum lycopersicum, cultivar Seokwang) leaves to investigate transcriptional responses under treatment with JCK1241 and/or challenge with the bacterial wilt pathogen Ralstonia solanacearum. A total of 12 samples were analyzed, including control, pathogen-infected, treatment-only, and combined treatment-plus-pathogen conditions

overall_design: Tomato leaves were sampled from cultivar PNU 01 grown under controlled conditions. Four groups were studied: (i) control, (ii) R. solanacearum-infected, (iii) JCK1241-treated, and (iv) JCK1241 treatment plus pathogen infection. Three biological replicates were included per group. RNA was extracted, sequenced using Illumina paired-end sequencing, and analyzed for differential gene expression, annotation, and clustering

first: Mohamed

last: Mannaa


title: A biomemetic senotherapy targeting MAT2A-mediated senescence-inflammation promotes wound regeneration through moonlighting reprogramming

status: Public on Aug 24 2025

first: Dongming

last: Lv

state: None Selected

address: No.58 Zhongshan 2nd Road, Guangzhou, Guangdong Province, China,

institute: Sun Yat-sen University

summary: To evaluate the role of Mat2a in the wound healing, we generated the Mat2a KO mouse. We investigate the changes in wound healing process between the Mat2a KO mouse and WT mouse.

overall_design: Wound margin tissues of three Mat2a KO and WT mouse were collected, and diagested for single-cell sequencing analysis.

first: Lei

last: Ren

first: Zirui

last: Zhao

first: Yanchao

last: Rong

first: Xiaoling

last: Cao

first: Bing

last: Tang


title: Metabolomic landscape of fetal organs development during late gestation in mice

status: Public on Aug 23 2025

city: Shanghai

first: Chanyi

last: Li

address: 168 Changhai Road

institute: The First Affiliated Hospital of Naval Military Medical University

summary: This experiment investigates the differential gene expression of the heart during different developmental stages of mouse embryonic development

overall_design: This experiment collected the hearts of ICR mice at embryonic stages 16.5 and 18.5, with three biological replicates per group for transcriptome sequencing.

first: Wuping

last: Liu

first: Xiaodong

first: Bo

first: Jiaying

last: Qin

first: Ning

last: Yi

first: Bianling

last: Xu

first: Jing

first: Zhigang

last: Xue

first: Hongli

last: Yan

first: Jinfeng


title: Genome-wide identification of transcriptional targets for H3K18la in adipose stem and progenitor cells

status: Public on Aug 25 2025

first: Hongrui

last: Chen

address: 639 Zhizaoju Road, Shanghai 200011, P.R.China.

department: Plastic and reconstruction surgery

institute: Shanghai ninth people's hospital

summary: In this study, we found that H3K18la level is elevated in adipose stem and progenitor cells of facial infiltrating lipomatosis (FIL-ASPCs). To further explore the potential functional significance of H3K18la in FIL, we performed genome-wide cleavage under targets and tagmentation (CUT&Tag) analysis to identify candidate genes regulated by H3K18la in FIL-ASPCs and CON-ASPCs. Following CUT&Tag, H3K18la-associated DNAs were amplified using non-biased conditions, labeled, and sequenced with Illumina NovaSeq 150PE.

overall_design:
Group 1: FIL-ASPCs. Group 2: CON-ASPCs
CUT&Tag

first: Chen

last: Hua

first: Xiaoxi

last: Lin


title: Comparison of human pluripotent stem cell-derived cardiomyocyte subtypes

city: Okayama

first: Yukihiro

last: Sato

address: 2-5-1 Shikata-cho Kita-ku

institute: Okayama University

summary: Different subtypes of cardiomyocytes were induced from human induced pluripotent stem cells.

overall_design: Human induced pluripotent cells were basically differentiated using cardic differentiation protocol with a GSK3 inhibitor and a Wnt inhibitor (GiWi). Cells were purified using no glucose medium supplemented with lactate. Standard GiWi mainly produced NKX2-5-positive/TBX5-positive cardiomyocytes and modified GiWi mainly produced NKX2-5-positive/TBX5-negative cardiomyocytes.

last: Saito

first: Dai

last: Kusumoto

first: Shinsuke

last: Yuasa


title: Transcriptome of the hindgut of Aedes aegypti wild type females fed on sucrose ad libitum

status: Public on Aug 26 2025

city: New York

first: Laura

middle: B.

last: Duvall

state: NY

address: 1212 Amsterdam Ave

institute: Columbia University

summary: Aedes aegypti mosquitoes are efficient vectors of human disease including Zika, Dengue and Chikungunya. After taking a blood meal, proteins from the blood are broken down into amino acids that are essential for egg development and growth. We have discovered a novel role for a neuropeptide receptor in the hindgut that coordinates blood utilization. The hindgut is not a tissue normally implicated in blood digestion, therefore we conducted RNA-seq profiling of the hindgut in wild type females to obtain a transcriptomic profile of these tissues in non-blood fed conditions.

overall_design: RNA-seq profiling of the hindgut of wild type 5-15 day old Aedes aegypti female mosquitoes fed on sucrose ad libitum

first: Chloe

last: Greppi

first: Kyle

last: Frank

first: Victoria

last: Saltz

middle: B


title: Single-dose cathepsin L CRISPR nanotherapy mitigates long COVID–like lung damage in hamsters

city: Milwaukee

first: Victor

last: Jin

state: WI

address: 8701 W Watertown Plank Rd

institute: MCW

summary: We investigate the long-term cellular response in the lungs of golden Syrian hamsters 31 days after SARS-CoV-2 infection.

overall_design: The SARS-CoV-2-infected golden Syrian hamsters received a single-dose CRISPR-CasRx nanotherapy targeting the host enzyme cathepsin L (SCNC), administered 4 hours post-infection, with a non-targeting CRISPR-CasRx nanotherapy serving as the control. At 31 days post-infection, the caudal lung lobe was isolated. Six samples were subjected to single-cell RNA sequencing, with three samples from the SCNC treatment group and the remaining three from the control group.

first: Zhifen

last: Cui

first: Tianxiang

last: Liu

middle: X

first: Qianben

last: Wang


title: Long noncoding RNA-dependent control of Myc transcriptional bursting [ATAC-Seq]

status: Public on Aug 22 2025

city: New Haven

first: Nadya

last: Dimitrova

state: CT

address: 260 Whitney Ave YSB211

department: MCDB

institute: Yale University

summary: Genes are transcribed in short periods of activity, called bursts. Bursts are initiated by enhancer-promoter contacts and dynamically controlled by the levels of enhancer- and promoter-produced RNAs through a negative feedback mechanism. Here, by direct visualization of nascent transcripts, we show that chromatin-associated long noncoding RNAs (lncRNAs) contribute to the regulation of transcriptional bursting. We find that production of Pvt1 raises the baseline of RNA concentration in the locus of the Myc proto-oncogene and acts locally and in a dose-dependent manner to decrease the duration of Myc bursting. Premature termination of Pvt1 led to higher Myc expression and transcriptional activities, resulting in increased cellular proliferation and advanced tumor development in autochthonous models of lung cancer. These findings point to a critical lncRNA-mediated mechanism for Myc regulation and suggest a potentially widespread role for lncRNAs in fine-tuning gene expression through local control of transcriptional bursting.

overall_design: Primary Pvt1+/+ and Pvt1aP/P MEFs were isolated from littermate E13.5 MEFs and cultured in DMEM supplemented with 15% FBS, Pen/Strep, L-glutamine, NEAA, and b-ME. Samples were harvested in two biological replicates from two independent littermate pairs. For RNA-seq, total RNA was isolated using the Qiagen RNeasy Kit and submitted for library preparation and sequencing at the Yale Center for Genome Analysis (YCGA). For ATAC-seq and Hi-C, cryopreserved cells were submitted for library prepation and sequencing at YCGA.

first: Qiao

last: Li

first: Corinne

last: Dilsavor

first: Valid

last: Gahramanov

first: Erin

last: Floyd

first: Jane

last: Ding

first: Justin

last: Glynn

first: Ioannis

last: Chiotakakos

first: Christiane

middle: E

last: Olivero

first: Jesse

last: Zamudio


title: Long noncoding RNA-dependent control of Myc transcriptional bursting [HiC]


title: Normalizing body weight with a dietary strategy mitigates obesity-accelerated pancreatic carcinogenesis in mice

city: Davis

first: Gerardo

last: Mackenzie

state: California

address: 1 Shields Ave

institute: University of California Davis

summary: Although obesity is a modifiable risk factor for pancreatic cancer, the role of dietary changes that lead to weight loss in pancreatic carcinogenesis remains unknown. Thus, we determined the effects of weight normalization via dietary switch on pancreatic carcinogenesis and the associated mechanisms. Five-week-old male and female LSL-KrasG12D/+; p48Cre/+ (KC) mice (8-12/diet group/sex) were fed a high-fat, diet-induced obesity diet (DIO; 60 kCal% energy from fat) or a low-fat, control diet (CD; 11 kCal% energy from fat) for 21 weeks. A subset of mice was fed the DIO for 8 weeks, then switched to a CD for 13 additional weeks (DIO→CD). Cancer incidence was evaluated by histology. Lipidomics and RNAseq followed by bioinformatic analysis were conducted to identify possible mechanisms. The gut microbiome was characterized using 16s rRNA amplicon sequencing. After 21 weeks, DIO-fed mice had significantly higher body weight, fat mass, and pancreatic acinar-to-ductal metaplasia compared to the other 2 groups.  While none of the 21 mice fed a CD developed cancer, 2 out of 21 DIO-fed mice did. Switching from a DIO to a CD normalized body weight and composition, reduced acinar-to-ductal metaplasia and prevented cancer incidence with no mice developing cancer. Mechanistically, the DIO affected the expression of genes regulating cellular metabolism, immune function, and cell-signaling, while CD and DIO→CD had similar global gene expression. Moreover, DIO increased epoxy metabolites of linoleic acid, which were mitigated by the dietary switch. Finally, compared to a CD, DIO altered the gut microbiome and switching from a DIO to a CD restored the gut microbiome profile to one close to the mice fed a CD. Body weight normalization mitigates obesity-accelerated pancreatic carcinogenesis, in part, by affecting inflammatory and cell signaling pathways, reducing epoxy metabolites, and modulating the gut microbiome.

overall_design: RNA-seq of the pancreas from female LSL-KrasG12D/+; p48Cre/+ (KC) mice fed either: 1) a high-fat, diet-induced obesity diet (DIO) for 21 weeks, 2) a low-fat control diet (CD) for 21 weeks, or 3) a DIO diet for 8 weeks followed by a CD diet for 13 weeks (DIO→CD).

first: Joanna

last: Wirkus

first: Aya

middle: S

last: Ead

first: Irena

last: Krga

first: Yige

first: Matthew

last: Pontifex

first: Michael

last: Muller

first: David

last: Vauzour

first: Karen

last: Matsukuma

first: Guodong

last: Zhang


title: Colon tissue gene expression associated with vedolizumab treatment effectiveness in ulcerative colitis.

city: Tokyo

first: Mayu

last: Suzuki

address: 2-1-1 Nihonbashi-Honcho, Chuo-ku

department: Japan Medical Office

institute: Takeda Pharmaceutical Co., Ltd.

summary: Transcriptional profiling was performed on colorectal tissues, both inflammatory and non-inflammatory, collected from patients with ulcerative colitis.

overall_design: RNA was extracted from the tissues using RNeasy Mini Kit (Qiagen) and AmpliSeq libraries were prepared with the Ion AmpliSeq™ Transcriptome Human Gene Expression Kit (Thermo Fisher Scientific) using 10 ng of RNA. The resulting libraries were used for sequencing on the Ion 550™ Chip Kit , Ion 550™ Kit-Chef and Ion GeneStudio™ S5 Prime System (Thermo Fisher Scientific), and output data (BAM files) were obtained.

first: Mikihiro

last: Fujiya

first: Kaori

last: Ishiguro


title: TTK defines a high-risk Oral Squamous Cell Carcinoma subtype through dual mTORC1/NF-κB activation

city: Xi'an

first: Tianjie

last: Liu

state: Shannxi

address: No.277, Yanta West Road

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

summary: Oral squamous cell carcinoma (OSCC) remains challenging to treat due to significant tumor heterogeneity, highlighting the need for identifying molecular subtypes with distinct therapeutic vulnerabilities. Here, we present a comprehensive molecular analysis of 709 OSCC cases, integrating single-cell RNA sequencing and bulk transcriptomic data. We identify a distinct molecular subtype of OSCC characterized by co-activation of the mTORC1 and NF-κB pathways, with TTK emerging as a central regulator of this co-activation. This subtype exhibits heightened genomic instability. Using protein mass spectrometry and immunoprecipitation, we demonstrate that TTK activates the NF-κB pathway through interaction with the TAK1-TAB protein complex. Functional in vitro and in vivo experiments further reveal that TTK inhibition significantly enhances cisplatin sensitivity in OSCC. These findings provide a basis for patient stratification and underscore the potential of targeting TTK in therapeutic strategies for this high-risk OSCC subtype.

overall_design: RNA-seq profiling of wildtype SCC-15 and CAL-27 cells and their knockdown derivatives (shTTK).

first: Huan

last: Jin

first: Yucheng

last: Guo

first: Wenqing

last: Bu

first: Fei

first: Yuxia

last: Hou


title: Long noncoding RNA-dependent control of Myc transcriptional bursting [RNA-Seq]

first: Nadya

last: Dimitrova

first: Qiao

last: Li

first: Corinne

last: Dilsavor

first: Valid

last: Gahramanov

first: Erin

last: Floyd

first: Jane

last: Ding

first: Justin

last: Glynn

first: Ioannis

last: Chiotakakos

first: Christiane

last: Olivero

first: Jesse

last: Zamudio


title: Dynamical network biomarker analysis using multi-organ RNA sequencing in metabolic syndrome model mice

city: Toyama

first: Makito

last: Oku

address: 2630 Sugitani

department: Research Center for Pre-Disease Science

institute: University of Toyama

summary: Dynamical network biomarker (DNB) theory has emerged as a powerful framework for detecting early warning signals of pre-disease states. Based on our previous work demonstrating its utility in adipose tissue of metabolic syndrome model mice, we conducted a comprehensive DNB analysis using RNA sequencing data across 13 organs and 14 to 16 time points in high-fat diet-fed mice. Our findings revealed organ-specific variation in the timing of early warning signals, suggesting heterogeneous inter-organ dynamics during the pre-disease state of metabolic syndrome. These results highlight the potential of DNB theory for elucidating systemic early-stage pathophysiology in complex metabolic disorders.

overall_design: Male C57BL/6J mice were fed high-fat diet (HFD) from eight weeks of age. From zero days (HFD onset) to 12 weeks, RNA-seq was conducted for 13 organs: epididymal white adipose tissue (eWAT), inguinal white adipose tissue (iWAT), interscapular brown adipose tissue (BAT), pancreas, liver, small intestine, soleus muscle, gastrocnemius muscle, hypothalamus, pituitary gland, neocortex, hippocampus, and olfactory bulb. At 16 and 20 weeks, RNA-seq was conducted only for eWAT. Six mice were measured per time point.

first: Akiko

last: Inujima

first: Keiichi

last: Koizumi

first: Kazutaka

last: Akagi

first: Shiho

last: Fujisaka

first: Tsutomu

last: Wada

first: Yasuhiro

last: Onogi

first: Toshiyasu

last: Sasaoka

first: Kazuyuki

last: Tobe

first: Makoto

last: Kadowaki

first: Xun

last: Shen

first: Jun-ichi

last: Imura

last: Aihara

first: Shigeru

last: Saito


title: RNAs expression analyses in commercially used Marek’s disease vaccine viruses to identify their Latency associated transcripts splicing patterns

city: Namur

first: Camille

last: Ponsard

state: Namur

address: Rue de Bruxelles, 61

department: Veterinary Medecine

country: Belgium

institute: Unamur

summary: Circular RNAs (circRNAs) are covalently closed RNA molecules, supporting a wide diversity of functions. While aberrant circRNA expression stands as a recognized hallmark of cancer development, our attention has turned to investigate their role in viral infections, specifically Mardivirus Gallidalpha 2 (GaHV-2, MDV) infection. In a previous study focused on the virulent GaHV-2, RB-1B strain, we extensively cataloged circRNAs produced from virulence genes, notably from the MEQ-vIL-8 locus and the Latency Associated Transcripts (LATs) gene. Building upon this groundwork, our current investigation uncovers novel loci expressing viral circRNAs in distinct stages of GaHV-2 infection. Furthermore, we extend our focus to viral circRNA signatures in three commonly used MDV vaccines, the avirulent GaHV-2 (CVI988- Rispens strain), non-oncogenic Mardivirus Gallidalpha 3 (GaHV-3), and non-oncogenic Mardivirus Meleagridalpha 1 (MeHV-1) commercially called Herpesvirus of Turkey (HVT). In these vaccine viruses, we identified viral circRNA expression from a locus antisense to the immediate early ICP4 gene a conserved feature across the three species. This region has been characterized herein for the first time in term of candidate LATs exons and introns for GaHV-3 and MeHV-1. Potential LATs circRNAs were then deeply analyzed and we observed both similarities and distinctions when compared to those of the virulent GaHV-2. Another conserved gene, encoding the DNA packaging protein, was identified as a source of circRNAs in all three species. Eventually, different levels of circRNAs expression were found from the meq locus between virulent and avirulent GaHV-2 strains. Our findings highlight a conserved pattern of viral derived circRNA expression in these related avian alphaherpesviruses. This conservation underscores the potential significance of these transcripts in completing the viral cycle and facilitating viral spread.

overall_design:
To identify Latency associated transcripts splicing pattern from three viruses used in Marek's Disease vaccination program, we used in vitro  lytic infection of ESCDL-1 cells with GaHV-2 CVI-988 (Acc. n° DQ530348), GaHV-3 SB-1(Acc. n° NC_002577), and MeHV-1 FC-126 (Acc. n° NC_002641) viral strains .
We extracted RNAs from the infected cell lines and send them for paired-end RNA sequencing at Novogene.
We processed the data through vCircTrappist to identify spliced RNAs (sense and antisense).

first: Alexis

last: Chasseur

first: Pierre

last: Lombard

first: Béatrice

last: Danneels

last: Letellier

first: Ahmed

last: Kheimar

first: Yu

last: You

first: Caroline

last: Denesvre

first: Benedikt

last: Kaufer

first: Damien

last: Coupeau

first: Benoît

last: Muylkens


title: FXR1 dominates mRNA export fate via riboregulation during hESC differentiation

city: Beijing

first: Zhongyang

last: Chen

address: No.5, Dongdan Santiao, Dongcheng District

institute: School of Basic Medicine, Peking Union Medical College (PUMC)

summary: mRNA export is required for its translation into functional protein, facilitated by the interaction between mRNA transporters and nuclear pore complex (NPC). However, only a few mRNA transporters associated with NPC were identified. Here, we comprehensively depicted NPC interactome in human embryonic stem cells (hESCs), from which we identified a series of novel mRNA transporters. Among them, FXR1 functioned as a cytoplasmic mRNA acceptor, promoted the release of G-quadruplex containing mRNA from its export receptor, simultaneously mediated the localization of nucleoporins mRNA on nuclear pore. FXR1 bound G-quadruplex or nucleoporin AGAA RNA via its RGG and KH domain respectively, which in turn weakened or enhanced its binding to nuclear pore, thus resulted in mRNA release or localization. More importantly, the decline of FXR1 and nuclear pore activity helped hESCs to achieve fate transition by impeding the nuclear export of transcribed RNAs, which was required for hESC differentiation.

overall_design: RNA-seq and eCLIP-seq datasets.

first: Jiabin

last: Yang

first: Yanni

last: Ma

first: Jia

last: Yu


title: Conserved and distinct expression of circular RNAs in commercially used Marek’s disease vaccine viruses

type: Non-coding RNA profiling by high throughput sequencing

overall_design:
To identify circRNAs expression from three viruses used in Marek's Disease vaccination program, we used in vitro  lytic infection of ESCDL-1 cells with GaHV-2 CVI-988 (Acc. n° DQ530348), GaHV-3 SB-1(Acc. n° NC_002577), and MeHV-1 FC-126 (Acc. n° NC_002641) viral strains .
We extracted RNAs from the infected cell lines and treated them with RNase R before sending them for paired-end RNA sequencing at Novogene.
We processed the data through vCircTrappist to identify candidate circRNAs.


title: Gene expression profile at single cell level of an orthotopic mouse model with ZEB1 knockdown  in the KPC cell line and control group mouse [spatial transcriptomic]

status: Public on Aug 20 2025

city: Peking

first: Mingyang

last: Liu

address: No.17, Panjiayuan South, Chaoyang District

institute: State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital

summary: Pancreatic cancer is characterized by high resistance to chemotherapy and immunotherapy and there are no effective drugs which leads to poor overall survival for pancreatic cancer patients. The transcription factor ZEB1 promotes cellular plasticity and tumor metastasis in pancreatic cancer. We employed single-cell RNA sequencing and spatial transcriptomic sequencing to analyze ZEB1-mediated remodeling of the tumor microenvironment in pancreatic cancer.

overall_design: Spatial transcriptomic sequencing of an orthotopic mouse model injected with KPC-shV and KPC-shZEB1 cells.

first: Shaobo

last: Zhang

first: Yumeng

last: Hu

first: Zhijun

last: Zhou

first: Gaoyuan

last: Lv


title: ZMYND11 Functions in Bimodal Regulation of Latent Genes and Brain-like Splicing to Safeguard Corticogenesis [RNA-seq]

status: Public on Aug 21 2025

city: Cincinnati

first: Jason

last: Tchieu

address: 240 Albert Sabin Way

institute: Cincinnati Children's Hospital Medical Center

summary: While the identification of pathogenic variants linked to neurodevelopmental (NDD) and autism spectrum disorders (ASD) has advanced rapidly, the mechanisms underlying these genetic risks remain unclear. Here, we leveraged a human pluripotent stem cell model to uncover the neurodevelopmental consequences of mutations in ZMYND11, a newly implicated risk gene. ZMYND11, known for its tumor suppressor function, encodes a histone-reader that recognizes sites of transcriptional elongation and acts as a co-repressor. Our findings reveal that ZMYND11 deficient cortical neural stem cells exhibit upregulation expression of latent developmental pathways, leading to impaired production of secondary neural progenitors and neurons. In addition to its chromatin-related functions, we found ZMYND11 orchestrates a brain specific isoform switch that affects migration and proliferation of cortical neural stem cells. We further demonstrated that brain specificity is likely to involve the activity of the splicing regulator RBFOX2. Finally, we extended our findings to 10 additional lines with different chromatin-related NDD/ASD risk factors and identified a subset displaying similar activation of developmental pathways and splicing dysregulation, which could partially be rescued by leveraging the transcriptional repression and splicing coordination of ZMYND11. Collectively, our work highlights the critical role of ZMYND11 in regulating developmental signals and alternative splicing, offering novel insights into the molecular pathology of ZMYND11-associated NDDs. Moreover, these findings suggest broader convergence with other genetic risk factors for NDD/ASD, presenting potential therapeutic avenues for intervention.

overall_design: To investigate the role of ZMYND11 in corticogenesis, we performed RNA-seq on WT and ZMYND11 mutant human embryonic stem cells and d18 cortical neural stem cells, WT d18 cortical neural stem cells that overexpressed FLAG-ZMYND11 or not for 3 days, and d18 cortical neural stem cells differentiated from a subset of Autistic mutants (termed "Class I") and isogenic controls (UMOD edited).

first: Xuyao

last: Chang


title: N460S on PB2 and I163T on nucleoprotein synergistically enhance the replication and pathogenicity of influenza B virus

city: Guangzhou

first: yuting

last: Ye

address: Guangzhou Dongfengxi road

institute: Guangzhou Medical University

summary: Influenza B virus (IBV), though often overshadowed by influenza A viruses (IAVs), remains a significant global public health concern, particularly during seasons when it predominates. However, the molecular mechanisms underlying IBV pathogenicity remain largely unknown. In this study, we analyzed polymerase polymorphisms in an IBV isolated from a single patient’s oropharyngeal swab and identified two plaque colonies with distinct replication and pathogenicity phenotypes, associated with the PB2:N460S and NP:I163T substitutions. Using reverse genetics, we generated recombinant IBV mutants to evaluate the impact of these substitutions. The results showed that while neither mutation alone significantly affected viral replication or pathogenicity, their combination markedly enhanced both. Transcriptomic analysis of infected lung tissues revealed heightened immune activation, including upregulation of antiviral and immune-related genes, contributing to excessive inflammation and disease severity. Mechanistically, both substitutions increased protein expression and strengthened PB2-NP interaction, but only together did they enhance polymerase activity. Structural modeling suggested that PB2:460 is positioned at the PB2-NP interface, whereas NP:163 is not, indicating an indirect functional interplay. These findings provide new insights into the molecular determinants of IBV pathogenesis, highlighting the synergistic effect of PB2:N460S and NP:I163T in enhancing viral fitness and exacerbating disease outcomes.

overall_design: Mice lungs intranasally infected with the recombinant influenza B viruses rgPB2460N/NP163I or rgPB2460S/NP163T were harvested at 5 dpi for RNA sequencing. Control mice were inoculated with 50 μl of PBS only. Total RNA was extracted using the Tissue RNA Purification Kit PLUS (EZBioscience). RNA libraries for mRNA sequencing were prepared with the NEBNext® Ultra™ RNA Library Prep Kit for Illumina (NEB), following the manufacturer's instructions.

first: Weiqi

last: Pan

last: Gao


title: BRRIAR lncRNA alters breast cancer risk by modulating interferon signaling in cis and in trans through BHLHE40 and RIG-I

status: Public on Aug 19 2025

city: Brisbane

first: Juliet

last: French

address: 300 Herston Rd

country: Australia

institute: QIMRB

summary: Interferons (IFNs) are key regulators of cell proliferation and anti-tumor immunity. We identified a breast cancer-associated long noncoding RNA (lncRNA), BRRIAR, that modulates IFN signaling in estrogen receptor-positive (ER+) breast cancer. BRRIAR is transcribed from an 11 kb enhancer cluster at 3p26, and its reduced expression is linked to breast cancer GWAS risk variants. Primarily expressed in ER+ breast tumors, BRRIAR exhibits dual functionality, acting both in cis and in trans. Nuclear BRRIAR regulates BHLHE40 expression through its enhancer, while cytoplasmic BRRIAR binds to the pattern recognition receptor RIG-I, modulating its activation. BRRIAR RNA overexpression activates RIG-I signaling, inducing IFN responses that selectively trigger apoptosis in ER+ breast tumor cells in vitro and in vivo, while promoting immune activation in human peripheral blood mononuclear cells. These findings emphasize the complex regulatory mechanisms at GWAS risk regions, reveal the critical role of lncRNAs as modulators of tumor immunity and identify BRRIAR as a promising RNA-based therapeutic for ER+ breast cancer.

overall_design: H3K27ac ChIPseq data in T47D cells after CRISPRi-BRRIAR or using gRNAs targeted to the 3’ end of the enhancer cluster. T47D cells were cross-linked with 1% formaldehyde (Merck) at 37oC for 10 min, rinsed with phosphate buffered saline (PBS; TMO) containing 5% bovine serum albumin (BSA; Scientifix) and harvested in PBS containing protease inhibitor cocktail (PIC; Roche). Harvested cells were centrifuged for 2 min at 3,000 rpm. Cell pellets were resuspended in lysis buffer (1% sodium dodecyl sulfate (SDS; Merck), 10 mM EDTA (TMO), 50 mM Tris-HCl, pH 8.1, PIC) and sonicated three times for 15 s at 70% duty cycle (Branson SLPt) then centifuged at 13,000 rpm for 15 min. Supernatants were resuspended in dilution buffer (1% Triton X-100, 2 mM EDTA, 150 mM NaCl, 20 mM Tris-HCl, pH 8.1). Antibodies detecting H3K27ac (2 μg; Abcam) or an IgG control (2 μg; Abcam) were prebound for 6 h to protein G Dynabeads (TMO), then incubated with the chromatin for 16 h. The complexes were then washed six times in RIPA buffer (50 mM Tris-HCl, pH 8.0, 150 mM NaCl, 1% IGEPAL CA-630, 0.5% sodium deoxycholate (Merck), 0.1% SDS, 1 mM DTT, PIC). To reverse cross-links, the complexes were incubated at 65oC for 16 h in elution buffer (1% SDS, 0.1 M NaHCO3), then DNA fragments purified using the QIAquick spin kit (Qiagen). Libraries were prepared using the NEBNext Ultra II DNA library prep kit (NEB), according to manufacturer’s instructions.

first: Mainá

last: Bitar

first: Stacey

last: Edwards

first: Jonathan

last: Beesley


title: Antisense transposon insertions into host genes trigger piRNA mediated immunity

city: Vienna

first: Dominik

last: Handler

address: Dr. Bohr-Gasse 3

country: Austria

institute: IMBA-Institute of Molecular Biotechnology of Austrian Academy of Sciences

summary: Transposable elements pose a persistent threat to genome integrity, yet how host defense systems adapt to newly invading elements remains poorly understood. Here, we reveal how Drosophila melanogaster acquired PIWI-interacting RNA (piRNA)-mediated immunity against the recently invading endogenous retrovirus tirant. By integrating genetics, small RNA profiling, and population genomics, we identify two distinct modes of de novo piRNA biogenesis. The primary mechanism involves antisense insertions into the flamenco cluster, a well-established master locus for transposon control. Strikingly, we also find that antisense tirant insertions into 3′ UTRs of host genes robustly trigger piRNA production, a process driven by host gene transcription but independent of gene identity. These findings challenge prevailing models that link piRNA precursor specification to genomic origin or nuclear processing context. Instead, they uncover a flexible, general mechanism in which transposition into host gene exons represents a critical vulnerability for transposons: by generating chimeric antisense transcripts that are exported to the cytoplasm, transposons inadvertently initiate their own silencing, enabling rapid and adaptive genome defense against new invaders.

overall_design: small RNA-seq profiling from the Drosophila Synthetic Population Resources (DSPR) founder strains

first: Rafanel

last: Baptiste

first: Protsenko

last: Liudmila

first: Handler

last: Dominik

first: Brennecke

last: Julius

first: Senti

last: Kirsten-André


title: Single cell transcriptional landscape of liver transplant rejection reveals tissue persistence of clonally expanded, treatment-resistant T cells

first: Erica

last: DePasquale

state: OH

address: 3333 Burnet Ave.

department: Gastroenterology

institute: Cincinnati Children's Hospital

summary: T cell mediated rejection (TCMR) affects ∼50% of pediatric liver transplant recipients within 5 years, and late TCMR is associated with graft failure due to ineffective treatment. Although CD8+ T cells promote late TCMR, their clonal expansion, intragraft persistence, localization, and gene expression remain largely undefined. Herein, single-cell RNA sequencing and immune repertoire profiling of 30 cryopreserved liver biopsies from rejecting and non-rejecting pediatric patients identified expanded intragraft CD8+ T cell clonotypes (CD8EXP) and their gene expression profiles. Expanded CD8+ clonotypes (CD8EXP) bore markers of effector and CD56hiCD161- 'NK-like' T cells, retaining their clonotype identity and phenotype in serial biopsies despite histologic TCMR resolution. CD8EXP clonotypes localized to portal infiltrates during active TCMR and persisted in the lobule after histologic TCMR resolution. MultiNicheNet analysis revealed differential crosstalk between Kupffer cells (KC) and CD8EXP, with activation of TGFß and downregulation of CD47 immune checkpoint signaling. Therefore, persistenting intragraft CD8EXP clones remain active despite TCMR treatment and may contribute to long-term allograft fibrosis and failure of operational tolerance.

overall_design: 10X Genomics Chromium Next GEM Single Cell V(D)J Reagent Kit was used on needle biopsies from human liver rejection patients and associated healthy controls (pre-transplantation donors).

first: Anna

middle: L

last: Peters

first: Gousia

last: Begum

first: Krishna

last: Roskin

first: Michael

last: Kotliar

first: Artem

last: Barski

first: Nathan

last: Salomonis

first: Tiffany

last: Shi

first: Sarangarajan

last: Ranganathan

first: E

last: Woodle

first: David

last: Hildeman


first: Mulin Jun

last: Li

state: Guangdong

address: No. 9 Jinsui Road, Guangzhou

institute: Guangzhou Women and Children's Medical Center

summary: To investigate the internal regulatory mechanisms governing the CD28 gene region during T cell activation and to screen for truly active dynamic chromatin regulatory elements responsive to stimulation, we employed the CRISPRa gene editing technology to design specific sgRNAs targeting this region and conducted a tilling CRISPRa screen sequencing on the CD28 gene region.

overall_design: We performed tilling CRISPRa screening of CD28 gene region in Jurkat cells. Anti-CD28 and anti-CD3 antibodies were utilized to activate T cells as previously described (Simeonov et al. Nature, 2017). Briefly, the culture plate was coated with 10 µg/ml of anti-CD28 (TONBO Biosciences, 40-0289) for 12 hours at 4°C prior to cell inoculation. Jurkat or CD4+ T cells were then seeded with 10 µg/ml of anti-CD3 (40-0038). The cells were harvested 24 hours later for subsequent experimental analysis.

first: Zhao

last: Wang

first: Wei

last: Dong


title: Campylobacter hepaticus transcriptomics revealed the genes involved in the Spotty Liver Disease (SLD)  pathogenesis

status: Public on Aug 18 2025

city: Gainesville

first: Subhashinie

last: Kariyawasam

state: Florida

address: 1945 SW 16th Ave

department: Comparative, Diagnostic, and Population Medicine

institute: University of Florida

summary: Campylobacter hepaticus, the causative agent of spotty liver disease (SLD) in commercial layer hens, leads to liver necrosis, reduced egg production, and increased mortality. Despite its impact, the pathogen’s virulence mechanisms remain poorly understood. This study used high-throughput transcriptomics to analyze gene expression profiles of C. hepaticus cultured in vitro bile, infected with LMH cells, and SLD affected chicken livers (in vivo) obtained from field cases to uncover key factors involved in host adaptation and pathogenicity

overall_design: To investigate the differential gene expression profiles of C. hepaticus in three distinct conditions (bile, LMH cell line, and SLD infected- liver)

first: Varsha

last: Bommineni

first: Lekshmi

middle: K

last: Edison

first: Chaitanya

last: Gottapu

first: Gary

middle: D

last: Butcher


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

status: Public on Aug 16 2025

first: Xiao-Hui

last: Tan

address: 8, Xishiku Street, Xicheng District

institute: Peking University First Hospital

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

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

first: Rui-Li

last: Guan


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

status: Public on Aug 15 2025

first: Yu

last: Chen

state: Select...

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

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

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

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


title: Transcriptomic insights and feeder-free culturing of porcine expanded potential stem cells from cloned embryos

city: Cheongju

first: Lian

last: Cai

state: Chungcheongbuk-do

address: 1 Chungdae-ro, Seowon-gu

institute: Chungbuk national university

summary: Background: Generating expanded potential stem cells from cloned porcine embryos (pEPSCsNT) represents a notable advancement in regenerative medicine and agricultural biotechnology. However, challenges, including low derivation efficiency, limited understanding of transcriptomic features, and unknown feasibility of culturing under feeder-free conditions, remain. This study aimed to generate pEPSCs using blastocysts derived from parthenogenetic activation, in vitro fertilization, and somatic cell nuclear transfer (SCNT) using a modified culture system. Methods: We derived pEPSCNT lines using an optimized culture system. We characterized the pEPSC lines from all three origins by analyzing pluripotent marker expression, performing karyotyping, and assessing their differentiation potential into the three germ layers. Furthermore, we performed a comparative transcriptomic analysis using in vivo and cloned embryo data, with a major focus on cell lines derived from SCNT (pEPSCsNT). We optimized feeder-free culture conditions for the pEPSCNT line and derived the pEPSCNT lines using an optimized culture system with an efficiency of ~14%. Results: The cells were closely correlated with 8-cell to morula-stage embryos and exhibited significant enrichment of EPSC signature genes, suggesting a unique pluripotent state relatively close to the naïve state, specifically within a formative state. The pEPSCsNT possessed broad differentiation capacity, indicative of Hippo signaling pathway enrichment, blastocyst-like structure formation ability, and potential differentiation into trophoblast lineage cells. Conclusions: Our modified culture medium combined with the 2× Matrigel coating system facilitated the transition to feeder-independent culture conditions. These findings facilitate the establishment of a feeder-free culture system while preserving pluripotency and differentiation potential.

overall_design: RNA-seq profiling of the EPSCsNT line, SCNT-derived blastocysts at Day 7, and induced pluripotent cells (iPSCs) line of pig

first: Mirae

last: Kim

first: Hyerin

last: Choi

first: Haneul

first: Sang-Hwan

last: Hyun

first: Eunhye


title: Pan organ and time course analysis of T cells in acute LCMV (armstrong) infection (day 60) [I40]

city: Boston

first: Liang

last: Yang

state: MA

address: 77 Avenue Louis Pasteur

department: Pathology

institute: Harvard Medical School

summary: This study is part of the immgenT Open Source Project, specifically from IGT40, which focuses on a pan-organ and time course analysis of T cells in acute LCMV (Armstrong) infection at day 60 post-infection. The dataset includes T cells isolated from multiple organs: spleen, prostate, submandibular gland, bone marrow, mesenteric lymph node, small intestine epithelium, small intestine lamina propria, lung, and mediastinal lymph node. 7-week-old male C57BL/6J mice infected intraperitoneally with 2×10^5 PFU LCMV Armstrong, and T cells were analyzed at 60 days post-infection (dpi). The study includes both endogenous T cells and adoptively transferred P14 and SMARTA TCR transgenic T cells. Mice received IV 100,000 SMARTA (CD45.1.2) and 50,000 P14 (CD45.1) T cells one day before infection.

overall_design: T cells were isolated from individual organs using mechanical dissociation, enzymatic digestion (collagenase I or DTE), and anti-CD45 intravenous labeling to distinguish tissue-resident from circulating cells. Sorted CD3e+ or IV- CD3e+ were profiled using single-cell RNA sequencing (10x Genomics), combined with CITE-seq (TotalSeq C) and paired TCR α/β sequencing. Samples were pooled using hashtags.

first: Giovanni

last: Galletti

first: Sara

last: Quon

first: Nicole

last: Scharping

first: Kennidy

last: Takehara

first: Amir

last: Ferry

first: Ananda

last: Goldrath


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

status: Public on Aug 17 2025

city: Hangzhou

first: Songying

last: Zhang

address: No.3 Qingchun East Road

department: Department of Obstetrics and Gynecology

institute: Sir Run Run Shaw Hospital

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

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


title: Pan organ and time course analysis of T cells in acute LCMV (armstrong) infection (day 7) [I36]

summary: This study is part of the immgenT Open Source Project, specifically from IGT36, which focuses on a pan-organ and time course analysis of T cells in acute LCMV (Armstrong) infection at day 7 post-infection. The dataset includes T cells isolated from multiple organs: spleen, prostate, submandibular gland, bone marrow, mesenteric lymph node, small intestine epithelium, small intestine lamina propria, lung, and mediastinal lymph node. 7-week-old male C57BL/6J mice infected intraperitoneally with 2×10^5 PFU LCMV Armstrong, and T cells were analyzed at 60 days post-infection (dpi). The study includes both endogenous T cells and adoptively transferred P14 and SMARTA TCR transgenic T cells. Mice received IV 100,000 SMARTA (CD45.1.2) and 50,000 P14 (CD45.1) T cells one day before infection.


title: Enterocyte dedifferentiation drives colonic regeneration following irradiation injury [scRNA-seq]

first: Mengxian

address: Beijing

institute: Tsinghua University

summary: The intestinal epithelium consistently exposes to various injuries and exhibits remarkable regenerative capacity. Although small intestinal regeneration has been extensively investigated, the mechanisms governing colonic regeneration remain poorly understood. Here, we identify irradiation-induced regenerative cells (IRECs), a previously unrecognized colonic enterocyte population, emerges following irradiation injury. IRECs, marked by the gene YuanShangCao (Ysc), undergo dedifferentiation and transition into a stem-like state, contributing to epithelial regeneration. IREC ablation severely impairs colonic repair. Mechanistically, YSC promotes colonic regeneration by preventing the lysosomal degradation of YAP. Furthermore, we demonstrate a critical role of p53 in colonic regeneration by inducing Ysc expression. Together, our findings define IRECs as an irradiation injury-induced enterocyte population that dedifferentiate into stem cells in colon epithelial repair and establish the p53-YSC-YAP axis plays a key role in this process, deepening the understanding of colonic diseases.

overall_design: In this study, leveraging a colon irradiation injury model coupled with single-cell sequencing, we identified a population of irradiation-induced Ysc+ cells. Through RNA velocity analysis and lineage tracing experiments, we demonstrated that these cells are a population of colonic absorptive enterocytes capable of dedifferentiation. They are activated by p53 and play a crucial role in colon regeneration, thereafter we call them irradiation-induced regenerative cells (IRECs). Further, we revealed that as the marker of IRECs, Ysc plays an important role in epithelial injury repair. Organoids deficient of Ysc were found to be more sensitive to irradiation damage, and the colonic injury repair capacity was impaired in mice lacking Ysc. Mechanistically, Ysc can affect lysosome function and activating YAP signaling by inhibiting its lysosomal degradation.

first: Ye-guang

first: Zeyu

last: Zang

first: Wanlu

last: Song


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

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

overall_design: Refer to individual Series


title: Evolution of the human autopod skeleton [ATAC-seq]

city: Cambridge

first: Terence

last: Capellini

address: 11 Divinity Avenue

department: Human Evolutionary Biology

institute: Harvard University

summary: We investigate the genetic architecture of autopod development at the regulatory and transcriptomic level.

overall_design: Examination of open chromatin regions (ATAC-seq) and differentially expressed genes (RNA-seq) in the developing autopod skeleton.

first: Alexander

last: Okamoto


title: Crotonate-activated histone H3K14 crotonylation enhances intestinal regeneration after injury [RNA-seq]

status: Public on Aug 13 2025

first: Ye-Guang

last: Chen

state: China

address: Haidian  District

summary: The intestinal epithelium undergoes rapid turnover driven by Lgr5+ intestinal stem cells (ISCs) at the crypt base, and can recover despite ISC loss during damage. However, the role of epigenetic modifications in regulating this regeneration remains unclear. In this study, we report that H3K14 crotonylation (H3K14cr), a vital histone modification mediated by the acyltransferase HBO1, is essential for intestinal regeneration. HBO1 ablation in the intestinal epithelium exacerbates dextran sulfate sodium (DSS)-induced colitis.

overall_design:
Part1:
We performed  gene expression analysis with RNA-seq data  from control and HBO1 KO small intestinal organoids. Otherwise,to study the function of HBO1 in intestinal regeneration, we analyzed RNA-seq data from control and HBO1 KO colonic epithelial cells  derived from DSS-treated mice.
Part2:
This study aims to characterize transcriptional dynamics during tissue damage and subsequent regeneration. Mice are treated with 3% DSS for 5 days, followed by normal drinking water. Colonic crypts were isolated at the indicated time points for bulk RNA-seq.

first: Yanhui

last: Xiao

first: Shicheng

last: Yu


title: Analyzing the effects of benzodiazepines on key virulence-related parameters of Pseudomonas aeruginosa

status: Public on Aug 11 2025

city: Palma de Mallorca

first: Carlos

last: Juan

address: Crta. Valldemossa 79

country: Spain

institute: Health research Institute of the Balearic Islands

summary: Sedation with benzodiazepines (BZs) has eventual side-effects proved to entail incremented risks for ventilator-associated pneumonia (VAP) (e.g. immunity alterations and nervous/mechanical responses increasing the aspiration of upper respiratory tract-colonizing bacteria), but some knowledge gaps on the topic exist. For instance, it has never been approached whether BZs could cause a modulation of intrinsic bacterial virulence, and/or influence the host-pathogen interaction in neglected contexts (e.g. respiratory epithelium features, or the lytic/opsonic activity of complement) to facilitate VAP development. Thus, to enrich the picture of factors contributing to the BZs-associated higher risk for VAP, we analyzed relevant in vitro, ex vivo and in vivo infection-related parameters to decipher whether they could be affected by these sedatives in the top VAP-causing pathogen Pseudomonas aeruginosa.  While most variables were unaltered (including among others invertebrate infection assays and a rat model of VAP), a significantly attenuated pathogenic impact of infection on human respiratory A549 cells (invasion, cytotoxicity and inflammation reduced up to ≈50%) appeared upon BZ exposure at high therapeutic concentrations (diazepam/midazolam 10 µg/ml), potentially because of effects of the drugs mostly on the cultured cells. These facts could entail a BZs-associated stealth pathogen-like behavior of P. aeruginosa on the respiratory epithelium, consisting of a weak immune activation proportional to the mild damage caused, perhaps favoring VAP onset. Strikingly, BZs triggered a significantly increased biofilm formation (up to ≈2-fold > controls) on plastic plates and endotracheal tubes (supported by the upregulation of various biofilm-related genes and c-di-GMP accumulation), suggesting a groundbreaking idea: the BZ-dependent boosted formation of these P. aeruginosa sessile reservoirs, likely enabling bacterial release to deep airways and thus VAP progression. Animal models with prolonged sedation/ventilation periods should be conducted to confirm that BZs pose an added trigger for VAP through the surprising hitherto unknown phenomena revealed here.

overall_design: RNA-seq prfiling of Pseudomonas aeuginosa (from Denmark collection, DK) grown in planktonic (PL) or biofilm (BF) mode of life in response to midazolam 10 ug/ml treatment (M) vs untreated control (C)

first: Isabel mª

last: Barceló

first: Elena

last: Jordana-Lluch

first: Maria

last: Escobar-Salom

first: Jordi

last: Sansó-Sastre

first: Miguel Ángel

last: Estéve

first: Mar

last: Marí-Riba

first: Àlex

last: González-Alsin

first: Anna

last: Tomàs

first: María

last: Tortosa

first: Gabriel

last: Torrens

first: Sebastián

last: Albert

first: Antonio

last: Oliver


title: STAT1-dependent expression in kidney endothelium from mice challenged with LPS

city: Albany

first: Ramon

last: Bossardi Ramos

state: Ny

address: 43 New Scotland Avenue

department: Department of Molecular and Cellular Physiology

institute: Albany Medical College

summary: Severe systemic inflammatory reactions, including sepsis, often lead to shock, organ failure and death, in part through an acute release of cytokines that promote vascular dysfunction. However, little is known about the vascular endothelial signaling pathways regulating the transcriptional profile in failing organs. Among all the cytokines altered during a cytokine storm, IL-6 levels are particularly informative, as they correlate with systemic disease severity and are highly predictive of mortality. Here, we show that loss of endothelial expression of the IL-6 pathway inhibitor, SOCS3, promotes a type I interferon (IFNI)-like gene signature in response to endotoxemia in mouse kidneys and brains. In cultured primary human endothelial cells, IL-6 induces a transient IFNI-like gene expression in a non-canonical, interferon-independent fashion. We further show that STAT3, which we had previously shown to control IL-6-driven endothelial barrier function, is dispensable for this activity. Instead, IL-6 promotes a transient increase in cytosolic mitochondrial DNA and requires STAT1, cGAS, STING, and the IRFs 1, 3, and 4. Inhibition of this pathway in endothelial-specific STING knockout mice or global STAT1 knockout mice leads to reduced severity of an acute endotoxemic challenge and prevents the endotoxin-induced IFNI-like gene signature. These results suggest that permeability and DNA sensing responses are driven by parallel pathways downstream of this cytokine, provide new insights into the complex response to acute inflammatory responses, and offer the possibility of novel therapeutic strategies for independently controlling the intracellular responses to IL-6 in order to tailor the inflammatory response.

overall_design: STAT1KO (JAX #012606) or control C57Bl/6J (JAX #000664) were challenged with 250 ug of LPS and sacrificed 15 hours later. Whole organ RNA was oobtained from an aliquot of kidney single cell suspensions, while the reminder was processed for endoothelial cell enrichment prior to RNA isolation. Each experimental group includes two male and two female mice.

first: Martino

last: Nina

first: Bossardi Ramos

last: Ramon

first: Adam

last: Alejandro Pablo


title: Crotonate-activated histone H3K14 crotonylation enhances intestinal regeneration after injury

first: Ye-Guang

last: Chen


title: Crotonate-activated histone H3K14 crotonylation enhances intestinal regeneration after injury [ChIP-seq]

overall_design: To study how HBO1 regulates ISC and fetal genes expression, the control and HBO1 KO colonic crypts were subject to CUT&Tag and ChIP-seq with HBO1, H3K14ac and H3K14cr antibodies.Otherwise, the control and HBO1 KO mice were treated with 3% DSS, and the crypts were isolated at day 3 for ATAC-seq.

first: Yanhui

last: Xiao

first: Shicheng

last: Yu


title: Role of endothelial SOCS3 in the transcriptional response to LPS

summary: Translating affinity purification (TRAP)-mediated analysis of kidney endothelial translatome of bulk kidney RNA-seq from mice 15 hours after an intraperitoneal challenge with 250 micrograms of LPS per mouse.

overall_design: Total RNA from kidney or endothelial especific. Four groups: WT+Saline, WT+LPS, SOCS3iEKO+Saline, SOCS3iEKO+LPS


title: Rapalink-1 reveals novel TOR dependent genes and the role of agmatinases  in growth and lifespan

city: London

first: Charalampos

last: Rallis

address: Mile End Road

department: School of Biological and Behavioural Sciences

country: United Kingdom

institute: Queen Mary University of London

summary: mTOR is a conserved proaging pathway with characterised inhibitors like rapamycin and torins. A third-generation inhibitor, rapalink-1, has been developed, however, its effects on organismal gene expression and lifespan have not been evaluated. Here, we demonstrate that rapalink-1 affects fission yeast spatial and temporal growth and prolongs chronological lifespan. Endosome and vesicle-mediated transport and homeostasis processes related to autophagy and Pik3, the orthologue of human PI3K, render cells resistant to rapalink-1. Our study reveals mTOR-regulated genes with unknown roles in aging including all fission yeast agmatinases, the enzymes responsible for processing agmatine to putrescine and urea. We identify sensitive and resistant mutants to agmatine and putrescine and show that all fission yeast agmatinase enzymes are required for normal lifespan. Genetic interactome assays for the agmatinase agm1 and further analyses demonstrate that impairing the agmatinergic branch of arginine catabolism results in mTOR activity levels that are beneficial for growth but detrimental for chronological aging. Our study reveals metabolic circuits with possible implications to other systems, including human cells.

overall_design: To compare the effects of Rapamycin and Rapalink-1 on gene expression, S.pombe cells were treated with 100nM of Rapamycin and Rapalink-1 for 5 hours, followed by downstream processing to extract RNA and compare transcriptomic profiles between untreated and treated yeast cells.

first: Rallis

last: Charalampos

first: Kumar

last: Juhi