title: RNA-seq profiling of ADAM10 inhibition in DLD-1 and SW620 colorectal cancer cell lines

city: Brooklyn

first: Pargol

last: Mashati

state: New York

address: 2100 Bedford ave, BSB 2-95

institute: SUNY Downstate

summary: This study examines the transcriptomic effects of ADAM10 inhibition in two human colorectal cancer cell lines, DLD-1 and SW620. Cells were treated with vehicle control or the conformation-specific ADAM10 monoclonal antibody 1H5 for 48 hours, followed by extraction of total RNA and paired-end RNA sequencing. The dataset enables comparative analysis of ADAM10-regulated pathways across different CRC genetic backgrounds, including alterations in Notch and EGFR signaling, metabolic gene programs, and other pathways associated with tumor progression.

overall_design: Total RNA was extracted from human colorectal cancer cell lines DLD-1 and SW620 following treatment with either vehicle control or the ADAM10-targeting monoclonal antibody 1H5 (40 μg/mL) for 48 hours. Cells were cultured under standard conditions, and RNA isolation was performed using a column-based extraction method. RNA-seq was conducted to characterize global transcriptional changes induced by ADAM10 inhibition across two colorectal cancer genetic backgrounds and to identify regulated pathways related to Notch signaling, EGFR signaling, and cancer metabolism.


title: GPR39 activation inhibits AQP2 trafficking and alters cytoskeletal organization

status: Public on Jan 20 2026

city: Baltimore

first: Mackenzie

last: Kui

state: Maryland

address: 725 N Wolfe Street

department: Physiology

country: USA

institute: Johns Hopkins

type: Expression profiling by high throughput sequencing

summary: G protein-coupled receptor 39 (GPR39) is an orphan receptor that is highly expressed in renal collecting duct principal cells. GPR39 activation in vivo leads to reduced urinary concentration capacity. In this study, we utilized mpkCCD cells, a model of principal cells in the collecting duct, to examine the cell biological effects of GPR39 activation. Pharmacological activation of GPR39 with the synthetic agonist cpd1324 impaired vasopressin-mediated aquaporin-2 (AQP2) apical trafficking and reduced total AQP2 expression following long-term treatment, consistent with its known in vivo role. These effects were absent in GPR39 knockout cells. In addition, GPR39 activation altered apical membrane morphology, disrupted the tight junction network, and reduced cortical F-actin expression, suggesting a shift toward a dedifferentiated phenotype. GPR39 activation also increased glycolytic ATP production while reducing mitochondrial ATP output without affecting proliferation. RNA-seq analysis of acutely treated mpkCCD cells revealed upregulation of inflammatory and dedifferentiation-associated gene programs, including cytokines. These findings indicate that the role of GPR39 in principal cells goes beyond AQP2 regulation and imply that GPR39 functions as a negative regulator of epithelial differentiation, perhaps acting to coordinate metabolic and inflammatory responses to stress.

overall_design: Without transformation (WT) and Gpr39 knockout (KO) mpkCCD cells were seeded onto 12-well transwell inserts and cultured in complete media without dDAVP for 9 days to allow for full polarization. Cells were then switched to simple media for 24 hours prior to treatment. Cells were treated with either 1 µM cpd1324 + 10 µM ZnCl₂ or vehicle control (0.1% DMSO + 10 µM ZnCl₂) for 2 hours. Following treatment, total RNA was extracted using the RNeasy Mini Kit (Qiagen, Cat# 74104) according to the manufacturer’s instructions.

first: Jessica

last: Zhang

first: Ibrahim

last: Ahmed

first: Shishir

middle: K

last: Patel

first: Tarah F

last: Rastegar

first: Hamid

last: Rabb

first: Jennifer

middle: L

last: Pluznick


title: Embryonic stem cell factors DPPA2/4 amplify active H3K4me3-H2AK119ub chromatin domains in non-small cell lung cancer (ChIP-seq)

city: Melbourne

first: Janith

last: Seneviratne

state: VIC

address: Peter MacCallum Cancer Centre, 305 Grattan Street

country: Australia

institute: Peter MacCallum Cancer Centre

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Embryonic regulators are often re-expressed in cancers, however the functional and molecular significance of this is not always understood. The epigenetic priming factors Developmental Pluripotency Associated 2 and 4 (DPPA2/4) have crucial roles in early development and are implicated in cancer pathogenesis. We reveal in non-small cell lung cancer (NSCLC), DPPA2/4 co-expression is associated with poorly differentiated tumours and impaired patient outcomes. Biochemically, human DPPA2/4 multimerise for their protein stability and enhanced nucleosome binding activity. In NSCLC cells, DPPA2/4 bind CG-rich sequences including promoters of developmental, Wnt signaling and catabolic genes. Chromatin state modelling revealed DPPA2/4 preferentially bind active H3K4me3 and H3K27ac domains that were intriguingly also enriched for PRC1 and its product H2AK119ub, validated by H3K4me3-H2AK119ub sequential ChIP. Knockdown experiments revealed DPPA2/4 were required to maintain RING1B and H2AK119ub at these domains. Surprisingly, despite the presence of PRC2.1, these regions lacked any detectable H3K27me3, suggesting an uncoupling between the recruitment of PRC2 to chromatin and its catalytic product. When exogenously over-expressed in NSCLC cells where they are not normally present, DPPA2/4 bind to and promote active chromatin states, resulting in an increase in vivo xenograft tumour growth. Our results demonstrate how in NSCLC cells, DPPA2/4 act as molecular amplifiers of active and poised chromatin. Together, this highlights how aberrant re-activation of embryonic factors in cancers may take on new functions, promoting tumourigenesis.

overall_design: The NCI-H661 cell line is derived from lung large cell carcinoma (subtype of non-small cell lung cancer) metastases and expresses both DPPA2 and DPPA4 highly at the mRNA and protein level. In order to investigate DPPA2/4 binding, transcription factor binding (KDM2A, SUZ12) and histone modifications (H3K4me3, H3K4me1, H3K36me3, H3K36me2, H3K9me3, H3K27me3, H2AK119ub and H3K27ac) in NCI-H661 cells we performed ChIP-seq analyses of these modifications at baseline. We also assessed histone modifications (H3K4me3, H3K4me1, H3K36me3, H3K9me3, H3K27me3, H2AK119ub and H3K27ac) in the NCI-H1299 cell line model following induced expression of DPPA2/4 after 7 days. All assays were controlled with genomic input controls with all conditions having duplicate replicates.

middle: A

first: Melanie

last: Eckersley-Maslin


title: TRMT6 mitigates susceptibility and progression of DSS-induced colitis multifacetedly via translational regulation

status: Public on Jan 19 2026

city: Hangzhou

first: Aiwei

last: Wu

state: Zhejiang

address: 2318 Yuhangtang Road

department: School of Basic Medical Sciences

country: China

institute: Hangzhou Normal University

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

overall_design: Refer to individual Series


title: Bariatric surgery reverses ORG and exhibits a distinct transcriptomic profiel compared to weight loss through a low-fat diet

city: Sant Joan Despí

first: Maruja

last: Navarro-Díaz

state: Barcelona

address: Oriol Martorell, 12

department: Nephrology

country: Spain

institute: Hospital Sant Joan Despí Moisès Broggi

summary: Weight loss is central to treating obesity-related kidney disease, yet the renal effects of low-fat diet (LFD) versus bariatric surgery (BS) remain incompletely understood. This study compared their impact on obesity-related glomerulopathy (ORG). Twenty-eight male Wistar rats were fed a high-fat diet (HFD) for 10 weeks to induce obesity. Eight rats were sacrificed (HFD group), eight switched to LFD for 10 weeks, and twelve underwent sleeve gastrectomy. Body weight, albuminuria, renal histology, and transcriptomic profiles were analyzed. Weight loss was modest in the LFD group (−1.6%) but substantial after BS (−13.2%), occurring 2.1 times faster. Albuminuria decreased in both interventions compared to HFD (LFD: 7228 ± 514 ng/mL, BS: 6242 ± 418 ng/mL; HFD: 10384 ± 1168 ng/mL; p < 0.01) and correlated strongly with weight loss (R² = 0.78). Glomerular area was reduced in both groups, but only BS achieved complete histological resolution of ORG. Tubular cells in BS-treated rats showed megamitochondria and cristae disruption, while LFD induced milder alterations. Transcriptomics revealed suppression of mitochondrial maintenance genes and upregulation of oxidative stress and immunometabolism pathways. Immune-related genes upregulated in BS clustered into pro-inflammatory/chemotactic and regulatory modules. To the best of our knowledge, this is the first evidence that BS fully reverses ORG, highlighting renal effects beyond weight loss alone.

overall_design: Twenty-eight Wistar rats were first fed a high-fat diet for 10 weeks to induce obesity. They were then divided into three groups: an obese control (HFD group), a low-fat diet (LFD) group, and a bariatric surgery (BS) group, all evaluated for weight, albuminuria, kidney histology, and transcriptomics. Raw data for the the HFD samples are available under PRJNA1092068 (GSE262503).

middle: M

last: Navarro

first: Mariapilar

last: Armengol

first: Mireia

last: Ferrer


title: Embryonic stem cell factors DPPA2/4 amplify active H3K4me3-H2AK119ub chromatin domains in non-small cell lung cancer (reChIP-seq)

overall_design: The NCI-H661 cell line is derived from lung large cell carcinoma (subtype of non-small cell lung cancer) metastases and expresses both DPPA2 and DPPA4 highly at the mRNA and protein level. In order to investigate H2AK119ub and H3K4me3 co-occupancy relative to DPPA2/4 in NCI-H661 cells we performed sequential ChIP (reChIP) analyses of these histone modifications. Analyses were conducted in parental H661 cells. All conditions were done in biological duplicates.


title: Embryonic stem cell factors DPPA2/4 amplify active H3K4me3-H2AK119ub chromatin domains in non-small cell lung cancer (ChIPRx-seq)

overall_design: The NCI-H661 cell line is derived from lung large cell carcinoma (subtype of non-small cell lung cancer) metastases and expresses both DPPA2 and DPPA4 highly at the mRNA and protein level. In order to investigate histone modifications (H3K4me3, H3K27me3, H2AK119ub and H3K27ac) in NCI-H661 cells we performed ChIP-seq analyses of these modifications with exogenous mouse spike-ins to account for potential global changes (E14 mouse embryonic stem cells) following either shRNA mediated knockdown of DPPA2/4 for 7 days or H3K27ac ablation with the catalytic p300/CBP inhibitor A-485 for 1 day. All assays were controlled with genomic input controls with all conditions having either duplicate or triplicate replicates.


title: GLASS-OD primary – recurrent oligodendrogliomas

city: Rotterdam

first: Youri

last: Hoogstrate

address: Wytemaweg 80

department: Neurology

country: Netherlands

institute: Erasmus MC

type: Methylation profiling by genome tiling array

summary: Background: Treatment decisions in IDH-mutant oligodendrogliomas are shaped by tumor aggressiveness, underscoring the need for objective grading of these malignant brain tumors. Material and Methods: We collect 302 primary and recurrent resections from oligodendrogliomas and perform Ki-67 staining, proteomics and DNA methylation profiling. Results & conclusion: During tumor progression, DNA methylation of oligodendrogliomas changes along a continuum. This continuum is linked to increased epigenetic aging, methylation of transcription factors and Ki-67+ cell density, and to large scale DNA demethylation. Demethylation correlates with CpGs flanking sequences preferred by TET enzymes. We confirm these findings in previously profiled astrocytomas, indicating IDH-mutant gliomas progress along a shared epigenetic axis. We develop an objective DNA methylation based prognostic continuous grading coefficient (CGCψ) that capturs these changes and outperformed WHO grading for oligodendrogliomas. Our findings underscore the potential of DNA methylation-based grading to more accurately reflect tumor biology and inform clinical decision-making in IDH-mutant gliomas.

overall_design:
Primary – Recurrent Oligodendroglioma pairs were collected as part of the GLASS-OD initiative. Validation set samples were not selected to be resected more than once.
The resection number is in the sample identifier: patient_id-R[surgery_number]
Sample identifiers ending with 2, 3, 4, or 5 (up to five brain surgeries...) are recurrent

first: Pim

middle: J

last: French


title: Embryonic stem cell factors DPPA2/4 amplify active H3K4me3-H2AK119ub chromatin domains in non-small cell lung cancer (ATAC-seq)

overall_design: The NCI-H661 cell line is derived from lung large cell carcinoma (subtype of non-small cell lung cancer) metastases and expresses both DPPA2 and DPPA4 highly at the mRNA and protein level. In order to investigate the functional consequence of peturbing DPPA2/4 we performed shRNA-mediated knockdown of DPPA2 or/and DPPA4 in NCI-H661 cells followed by ATAC-seq analyses. Analyses were conducted for shRNA models following 7 days of induction with either H20 vehicle control or 2ug/mL doxycyline, for control shRNA (shREN), shDPPA2, shDPPA4 or both shDPPA2+4. All conditions were done in biological duplicates.


title: YBX1 Drives Post-Myocardial Infarction Angiogenesis via an m⁶A-IGF2BP1/3 Dependent Stabilization of HIF-1α mRNA

status: Public on Jan 18 2026

city: Xiamen

first: Yuhong

last: Zhou

state: Fujian

address: No. 1999, Guankou Middle Road, Jimei District

department: Department of Basic Medicine

institute: Xiamen Medical College

summary: Angiogenesis plays a vital role in myocardial repair following myocardial infarction (MI). Y-box binding protein 1 (YBX1), an RNA-binding protein known for its role in cancer, is found to be significantly upregulated in endothelial cells within the peri-infarct zone and in hypoxic human umbilical vein endothelial cells (HUVECs). Using in vitro and in vivo models, we demonstrate that YBX1 enhances endothelial cell viability, proliferation, migration, and tube formation. Endothelial-specific overexpression of YBX1 in a murine MI model improved cardiac function and angiogenesis, while YBX1 knockdown aggravated cardiac injury. Transcriptome (RNA-seq) analysis revealed that YBX1 deficiency disrupts HIF-1α signaling. Mechanistically, YBX1 forms a complex with IGF2BP1/3 to stabilize HIF-1α mRNA through N⁶-methyladenosine (m⁶A) modification, thereby promoting angiogenesis and cardiac repair.

overall_design: RNA-seq was performed to analyze global gene expression changes in human umbilical vein endothelial cells (HUVECs) under YBX1 knockdown and control conditions. HUVECs were transfected with siRNA targeting YBX1 (siYBX1) or negative control (siNC). Total RNA was extracted using Trizol reagent, and sequencing libraries were prepared using standard Illumina protocols. Each group contained two biological replicates. Differential expression analysis was conducted using DESeq2 to identify YBX1-dependent transcripts, with particular focus on the HIF-1α signaling pathway.

first: Fangfang

last: Bi

first: Tong

last: Yu

first: Hanyu

last: Liu

first: Miao

last: Cao

first: Yijie

last: He

first: Jin

last: Li

first: Haoshu

last: Wang

first: Chengyu

last: Kong

first: Hongwen

last: Xiao

first: Hua

last: Tian

first: Fu

first: Yun

first: Hongli

last: Shan


title: Effect of stem cell-derived exosome treatments on gene expression during corneal cell differentiation

status: Public on Jan 16 2026

city: Taiyuan

first: yuxing

last: gong

state: Shanxi

address: yingze street

department: Ministry of Education, and the Department of Physiology

institute: Shanxi medical university

summary: To investigate the therapeutic mechanisms of stem cell-derived exosomes in dry eye disease (DED), we conducted a comparative transcriptomic analysis in a murine model. C57BL/6 mice were divided into four experimental groups: (1) Control group (untreated healthy mice); (2) DED model group (induced dry eye disease without treatment); (3) Exosome eye drop group (DED mice treated with topical stem cell-derived exosome eye drops); and (4) Exosome intravenous group (DED mice treated with systemic exosome infusion). After the treatment period, corneal tissues were harvested from each group and subjected to RNA sequencing (RNA-seq) to assess genome-wide gene expression changes. Our analysis revealed distinct transcriptional profiles across groups, highlighting key pathways modulated by exosome administration via both delivery routes. This study provides systematic insights into the molecular responses of corneal cells to exosome-based therapy and offers a basis for optimizing delivery strategies for ocular surface regeneration.

overall_design: RNA-seq profiling of corneal tissue from DED model mice across four treatment groups: untreated control, disease model, exosome eye drop therapy, and exosome intravenous therapy, focusing on pathway-level alterations.


title: TRMT6 mitigates susceptibility and progression of DSS-induced colitis multifacetedly via translational regulation [RNA-seq]

first: Aiwei

last: Wu

summary: The intestinal epithelium, a self-renewing single-cell layer, acts as a physical barrier isolating gut microbiota from deeper tissues. In human IBD and experimental IBD mouse models, this barrier is compromised, causing microbial infiltration and inflammation. However, the pathogenesis of IBD remains to be fully understood. Our research shows that the absence of TRMT6 in the mouse gut impairs the intestinal mucosal barrier, increasing susceptibility to DSS-induced colitis. Mechanically, loss of TRMT6 in intestinal epithelial cells disrupts m¹A modification-mediated translational control and impairs MYC protein synthesis–a deficiency that inhibits epithelial cell proliferation and differentiation. Further multi-omics analyses suggest that TRMT6 deficiency may be associated with perturbations in intestinal lipid metabolism, nutrient absorption, metabolite homeostasis, and gut microbiota composition–changes that could collectively contribute to the acceleration of colitis progression. In summary, TRMT6 is crucial for maintaining small intestinal mucosal barrier function, offering insights into how its deficiency may drive gastrointestinal inflammation in IBD. Given the critical role of TRMT6 in maintaining intestinal homeostasis, our findings highlight its potential as a therapeutic target for IBD treatment.

overall_design: RNA-seq of intestinal tissue of WT (n=3) and Trmt6-/- (n=3) DSS-induced colitis mice.

first: Xianli

last: Zhang

first: Yanting

last: Du

first: Yuefang

last: Ye

first: Xueqing

last: Zhong

first: Chengsong

last: Cai

first: Guodong

first: Hu

first: Liquan

last: Hong


title: Evolutionarily divergent transcriptomic programs in ovarian folliculogenesis across mice, monkeys and humans

city: Kyoto

first: Yukihiro

last: Yabuta

state: Kyoto

address: Yoshida-Konoe-cho, Sakyo-ku

department: Anatomy and Cell Biology

country: Japan

institute: Kyoto University, Graduate school of medicine

sample_organism:
Macaca fascicularis
Homo sapiens
Mus musculus


title: Direct reprogramming of human dermal fibroblasts into functional osteoblasts using cell-permeable Oct4-30Kc19 and Cbfβ-30Kc19

status: Public on Jan 17 2026

city: Chuncheon-si

first: Manho

last: Kim

address: Kangwondaehakgil 1

department: Biomedical science

country: South Korea

institute: Kangwon National University

summary: This study aimed to induce the direct reprogramming of human dermal fibroblasts (HDFs) into osteoblast-like cells using the recombinant fusion proteins Oct4-30Kc19 and Cbfβ-30Kc19. Oct4 is a transcription factor known to play a crucial role in the direct reprogramming of various cell types, while Cbfβ facilitates the differentiation of bone marrow-derived mesenchymal stem cells into osteogenic lineages. To enable intracellular delivery, both transcription factors were fused with 30Kc19, a bombyx mori-derived cell-permeable protein, and expressed using an Escherichia coli system. Oct4-30Kc19 and Cbfβ-30Kc19 were successfully delivered into HDFs, and the treated cells exhibited calcium deposition, a hallmark of functional osteoblasts. RNA sequencing was performed on control, treatment, and positive control (osteoblast) groups, revealing that Oct4-30Kc19 and Cbfβ-30Kc19 treatment shifted the gene expression profile of HDFs toward an osteoblast-like state. These findings suggest that recombinant fusion protein-based transcription factor delivery may serve as a potential strategy for direct cell reprogramming into osteogenic lineages.

overall_design: Oct4-30Kc19 and Cbfβ-30Kc19 were applied to induce the direct reprogramming of human dermal fibroblasts (HDFs) into osteoblasts. To achieve this, HDFs (Gibco) were cultured in osteogenic medium supplemented with Oct4-30Kc19 and Cbfβ-30Kc19, and their gene expression profiles were analyzed by RNA sequencing (RNA-seq) and compared with those of human osteoblasts.

first: Jaeyoung

last: Lee

first: Wijin

first: Songrae

first: Ju Hyun

last: Park


title: Evolutionarily divergent transcriptomic programs in ovarian folliculogenesis across mice, monkeys and humans [Cynomolgus]

summary: Understanding the mechanisms for human ovarian folliculogenesis is fundamental to reproductive biology and medicine. Here, we investigated transcriptomic dynamics in individual oocytes and their associated granulosa cells (GCs) during folliculogenesis in mice, monkeys and humans. Unlike mouse oocytes, which exhibited stage-specific, stepwise transcriptomic maturation, monkey and human oocytes showed minimal transcriptomic changes until the secondary follicle stage and could be broadly categorized as either immature or mature. In all three species, most highly variable genes (HVGs) during oocyte growth displayed monotonic up- or downregulation, with limited overlap in HVGs across species. GCs exhibited similarly species-specific transcriptomic trajectories. Correspondingly, intercellular communication pathways, including ligand–receptor signaling, gap junctions, and metabolic coupling between oocytes and GCs, demonstrated substantial species-specific differences. Nonetheless, X-chromosome dosage compensation and repression of evolutionarily young transposons were conserved across species. We established in vitro culture systems supporting preantral to antral follicle development in monkeys and humans, revealing relatively normal oocyte transcriptome maturation but aberrant GC profiles. By delineating interspecies differences in folliculogenesis, this study provides a framework for understanding human ovarian development and advancing its in vitro reconstruction.

overall_design:
Expression profiling by high throughput sequencing
gene expression datasets for oocytes and granulosa cells

first: Baku

last: Nakakita

first: Ken

last: Mizuta

first: Yoshitaka

last: Katou

first: Hidetaka

last: Tasaki

first: Tomonori

last: Nakamura

first: Chizuru

last: Iwatani

first: Hideaki

last: Tsuchiya

first: Ikuo

last: Kawamoto

first: Tomoyuki

last: Tsukiyama

first: Xun

last: Chen

first: Guillaume

last: Bourque

first: Junko

last: Otsuki

first: Mikiya

last: Nakatsuka

first: Akihito

last: Horie

first: Masaki

last: Mandai

first: Mitinori

last: Saitou

first: Hiroshi

last: Ohta


title: Comparative multi-omics analysis reveals shared and derived mechanisms of fin and limb regeneration [ATAC-seq]

status: Public on Jan 15 2026

city: Baton Rouge

first: Igor

last: Schneider

state: Louisiana (LA)

address: 386 Life Sciences Building, LSU

department: Biological Sciences

institute: Louisiana State University

summary: Comparative studies of vertebrate appendages offer a powerful framework for uncovering shared components of an ancestral regeneration toolkit. Here, we employed a multi-omics comparative approach leveraging the regenerative capacity of the axolotl, zebrafish, and Polypterus senegalus, a fish capable of full fin regeneration. We identified conserved markers of proximal and distal blastema territories, shared activation of DNA damage repair, hif1a-mediated hypoxia response, and sequential activation of pro- and anti-inflammatory program. Apical epithelial ridge markers were expressed in both the wound epidermis and distal mesenchyme during limb and fin regeneration. Notably, hif4a-expressing erythrocytes were uniquely associated with proximal limb and fin amputations but not fin rays, while epidermal myoglobin expression was upregulated only in Polypterus and zebrafish fins. Genome-wide chromatin profiling identified candidate regeneration-responsive elements and a conserved enrichment for AP-1 transcription factor binding. Together, these finding identify shared and derived mechanisms of limb and fin regeneration.

overall_design: ATAC-seq profiling of Polypterus senegalus pectoral fins at homeostasis (uninjured) and at 3 dpa (days post-amputation)

first: Josane

last: F. Sousa

first: Gabriela

last: Lima

first: Louise

last: Perez

first: Hannah

last: Schof


title: The Sh3Pxd2bnee-/- mouse: an attractive model unveiling developmental features in Frank-ter-Haar Syndrome

city: Stanford

first: Julika

last: Huber

state: CA

address: 257 Campus Drive

institute: Stanford University

summary:
Frank-ter Haar syndrome (FTHS) is an inherited disease associated
with variants of the SH3PXD2B gene, encoding for the podosomal
adaptor protein known as TKS4. FTHS is characterized by multiple
skeletal abnormalities, developmental delay and severe craniofacial
dysmorphology. This study provides an in-depth characterization of
the calvarial phenotype of a mouse model of FTHS and investigates
the potential underlying molecular and transcriptomic mechanisms.
The Sh3Pxd2bnee−/− mouse presents with craniofacial malformations,
AQ4 disrupted suture patterning, decreased osteoregeneration, cell
proliferation and migration both in vitro and in vivo, and impaired
podosome formation. Transcriptomic analysis revealed
downregulation of genes involved in ribosome biogenesis. Moreover,
ribosomal RNA accumulates in cell protrusions of migrating cells. We
established that the craniofacial phenotype of the Sh3Pxd2bnee−/−
mouse is governed by impaired cell migration and proliferation due
to dysfunctional podosome formation, particularly in neural crest-derived
tissues. Transcriptomic and molecular data suggest altered
ribosome-related processes, although further investigation is needed
to clarify the underlying mechanisms.

overall_design: RNA-seq profiling of RNA extracted from skulls of WT and Sh3Pxd2bnee-/- mice at postnatal day 15

first: Siddharth

last: Menon

first: Michael

last: Lopez-Torres

first: Jason

last: Guo

last: Longaker


title: Differential downstream signaling in microglia lacking Alzheimer’s-related TREM2 or its adaptor TYROBP/DAP12

city: Hartsdale

first: michelle

last: ehrlich

address: 88 Mercer Ave.

institute: Mount Sinai Hospital

summary: Microglia, the primary immune cell in the brain, have multiple activation phenotypes involved in broad functions within the brain, playing roles in neurotoxicity/neuroprotection, release of inflammatory and anti-inflammatory cytokines, and in cell survival, proliferation, and phagocytosis. TREM2 and TYROBP form a transmembrane complex in microglia that modulates intracellular signaling networks, and these proteins are essential regulators of the transition from homeostatic to activated microglia. Recent findings support a TREM2-independent molecular signature that is involved in the early transition of homeostatic to disease-associated microglia (DAM), with the next sequential step of DAM activation from stage 1 to stage 2 being TREM2-dependent. However, the underlying mechanisms determining how TREM2 or TYROBP regulate these downstream phenotypes are largely unknown. We isolated primary microglia from C57BL/6 wild-type (WT) controls, Trem2 knock-out (KO), and Tyrobp KO mice at post-natal day 0-3. Cells were treated with Alzheimer’s disease (AD)-relevant stimuli, such as amyloid beta (Aβ) oligomers or fibrils, or ‘neuroinflammatory-like’ stimuli, such as lipopolysaccharide (LPS). We explored protein and gene expression in the presence or absence of inhibitors of the TREM2/TYROBP downstream signaling pathway. We also performed a high-throughput Olink proteomic analysis of conditioned media from WT, Trem2 KO, and Tyrobp KO stimulated with either LPS or Aβ oligomers or fibrils. Our results show that the absence of either TREM2 or TYROBP is associated with increased basal levels of phosphorylated ERK in primary microglia compared to WT controls. In addition, Trem2 KO and Tyrobp KO cells show a less ramified cell morphology at baseline, as compared to WT microglia. Moreover, stimulating primary microglia with either Aβ oligomers or LPS leads to differential protein and gene expression in cells lacking TREM2 or TYROBP. The dysregulated downstream signal transduction and morphology in the absence of TREM2 or TYROBP suggest their essential roles not only in microglial homeostasis but also in their activation in response to different stimuli.

overall_design: RNA-seq profiling of cortical and hippocampal primary microglia isolated from WT, Trem2 KO, and Tyrobp KO mice at baseline, or after a 24hr-treatment with LPS, A11/OC mix, or OC-only preparations.

middle: E

last: Farias Quipildor

first: Ramona

last: Belfiore

first: Khaled

last: Althobaiti

first: Zahra

last: Najarzadeh

first: Charles

last: Glabe

first: Benjamin

middle: P

last: Readhead

first: Sam

last: Gandy

first: Stephen

last: Salton

first: Michelle

last: Ehrlich


title: Comparative multi-omic analysis reveals conserved and derived mechanisms of fin and limb regeneration [spatial transcriptomics]

first: Igor

last: Schneider

overall_design: Cryosections of Polypterus pectoral fins at homeostasis (uninjured) and at different time points of regeneration (1, 3 and 7 dpa) were used for spatial transcriptomics analysis.

first: Josane

middle: F

last: Sousa

last: Lima

last: Perez


title: TRMT6 mitigates susceptibility and progression of DSS-induced colitis multifacetedly via translational regulation [16S rRNA-seq]

first: Aiwei

last: Wu

overall_design: 16s rRNA gene sequencing of stool samples from WT (n=3) and Trmt6-/- (n=3) DSS-induced colitis mice to investigate the changes in gut microbiota (GM) composition.

first: Xianli

last: Zhang

first: Yanting

last: Du

first: Yuefang

last: Ye

first: Xueqing

last: Zhong

first: Chengsong

last: Cai

first: Guodong

last: Li

first: Hu

last: Wang

first: Liquan

last: Hong


title: Comparative multi-omic analysis reveals conserved and derived mechanisms of fin and limb regeneration

overall_design: snRNA-seq profiling of Polypterus senegalus regenerating fins. Single nucleus suspensions were prepared from uninjured and regenerating pectoral fins at 1, 3 and 7 dpa (days post-amputation). Regenerating fins were either from fish treated with DMSO (control) or 2.5 uM rapamycin (mTOR inhibition). Nuclei were fixed and frozen using the Evercode Nuclei Fixation Kit v3 (#NF100, #NF200) from Parse Biosciences following the manufacturer’s protocol. Fixed and frozen nuclei were then processed to generate snRNA-seq libraries following the combinatorial barcoding protocol from Parse Biosciences, using the Evercode WT v3 Kit (#WT100A-D, #WT200) as per manufacturer’s instructions.

first: Gabriela

first: Louise

first: Hannah

last: Schof


title: A beneficial environment promotes immune resilience through epigenetic regulation [scRNA-seq]

city: München

first: Thomas

last: Conlon

address: Ingolstädter Landstraße 1

country: Germany

institute: Helmholtz Zentrum München

summary: Environmental factors are often detrimental; however, certain environments enhance immune resilience. Notably, children raised on traditional farms show reduced allergies and asthma prevalence. Here, we investigated how a beneficial environment, using farm dust (FD) extract, influenced lung immune function in OVA-induced allergic inflammation. FD-exposure reduced allergic lung inflammation and increased monocyte-derived macrophage (MDM) recruitment. scRNA-seq revealed that FD-exposed MDMs had altered gene expression, including dampened Ccl8 and MHCII expression, impairing eosinophil recruitment and antigen presentation. RNA-seq and ATAC-seq confirmed FD-induced epigenetic reprogramming ex-vivo, on bone marrow-derived macrophages. This modulation, seen in both human and murine cells, relied on HDAC activity sustained by PPARγ signaling. These findings suggest that beneficial environmental exposures can reprogram immune cells and may offer a novel strategy for asthma prevention.

overall_design: Farm dust (FD) was collected from 9 traditional European cow farms (EUC) in Southern Germany and Austria that did not house sheep. Dust was collected from stables by sweeping settled dust from ledges, windowsills, and other, higher shelves (at least 1 m above ground) to obtain dry airborne dust. Animals were sensitized to ovalbumin (OVA) on days 0, 7, and 14 by intraperitoneal injection of 10 μg OVA emulsified in 1.0 mg aluminum hydroxide  and diluted to 200 μL with PBS. Subsequently, mice were challenged on days 26, 27 and 28 with intranasal administration of 100ug OVA. FD administration was carried out via intranasal administration of 25 μL from a 100ug/ml stock solution of FD extract on days 0, 2, 5, 7, 9, 12, 14, 16, 19, 21, 23 and 26, for a total of 12 administrations. 24h after the last challenge wit OVA, mice were deeply anesthetized in MMF, exsanguinated via the hepatic artery, and one whole lung was processed for scRNAseq.

first: Theodoros

last: Kapellos

first: Guilherme

last: Dragunas

first: Yuexin

last: Chen

first: Herbert

last: Schiller

first: Zeynep

last: Ertrüz

first: Ali Önder

last: Yildirim


title: Stem cell-like CD8+ T cells lacking PD-1 adapt to chronic stimulation by reducing TCR signaling and self-renewal capacity [RNA-seq]

city: Lausanne

first: Tania

last: Wyss

address: Rue du Bugnon 25A

country: Switzerland

institute: SIB Swiss Institute of Bioinformatics

summary: CD8+ T cells responding to chronic viral infection adapt to continuous antigenic stimulation by the upregulation of inhibitory receptors. Here we addressed how memory-like CD8+ T cells (TML), which sustain the immune response in chronic infection due to their stem cell-like properties, adapt to chronic stimulation when they cannot express the co-inhibitory receptor PD-1. We found that PD-1 deficient TML cells did not show evidence of a compensatory increases in the expression of other inhibitory receptors or exhaustion-related genes. Rather, these cells displayed a reduced ability to activate multiple signaling pathways downstream of the TCR. By-passing proximal TCR signaling events restored the activation of PD-1-deficient TML cells. Consistent with reduced TCR signaling, PD-1-deficient TML cells had a reduced ability to expand and self-renew in response to recall stimulation. Transient blockade of PD-1/PD-L1 interaction similarly reduced the stemness of TML cells. Thus, in the absence of PD-1, stem-like CD8+ T cells adapt to chronic stimulation by reducing the capacity of the TCR to transmit activating signals, which limits the stemness of these cells. Thus, PD-1 preserves the stemness of TML cells ensuring the long-term maintenance of the immune response to chronic infection.

overall_design: We transferred wild type (WT) or Pdcd1-/- (PD-1 KO) CD8+ T cells expressing a TCR specific for the LCMV epitope gp33-41 (P14 cells) (CD45.2) into Vbeta5 mice (CD45.1) prior to infection with LCMV cl13.  Naive, TML and TEX cells were flow sorted based on their Tcf7-GFP and subjected to bulk RNAseq. The bulk RNAseq experiment also included the corresponding P14 subsets fromWT mice subjected to PD-L1 blockade. Two biological replicates were included for each sorted population.

first: Werner

last: Held

first: Julia

last: Maier

first: Melanie

last: Charmoy


title: Comparative multi-omic analysis reveals conserved and derived mechanisms of fin and limb regeneration [spatial transcriptomics II]

first: Igor

last: Schneider

overall_design: Cryosections of axolotl  limbs at homeostasis (intact) and at different time points of regeneration (3, 7 and 14 dpa) were used for spatial transcriptomics analysis.

first: Josane

last: Sousa

last: Lima

last: Perez


title: Stem cell-like CD8+ T cells lacking PD-1 adapt to chronic stimulation by reducing TCR signaling and self-renewal capacity [scRNA-seq]

overall_design: Mouse P14 cells were flow sorted from the spleen of Vbeta5 hosts (CD45.1) transferred with WT or PD-1 KO Tcf7GFP P14 cells at d28 post LCMV infection. WT P14 cells were sorted from hosts infected with either Armstrong (Arm) or clone13 (cl13), while PD-1 KO Tcf7GFP P14 cells were exposed to cl13 only.  The sorted cells were restimulated in vitro with plate bound anti-CD3/28 antibodies for 4 h (stimulated) or were cultured without activation (rested) and then subjected to scRNAseq analysis. Rested and stimulated cells derived from the same donor mouse.


title: Chronic intermittent hypoxia mimicking sleep apnea reshapes the liver circadian metabolic architecture

city: Irvine

first: Kousha

last: Changizi

address: 4038 Donald Bren Hall

department: Computer Science

institute: University of California, Irvine

summary: Obstructive sleep apnea (OSA), characterized by chronic intermittent hypoxia (IH) during sleep, is increasingly recognized as a driver of metabolic dysfunction. However, its impact on circadian metabolic regulation remains poorly understood. Here, we investigated how chronic IH reshapes 24- hour hepatic and systemic metabolic programs in a mouse model mimicking OSA-associated hypoxia. Through integrated circadian transcriptomic, metabolomic, and physiological profiling, we show that four weeks of rest phase-restricted IH reprogram hepatic metabolism in a time-specific manner. This reorganization involves the coordinated circadian regulation of glucose, lipid, and redox pathways, with a shift away from oxidative metabolism and toward oxygen-sparing processes such as gluconeogenesis, glycogen turnover, and lipid mobilization. These changes align with the hypoxic phase and coincide with altered metabolite oscillations and autonomic rhythms, supporting a functional adaptation to intermittent oxygen availability. Mechanistically, we identify rhythmic activation of the cAMP–CREB1 axis as a key transcriptional driver linking adrenergic signaling to circadian metabolic remodeling under IH. Our findings establish chronic IH as a potent metabolic zeitgeber that entrains hepatic transcriptional and metabolic rhythms, revealing a circadian dimension to the metabolic consequences of sleep-disordered breathing.

overall_design: Male C57BL/6JRj mice were exposed to chronic intermittent hypoxia (60 cycles h-¹, 5 % FiO₂, ZT0 – ZT8) or normoxic air for four weeks. Livers were collected every 4 h over a 24-h cycle (ZT0, 4, 8, 12, 16, 20) and poly-A-selected, strand-specific RNA-seq libraries were prepared and sequenced (2 × 100 bp, Illumina NovaSeq 6000). n = 3 biological replicates per time-point and condition.

first: Emilie

last: Montellier

first: Guillaume

last: Vial

first: Sophie

last: Bouyon

last: Changizi Ashtiani

first: Sherif

last: Abdelkarim

first: Emeline

last: Lemarie

first: Antoine

last: Boutin

first: Kenichiro

last: Kinouchi

first: Pierre

last: Baldi

first: Jean-Louis

last: Pepin

first: Jonathan

last: Gaucher


title: Comparative multi-omic analysis reveals conserved and derived mechanisms of fin and limb regeneration [Bulk RNA-seq]

overall_design: Bulk RNA-seq profiling of Polypterus senegalus intact and 3 dpa (days post-amputation) regenerating fins

first: Gabriela

first: Louise

first: Hannah

last: Schof


title: Metabolic control of innate immune activation in TET2-mutant clonal hematopoiesis

city: Boston

first: Peter

middle: G

last: Kim

state: MA

address: 360 Longwood Ave, LC8202

department: Medical Oncology

institute: Dana Farber Cancer Institute

summary: TET2 mutations drive inflammation in clonal hematopoiesis of indeterminate potential (CHIP), but the mechanism by which TET2 inactivation leads to inflammation is not understood. Here, we used in vivo genome-wide genetic perturbations in primary wildtype (WT) or Tet2 knockout (KO) Cas9+ hematopoietic stem-progenitor cells (HSPCs) in a model of zymosan peritonitis to elucidate the basis of Tet2 KO inflammation. We found that Tet2 restrains O-linked N-acetylglucosamine (O-GlcNAc) glycosyltransferase (Ogt), a Tet2 binding partner and metabolic sensor that integrates nutrient availability. Tet2 loss disrupts this Tet2-Ogt interaction, and dysregulated Ogt facilitates widespread H3K4 trimethylation including lipid-related gene loci and inflammatory lipid droplet formation. We identified ATP citrate lyase (Acly) as a critical node for lipid accumulation, inflammation, and myeloid expansion in Tet2 deficiency. In summary, we reveal that Tet2 serves as a negative regulator of the nutrient sensor Ogt, and that Tet2 inactivation leads to aberrant lipid droplet formation and inflammation.

overall_design: RNAseq profiling from various sources including monocytes via single cell RNAseq and bone marrow derived macrophages exposed to various conditions.

first: Christopher

last: Hergott

first: Aidan

last: Miller

first: Amy

last: Deik

first: Meaghan

last: Boileau

first: Kevin

last: Bullock

first: Kerry

last: Pierce

first: Angeline

last: Choy

first: Wesley

last: Shin

first: Marie

last: McConkey

first: Justin

last: Loke

first: Birgitta

last: Ryback

first: Michael

last: Trinh

first: Hong

last: Yue

first: Hojong

last: Yoon

first: Paul

last: Park

first: Shourya

last: Burman

first: Matthew

last: Vander Heiden

first: Eric

last: Fisher

first: Scott

last: Armstrong

first: Clary

last: Clish

first: Benjamin

last: Ebert


title: The CD8 immgenT framework as a universal reference of mouse CD8 T cell differentiation states

status: Public on Jan 14 2026

city: Cambridge

first: Charles

middle: Ara

last: Demurjian

address: 31 Ames Street

institute: BioMicro Center at MIT

summary: Mouse CD8 T cell differentiation has been studied extensively in models of infections and cancer, yet no unified framework spans the full spectrum of immunological contexts. Here, we present the CD8 immgenT framework, integrating >200,000 single-cell transcriptomes and 128-plex surface proteomes from 734 samples across 45 perturbations, 45 tissues, and multiple timepoints. Unbiased analysis resolves 21 robust, recurrent states that capture naive, effector, circulating memory, tissue-resident memory, progenitor-exhausted, and terminally exhausted compartments, among others. These states reproducibly re-emerge with striking molecular convergence across acute and chronic infections, cancer, autoimmunity, aging, and homeostasis, revealing that highly similar transcriptional programs are deployed in dramatically different immunological contexts and can support protective or dysfunctional functions depending on developmental history and microenvironmental cues. Classic archetypes map to discrete clusters yet display previously unappreciated heterogeneity and extensive overlap, cautioning against rigid application of legacy subset nomenclature. We provide validated combinatorial markers, flow cytometry gating strategies, and T cell reference-based integration, a projection tool for reproducible annotation of new datasets. The CD8 immgenT framework thus establishes a universal coordinate system for mouse CD8 T cell biology that harmonizes fragmented literature and clarifies biological relationships across the entire spectrum of immune challenges.

overall_design: Syngeneic MC38-SIY colon carcinoma and B16-SIY melanoma tumors were implanted subcutaneously in C57BL/6 mice. Tumors were harvested 14 days post-implantation, enzymatically digested, and live CD45⁺ immune cells were isolated by flow cytometric sorting. Single-cell 3′ gene expression libraries were generated to profile immune cell transcriptional states within the tumor microenvironment.


title: Essential role of NONO-HOXA1-Wnt axis in cardiomyocyte differentiation [scRNA-seq]

city: Shanghai

first: Feizhen

last: Wu

state: Shanghai

address: Zhangheng Road 825, Pudong

department: Intelligent Medicine Institute

institute: Fudan Univ, Shanghai, China

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

overall_design: We performed scRNA-seq in days 2, 5, and 15 differentiated cells derived from WT and NONO-KO hiPSC.

first: Wei

last: Sheng

first: Guoying

last: Huang

first: Zhiyu

last: Feng

first: Yuan

last: Gao


title: Toll signalling controls intestinal regeneration in Drosophila

city: Oxford

first: Petros

last: Ligoxygakis

address: South Parks Rd

department: Biochemistry

country: United Kingdom

institute: University of Oxford

summary: This study is part of a manuscript approved for publication in Development (Cambridge UK) showing that the Toll pathway in Drosophila is necessary and sufficient for intestinal stem cell mitosis following infection and under homeostatic conditions. Chronic activation of Toll using a gain of function mutation (Toll10b) induces intestinal stem cell proliferation while blocking differentiation of enteroblasts to enterocytes. Thus, the intestinal tissue becomes replete with progenitor cells. The RNA-seq data deposited here are on whole guts of 20-day old flies where Toll has been activated in intestinal progenitor cells post-developmentally (in adults) from day 1 using the GAL4/GAL80ts system.

overall_design: Whole guts were dissected from flies with the following genotypes: esgts/w1118 (control genetic background), esgts/UAS-Toll10b (overactivation of the Toll pathway), esgts/UAS-Toll10b/UAS-BskDN (blocked overactivity of the Toll pathway by a dominant negative form of JNK). Libraries were generated using the MGIEasy RNA-seq Library Preparation Universal Kit in BGI HongKong. RNA-seq was performed on the DNBSEQ-G400 using the 150 paired-end sequencing protocol. 3 samples (esgts/w1118, esgts/UAS-Toll10b, esgts/UAS-Toll10b/UAS-BskDN) with 3 independent biological repeats were used.

first: Aiswarya

last: Udayakumar

first: Qi

last: Xiao


title: Metabolic control of innate immune activation in TET2-mutant clonal hematopoiesis [ChIP-seq]

first: Peter

last: Kim

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: Chipseq profiling from various sources including bone marrow derived macrophages and monocytic human U937 cell line with or without TET2 KO, exposed to various conditions.

first: Christopher

last: Hergott

first: Aidan

last: Miller

first: Amy

last: Deik

first: Meaghan

last: Boileau

first: Kevin

last: Bullock

first: Kerry

last: Pierce

first: Angeline

last: Choy

first: Wesley

last: Shin

first: Marie

last: McConkey

first: Justin

last: Loke

first: Birgitta

last: Ryback

first: Michael

last: Trinh

first: Hong

last: Yue

first: Hojong

last: Yoon


title: Late-onset sporadic Alzheimer’s disease modeling using patient-derived cells: A review

city: montreal

first: Gilbert

last: Bernier

state: Quebec

address: 5415 Assomption Blvd

country: Canada

institute: Hopital Maisonneuve-Rosemont Research center

summary: Late-onset sporadic Alzheimer’s disease (LOAD) is the most common form of dementia. The disease is characterized by progressive loss of memory and behavioral changes followed by neurodegeneration of all cortical areas. While the contribution of genetic and environmental factors is important, advanced aging remains the most important disease risk factor. Because LOAD does not naturally occur in most know animal species, except humans, studies have traditionally relied on the use of transgenic mice modeling rare, early-onset genetic forms of Alzheimer’s disease. Hence, the development of more representative LOAD models through reprograming of patient-derived cells into neuronal, glial, and immune cells became a necessity to better understand the disease origin and pathophysiology. Herein, and focusing on neurons, we review current work in the field and compare results obtained with two different reprograming methods to generate patient-derived neuronal cells: the induced pluripotent stem cell and induced neuron technologies. We also evaluate if these models can faithfully mimic cellular and molecular pathologies observed in LOAD patient’s brains. Here, we show new ATAC-seq data that support that iPSC can faithfully model LOAD, with an increased number of peaks showing chromatin relaxation in LOAD neurons

overall_design: iPSC reprogrammed from LOAD patient fibroblasts were differentiated into neurons for 60 days followed by an ATAC-seq

first: Katbe

last: Alisar

first: Diagne

last: Ismaila

first: Bernier

last: Gilbert


title: Evolutionarily divergent transcriptomic programs in ovarian folliculogenesis across mice, monkeys and humans [Human]

first: Yukihiro

last: Yabuta

overall_design:
Expression profiling by high throughput sequencing
gene expression datasets for oocytes and granulosa cells

first: Baku

last: Nakakita

first: Ken

last: Mizuta

first: Yoshitaka

last: Katou

first: Hidetaka

last: Tasaki

first: Tomonori

last: Nakamura

first: Chizuru

last: Iwatani

first: Hideaki

last: Tsuchiya

first: Ikuo

last: Kawamoto

first: Tomoyuki

last: Tsukiyama

first: Xun

last: Chen

first: Guillaume

last: Bourque

first: Junko

last: Otsuki

first: Mikiya

last: Nakatsuka

first: Akihito

last: Horie

first: Masaki

last: Mandai

first: Mitinori

last: Saitou

first: Hiroshi

last: Ohta


title: Cross-species analysis of transcriptomic response to alphaherpesvirus infection in human, bovine and equine cells

city: Freiburg

first: Florian

last: Full

address: Hermann-Herder-Str. 11

institute: Institute of Virology, University Medical Center Freiburg

summary: Comparative transcriptomics offers a powerful approach to elucidate host–virus interactions across related pathogens, yet systematic evaluations across spe-cies-matched cellular systems remain limited. Here, we performed a cross-species RNA-sequencing analysis of respective species’ cells infected with three alphaherpesviruses - herpes simplex virus 1 (HSV-1), bovine al-phaherpesvirus 1 (BHV-1), and equid alphaherpesvirus 1 (EHV-1) - to dissect conserved and virus-specific transcriptional responses. We show that certain orthologous genes and orthologous pathways are differentially regulated upon infection among the three species like pathways related to translation rRNA processing and TNF-alpha signaling. We find that the earliest sampled timepoint of infection, 2 hours post infection (hpi), shows the most commonly enriched pathways among the three species compared to later timepoints. At 6h and 9h post infection, BHV-1- and EHV-1-infections have more in common with each other in terms of enriched pathways than with HSV-1 infections. Moreover, we provide a comprehensive analysis of temporal viral gene expression for all three herpesviruses. Together, these findings provide a comparative framework for understanding alphaherpesvirus–host interactions and reveal both conserved core responses and species-specific transcriptional signatures. This work estab-lishes a foundation for identifying broadly acting antiviral targets as well as vi-rus-specific vulnerabilities that may inform host-directed therapies and cross-species disease management.

sample_organism:
Homo sapiens
Equus caballus
Bos taurus

platform_organism:
Homo sapiens
Equus caballus
Bos taurus

overall_design: RNA-sequencing was performed for MDBK cells infected with BHV-1, EDerm cells infected with EHV-1 and HFF cells infected with HSV-1 in the following conditions: Mock, 2hpi, 6hpi and 9hpi. The HFF cells have the following additional conditions: 6hpi + PAA treatment, 9hpi + PAA treatment and 16hpi.

first: Mirko

last: Schmitz

first: Eva

last: Neugebauer

first: Kristen

last: Conn


title: Human microglia in brain assembloids display region-specific diversity and respond to hyperexcitable neurons carrying SCN2A mutation

city: West Lafayette

first: Harish

last: Kothandaraman

state: IN

address: 201S South State St

department: Purdue Institute for Cancer Research

institute: Purdue University

summary: Microglia critically shape neuronal circuit development and function, yet their region-specific properties and roles in distinct circuits of the human brain remain poorly understood. In this study, we generated region-specific brain organoids (cortical, striatal, and midbrain), each integrated with human microglia, to fill this critical gap.

overall_design: Single-cell RNA sequencing was performed on human iPSC-derived cortical (hCO+Mg), striatal (hStrO+Mg), and midbrain (hMO+Mg) organoids containing microglia. For each condition, 4–5 organoids derived from three independent hiPSC lines (KOLF2.1J, B07 WT, B11 WT) were pooled into a single sample and processed using the PIPseq-T20 3′ single-cell RNA-seq workflow. Libraries were sequenced on an Illumina NovaSeq S4 platform (2 × 150 bp), and the resulting data were used to compare microglial transcriptional states across distinct brain region–like environments.

first: Jiaxiang

last: Wu

first: Xiaoling

first: Weihao

last: Li

first: Yang

last: Yang


title: Transcriptomic insights into metabolic reprogramming and exo-polysaccharide synthesis in Porphyridium purpureum under gradual nitrogen deprivation

city: AUBIERE

first: Maurean

middle: Tehani

last: Guerreiro

state: Auvergne-Rhône-Alpes

address: 4, Avenue Blaise Pascal

department: Axe GePEB : Génie des Procédés, Énergétique et Biosystèmes

country: France

institute: Institut Pascal, UMR 6602 – Université Clermont Auvergne (UCA)

summary: Porphyridium species are known red microalgae for producing valuable bioactive compounds such as sulfated exopolysaccharides (EPS) with diverse industrial biomed-ical applications due to their functional and rheological properties. Recent studies have investigated how abiotic stresses, particularly nitrogen deprivation, affect Porphyridium’s metabolic regulation and EPS production through transcriptomic analysis. Still, the mechanisms governing EPS biosynthesis and the involvement of carbohydrate-activated enzymes (CAZymes) remain poorly understood. This study investigated the progressive effects of nitrate consumption on unicellular red alga P. purpureum, by integrating physiological, biochemical, and transcriptomic analyses through RNA-Seq, further validated by RT-qPCR. P. purpureum displayed a gradual, phase-dependent metabolic response to progressive nitrogen stress. EPS release coincided with the decline in nitrate uptake, linking nitrogen availability to carbon redirec-tion towards polysaccharide secretion. Transcriptomic data revealed global metabolic downregulation with targeted upregulation of stress-responsive, carbohydrate catabolic, and nucleotide-sugar synthesis pathways, including upregulation of CAZyme families GT4, GT8, and GT77. Our results give insights into the coordinated nitrogen and carbon metabolic regulation underlying polysaccharide biosynthesis, while open-ing future perspectives on enzyme compartmentalization and regulatory flux distribution under nitrogen stress in P. purpureum.

overall_design: RNA-seq profiling of red microalga Porphyridium purpureum cultures exposed to four residual nitrate concentrations (1.5, 0.6, 0.5, 0.3 g·L⁻¹), with technical triplicates to study the onset of nitrate depletion.

first: Coline

last: Emmanuel

first: Céline

last: Dupuits

first: Christine

last: Gardarin

first: Said

last: Mouzeyar

first: João

last: Varela

first: Jane

last: Roche

last: Laroche


title: Clinical and Molecular differences of hypertensive disorders during pregnancy

city: La Jolla

first: Mariko

last: Horii

address: 2880 Torrey Pines Scenic Dr

department: Pathology

institute: UCSD

summary: Background: Hypertensive disorders of pregnancy (HDP) comprise a spectrum of four subtypes: chronic hypertension (cHTN), gestational hypertension (gHTN), preeclampsia (PE), and superimposed preeclampsia (siPE). Although often characterized as a spectrum of disease severity, there have been limited comparative studies of detailed clinical and molecular characteristics of these disorders. We hereby evaluate HDP subtypes using clinical, placental histopathological and molecular data to compare the similarities and differences between HDP subtypes. Methods: We utilize data from over 10-year-long pregnancy cohort with detailed clinical and placental pathology, as well as placental tissue RNA-sequencing. Clinical diagnosis was based on current ACOG criteria, and placental gross and histologic examination was based on the Amsterdam consensus statement. Results: Clinical data analysis showed cHTN and gHTN to be more likely to have normal placental pathology, while PE and siPE were more enriched in maternal vascular malperfusion (MVM). RNA-seq showed distinct gene expression signatures and pathway activation across  our HDP subgroups. We could not identify any molecular evidence that preeclampsia (PE or siPE) was an advanced stage of hypertensive disorder (gHTN or cHTN), but rather identified distinct gene expression profiles between these entities, suggesting preeclampsia (PE or siPE) and hypertension (gHTN or cHTN) are distinct pathophysiological conditions. Finally, we found that, in the presence of MVM, siPE and PE share significant gene expression profiles and pathway activation. Conclusion: Our findings suggest that MVM specifically differentiates pregnancies that progress to PE and siPE. MVM is thought to initiate in early gestation, indicating the cascade to PE/siPE maybe differentiated from gHTN/cHTN early in pregnancy. Incorporating placental evaluation into patient care is essential, in order to probe the etiology of HDP.

overall_design:
Placental tissue RNA-seq from hypertensive disorder that includes chronic hypertension (cHTN), gestational hypertension (gHTN), preeclampsia (PE), and superimposed preeclampsia (siPE).We used previously derived (GSE186257, GSE234729, PRJNA1027377) as well as newly derived data for this study. All the data were re-mapped as described in the data processing section.

***************************************************************
The table below lists GEO accessions reused/reanalyzed for this study.
***************************************************************

first: Marni

last: Jacobs

first: Robert

last: Morey

first: Jennifer

last: Chousal


title: Influenza A virus modulation of Streptococcus pneumoniae infection using ex vivo transcriptomics in a human primary lung epithelial cell [AEIC and AHFJ]

city: Baltimore

first: Adonis

last: D'Mello

address: Health Science Facility III, 670 W Baltimore St 3rd floor

institute: IGS- University of Maryland Baltimore

summary: Nanostring quantification of 76 pneumococcal probes representing 72 genes, for Streptococcus pneumoniae EF3030 (wildtype and mutants) bacteria during infection of normalized human broncial epithelial cells (nHBEC), together, or after coincubation with Influenza A virus pH1N1.

overall_design: HBECs isolated from human lung tissue of 2 donors [AEIC and AHFJ] were infected/mock infected with Influenza A [pH1N1, 72 hours] followed by Streptococcus pneumoniae EF3030 infection [wildtype WT, operon mutants EF3030_RS00905, EF3030_RS02325, EF3030_RS07890, EF3030_RS07920, 6 hours].

first: Erin

middle: Y

last: Earnhardt

first: Hervé

last: Tettelin

first: Kevin

middle: S

last: Harrod


title: REV-ERB-alpha and -beta coordinately regulate astrocyte reactivity and proteostatic function [II]

city: St. Louis

first: Eric

last: Tycksen

state: Missouri

address: 4444 Forest Park Avenue

department: McDonnell Genome Institute

institute: Washington University in St. Louis School of Medicine

summary: The molecular circadian clock is a ubiquitous transcriptional-translational feedback loop that regulates CNS function, glial responses, and neurodegenerative pathology. The druggable nuclear receptors REV-ERB-ɑ (gene: Nr1d1) and REV-ERB-.Beta. (gene: Nr1d2) are components of the core circadian clock. REV-ERB proteins regulate neuroinflammatory responses, synaptic pruning, and protein aggregation, though the cell type-specific effects and relative compensatory effects of REV-ERB-ɑ AND -.Beta. in the brain are unknown. To study the CNS functions of REV-ERBs, we developed mouse lines with global or astrocyte-specific, conditional knockout of both REV-ERB-ɑ and -.Beta.. We demonstrate that inducible post-natal global deletion of REV-ERB-ɑ and -.Beta. in vivo results in robust spontaneous astrocyte activation and increases gene expression of disease-relevant pathways such as protein catabolism, complement, and oxidative stress. Furthermore, in vivo astrocyte-specific deletion of REV-ERB-ɑ/-.Beta. recapitulates the spontaneous astrocyte activation phenotype seen in global REV-ERB-ɑ/-.Beta. KO mice, as well as in mice with deletion of key core clock gene Bmal1, indicating that REV-ERBs regulate astrocyte activation in a cell-autonomous manner downstream of the core circadian clock. REV-ERB-ɑ/-.Beta. repress transcription of Stat3 in the brain, and deletion of REV-ERBs in astrocytes induces increased astrocytic STAT3 expression and downstream STAT3-mediated gene changes, a mechanistic link to the astrocyte reactivity shift. This astrocyte activation phenotype decreases alpha-synuclein pathology in an in vivo model of Parkinson’s Disease-related alpha-synucleinopathy and increases astrocytic protein uptake and degradation in vitro. This study therefore provides insight into astrocyte function and could elucidate novel regulatory mechanisms that are candidates for therapeutic manipulation through modulating REV-ERB activity.

overall_design: To investigate the cell-autonomous role of REV-ERB-ɑ/-.Beta. in astrocytes, we generated inducible astrocyte-specific REV-ERB-ɑ/-.Beta. knockouts. REV-ERB-ɑ/-.Beta. was knocked out at 2 months of age and mice were aged a further two months before sacrifice. Brains were removed and RNA was extracted from the cortices and bulk RNA sequencing was performed to determine differentially expressed genes.

first: Collin

last: Nadarajah

first: Michelle

last: Li

first: Ibrahim

middle: O

last: Saliu

first: Elsa

middle: I

last: Quillin

last: Boyer

first: Julie

last: Dimitry

first: Yinying Cynthia

last: Chen

first: Melvin

middle: W

last: King

first: Jiyeon

last: Lee

first: Patrick

last: Sheehan

first: Albert

last: Davis

first: Mitchell

last: Lazar

first: Guoyan

last: Zhao

first: Erik

last: Musiek


title: Deciphering the molecular mechanism of flight loss in mulberry silkworm through the integration of single-cell and spatial transcriptomics [B_scRNA-seq]

first: Qiancheng

last: Xiao

address: Building 25, No. 1188, LIANHANG Road, Pujiang Town, Minhang District, Shanghai

institute: Shanghai OE Biotech Co., Ltd

summary: Loss of flight is recurrently observed in flying species and markedly abates threats to human health and agricultural production posed by flying pests. However, our understanding of the flight organs involved remains limited. The silkworm Bombyx mori, a lepidopteran model insect, loses flight most recently, while the Bombyx mandarina capable of flight, therefore it is a good model for studying flight loss. Here, we represent the first description of the spatiotemporal architecture of Bombyx flight organs. We demonstrated that the weakened cellular function of NFDCs and FECs determining the flight energy and wing vein and flight muscle development largely result in flight loss in B. mori, and single-cell analyses of cotton bollworm flight organs and RNA interference (RNAi) of key genes validated these findings, and the cellular and molecular determinants of flight may be conserved across Lepidoptera. These findings will contribute to the understanding of flight loss encountered in flying species.

sample_organism:
Bombyx mori
Bombyx mandarina

platform_organism:
Bombyx mori
Bombyx mandarina

overall_design:
We used scRNA of to gain a global understanding of the cell types and expressed genes in wing discs of B. mori, B.mandarina and H. armigera
Please note that "FWD" represents 'Fore wing discs' and "HWD" represents 'Hind wing discs', which will develop into the fore-wings of moth and hind-wings of moth, respectively.

first: Rongpeng

last: Liu

first: Chen

first: Jie

last: Hu

first: Yongbing

last: Ba

first: Yan

last: Ma

first: Yiting

last: Ran

first: Yuanyuan

last: Mu

first: Yinghao

first: Xiaoqing

last: Xu

first: Yiyun

last: Tang

first: Qingjun

first: Yuqin

first: Zhiming

last: Zhang

first: Kaiqi

last: Guo

first: Yuting

last: Wang

first: Zhiwei

first: Keshu

last: Dong

first: Xiao

first: Wei

last: Tan

first: Yumeng

last: Zhu

first: Zhonghuai

last: Xiang

first: Hanfu


title: Transcriptional profiling of skin cancer NK cells reveals the elevated glucocorticoid receptor activity alters their pro-inflammatory features.

city: Nanjing

first: Yuancheng

last: Li

state: JiangSu

address: No. 12 Jiangwangmiao Street

department: Institute of Dermatology

institute: Chinese Academy of Medicine Sciences and Peking Union Medical College

summary: The interplay between natural killer (NK) cells and tumor microenvironment (TME) is closely associated with tumor progression. We showed NK cells are common constituents in the tissue of skin cancers including basal cell carcinoma (BCC), cutaneous squamous cell carcinoma (cSCC), extramammary paget disease (EMPD) and acral melanoma (aMM). scRNA-Seq revealed an inter and intra-tumor transcriptional heterogeneity of NK cells in different skin TMEs. Unexpectedly, compared to peri-tumor, skin tumor NK cells down regulated the production of anti-tumor cytokines, IFN-γ and TNF-α, and up regulated the production of amphiregulin (AREG), a ligand of epidermal growth factor receptor (EGFR), which functions in promoting skin tumor growth and mediating immune tolerance.

overall_design: CD45+ cells from tumor and peri-tumor tissue were enriched and were subjected to scRNA-Seq, the NK cells sorted from PBMCs that were treated with glucocorticoid were subjected to bulk RNA-Seq

first: Yetao


title: Deciphering the molecular mechanism of flight loss in mulberry silkworm through the integration of single-cell and spatial transcriptomics [H_scRNA-seq]

first: Qiancheng

last: Xiao

first: Rongpeng

first: Chen

last: Zhao

first: Jie

first: Yongbing

first: Yan

first: Yiting

first: Yuanyuan

first: Yinghao

last: Chen


title: Robust effector memory features of human T-bet-hi B cells  induced by repeated mRNA vaccination

status: Public on Jan 13 2026

city: Daejeon

first: Jeongsoo

last: Lee

address: 291 Daehak-ro, Yuseong-gu

institute: KAIST

summary: The heterogeneity of memory B cells in response to repetitive cognate antigen challenges remains to be fully elucidated. Here we identified a transcriptionally distinct cluster of T-bethi B cells, among SARS-CoV-2 RBD-specific B cells in PBMCs from healthy individuals vaccinated with the BNT162b2 SARS-CoV-2 mRNA vaccine. Our findings indicate that T-bethi B cells can be defined by a combination of CD11c and FcRL5 receptors, and are distinguished by distinct gene regulatory networks associated with effector functions. Notably, these T-bethi B cells were affinity-matured and exhibited rapid differentiation into antibody-secreting cells (ASCs) producing neutralizing antibodies comparable to classical memory B cells, underscoring their role in early recall responses. Taken together, these findings illuminate the potent effector memory roles of T-bethi B cells in adaptive immunity following vaccinations.

overall_design: The stained B cells were sorted into tetramer+ cells and tetramer− cells and cells from 4 individuals were pooled, stained with CITE-seq antibodies to be included in a single gem (tube) , 2 gems per a single timepoint. Timepoints are as follows: T1 (D0), T2 (D7 after 1st dose), T3 (D14 after 1st dose), T4 (D14 after 2nd dose), T5 (D180 after 2nd dose), T6 (D14 after 3rd dose) and T7 (D90 after 3rd dose)


title: Transcriptomic signatures of immune suppression and cellular dysfunction distinguish latent from transcriptionally active HIV-1 infection in dendritic cells

city: Amsterdam

first: Neeltje

last: Kootstra

address: Meibergdreef 9

institute: AmsterdamUMC

summary: Dendritic cells (DCs) are essential for antiviral immunity but are also susceptible to HIV-1 infection. Although sensing and restriction pathways in DCs are well described, the mechanisms underlying latent infection and its functional consequences remain unclear. Here, we performed transcriptomic profiling of monocyte-derived DCs harboring transcriptionally active (Active-HIV) or latent HIV-1 (Latent-HIV) proviruses using a dual-reporter virus. Gene set enrichment analysis revealed suppression of metabolic and stress-modulatory programs in Active-HIV compared to unexposed DCs. In contrast, Latent-HIV showed broad downregulation of pathways, including interferon and innate responses and metabolic programs, indicating a hyporesponsive and dampened antiviral state despite the absence of differentially expressed genes (DEGs). DEG analysis of Active-HIV versus Latent-HIV showed that active transcription associates with cellular stress, cytoskeletal remodeling, and RNA-processing. Functional analyses further demonstrated activation of RNA processes, suppression of antigen-presentation pathways, and altered membrane and cytoskeletal signaling in Active-HIV. These pathways suggest that transcriptionally active HIV-1 leverages cellular machinery to support replication, creating a metabolically strained yet immunologically engaged state that disrupts antigen presentation. Conversely, latently infected DCs display a hyporesponsive state consistent with proviral silencing. This dichotomy reveals distinct mechanisms of DC dysfunction that may facilitate HIV-1 persistence and immune evasion.

overall_design: Primary monocyte-derived dendritic cells were infected with a VSV-G pseudotyped dual-reporter HIV-1 for five days. Transcriptionally active HIV-1-infected cells (MKO2+GFP+) and latently infected cells (MKO2+GFP-) were isolated by FACS. HIV-1-uninfected and -unexposed cells were included as controls.

first: Shirley

last: Man

first: Jade

last: Jansen

first: Neeltje A.

first: Teunis B.H.

last: Geijtenbeek


title: Liver-specific delivery of MDM2 antisense oligonucleotides counteracts diet-induced metabolic dysfunction-associated steatotic liver diseases

city: Hung Hom

first: Kenneth King Yip

last: Cheng

state: Kowloon

address: Y948, Lee Shau Kee Building, The Hong Kong Polytechnic University

department: Department of Health Technology and Informatics

country: Hong Kong

institute: The Hong Kong Polytechnic University

summary: Metabolic dysfunction-associated steatotic liver disease (MASLD) encompasses a spectrum of pathogenic conditions ranging from steatosis, inflammation and fibrosis with limited treatment options. We previously demonstrated an upregulation of hepatic murine double minute 2 (MDM2) in human subjects with MASLD. Genetic deletion of hepatic MDM2 and pharmacological inhibition of systemic MDM2 improves steatosis and fibrosis in mouse models. In this study, we further developed and investigated the therapeutic potential of a hepatocyte-specific triantennary N-acetylgalactosamine (GalNAc)-conjugated antisense oligonucleotide targeting MDM2 (GalNAc-Mdm2ASO) in two distinct dietary-induced mouse models of MASLD: a high-fat-high-cholesterol (HFHC) diet and a choline-deficient L-amino acid-defined high-fat diet (CDAHFD). In the HFHC-induced MASLD model, GalNAc‐Mdm2ASO not only alleviated liver injury, steatosis, and fibrosis but also improved obesity-related insulin resistance and hyperlipidaemia. The hepatoprotective effects of GalNAc-Mdm2ASO treatment were associated with a reduced accumulation of hepatic cholesterol and ceramide, both of which are known to trigger MASLD. In CDAHFD-induced MASLD mouse model, GalNAc‐Mdm2ASO significantly mitigated hepatic inflammation, cholesterol accumulation, and fibrosis but not triglyceride accumulation. Overall, we prove hepatic inhibition of MDM2 using GalNAc-Mdm2ASO as a promising therapeutic agent for MASLD in two rodent models with distinct pathogenesis.

overall_design: RNA-seq profiling of liver samples of GalNAc-conASO and GalNAc-Mdm2ASO groups (n = 4-5) fed the HFHC/CDAHFD diet.

first: Md Moinul

last: Hoque

first: Mengjie

last: Kong

first: Yuan

last: XinYi

first: Zhou

last: Xiangyu

first: Steve

last: Ting-Yuan Yeh

first: Kekao

last: Long

first: Huige

last: Lin

first: Kenneth

last: King Yip Cheng


title: Lack of synergy between AR targeted therapies and PARP inhibition in homologous recombination- proficient prostate cancer [ATAC-seq]

first: Nicole

last: Traphagen

address: 450 Brookline Ave

institute: Dana-Farber Cancer Institute

summary: Recent clinical trials have explored the combination of androgen receptor (AR) pathway inhibitors and poly (ADP-ribose) polymerase (PARP) inhibitors as a potential treatment for castration-resistant prostate cancer. This combination treatment is based on the premise that AR directly regulates expression of DNA repair genes, leading to synergy between PARP and AR inhibition. Despite some promising preclinical evidence, this combination therapy has shown limited efficacy in patients with homologous recombination (HR)-proficient tumors. To investigate this discrepancy between preclinical and clinical results, we profiled the effects of PARP inhibition in prostate cancer models in the presence or absence of AR inhibition. Surprisingly, AR inhibition impaired response to PARP inhibitors in castration-sensitive cells and had no effect on response in castration-resistant cells. AR inhibition also did not regulate DNA repair in either the castration-resistant or castration-sensitive setting. Instead, we find that cell cycle progression is required for response to PARP inhibition in homologous-recombination proficient prostate cancer.

overall_design: ATAC-seq profiling of LNCaP and 22RV1 cells treated with PARP inhibitors and AR inhibition

first: Myles

last: Brown


title: Deciphering the molecular mechanism of flight loss in mulberry silkworm through the integration of single-cell and spatial transcriptomics [stRNA-seq]

first: Qiancheng

last: Xiao

overall_design:
We used spatial transcriptome RNA sequencing (stRNA-seq) to gain a spatial transcriptome atlas of spatiotemporal architecture in wing discs of B. mori and B.mandarina
Please note that "FWD" represents 'Fore wing discs' and "HWD" represents 'Hind wing discs', which will develop into the fore-wings of moth and hind-wings of moth, respectively.

first: Rongpeng

last: Liu

first: Chen

last: Zhao

first: Jie

last: Hu

first: Yongbing

last: Ba

first: Yan

last: Ma

first: Yiting

last: Ran

first: Yuanyuan

last: Mu

first: Yinghao

last: Li

first: Xiaoqing

last: Xu

first: Yiyun

last: Tang

first: Qingjun

first: Yuqin

last: Chen

first: Zhiming

last: Zhang

first: Kaiqi

last: Guo

first: Yuting

last: Wang

first: Zhiwei

first: Keshu

last: Dong

first: Xiao

first: Wei

last: Tan

first: Yumeng

last: Zhu

first: Zhonghuai

last: Xiang

first: Hanfu


title: Phosphorylation of Barrier-to-Autointegration Factor (BAF) regulates anchoring of centromeric heterochromatin to the nuclear envelope (NE)

city: Barcelona

first: Camille

last: Stephan Otto Attolini

state: Select a State or Province

address: Baldiri Reixac 10

department: Biostatistics and bioinformatics Unit

institute: IRB Barcelona

summary: In eukaryotes, the spatial segregation of heterochromatin and euchromatin is key for the structural organization and function of the genome. Heterochromatin interacts with the nuclear envelope (NE) and occupies a more peripheral position than euchromatin. However, the mechanisms that govern tethering of heterochromatin to the NE are not fully understood. Here, we report that Barrier-to-Autointegration Factor (BAF), a highly conserved NE-associated protein, interacts with centromeric heterochromatin and regulates its anchoring to the NE in a phosphorylation dependent manner. We show that impaired BAF phosphorylation results in its persistent association with centromeric heterochromatin and reinforced anchoring. We also show that reinforced anchoring of centromeric heterochromatin to the NE has important functional consequences, compromising both NE integrity and heterochromatin coalescence, and disturbing mitosis progression and the assembly of functional centromeres. Altogether, our results suggest that anchoring of centromeric heterochromatin to the NE is a highly dynamic process regulated through BAF phosphorylation, and unveil the deleterious functional consequences of perturbing this dynamics.

overall_design: Torras-Llort, Mònica

first: Carbonell

last: Albert

first: Escudero-Ferruz

last: Paula

first: Serrat

last: Martina

first: Zhang

last: Chong

first: Reina

last: Oscar

first: Medina-Giró

last: Sònia

first: Moreno-Moreno

last: Olga

first: Lipinski

last: Zoltan

first: Fernando

last: Azorín


title: Systemic comparison  of dCas9-based DNA methylation editing systems for specificity and stability [Bisulfite-Seq (reduced representation)_TMS2]

city: Solna

first: Maria

last: Needhamsen

address: Solnavagen 1

department: Clinical Neuroscience

country: Sweden

institute: Karolinska Institutet

type: Methylation profiling by high throughput sequencing

summary: Manipulating epigenetic layers during transcriptional regulation poses significant challenges, yet advancements in dCas-based systems offer promising avenues for targeted manipulation. DNA methylation, a widely studied epigenetic mechanism in mammals, has benefited from recent methodological developments enabling comprehensive profiling across various tissues and conditions. While traditional methods for altering methylation levels lacked specificity and often induced pleiotropic effects, the advent of CRISPR technology has revolutionized this landscape, offering precise manipulation of methylation levels at specific loci. However, despite their advantages, these techniques have limitations, underscoring the need for thorough characterization of existing tools and the development of novel approaches. This study aimed to comprehensively compare the on-target/off-target effects of several available epimodifier systems and explore the potential of a multimerization strategy for epimodifier domains. Through our investigations, we provide insights into the methylation-mediated control of human gene expression and the utility of dCas9-based methylation editors.

overall_design: To investigate the on-target/off-target effects of several available dCas9-based DNA methylation epimodifier systems in HEK293T cells.

first: Majid

last: Pahlevan Kakhki

first: Fatemeh

last: Rangani

first: Ewoud

last: Ewing

first: Chiara

last: Starvaggi Cucuzza

first: Galina

last: Zheleznyakova

first: Tejaswi

last: Venkata S. Badam

last: Kalomoiri

first: Ruxandra

last: Covacu

first: Ioanna

last: Andreou

first: Lara

last: Kular

first: Maja

last: Jagodic


title: Systemic comparison  of dCas9-based DNA methylation editing systems for specificity and stability [RNAseq_firstRun]


title: Systemic comparison  of dCas9-based DNA methylation editing systems for specificity and stability [RNAseq_secondRun]

overall_design: Experimental design: HEK293T cells were transfected with plasmids encoding gRNA (BACH2-g8 or NTC) and dCas9-epimodifier-EGFP (3A, 3A3L, 3A3A, 3A-KRAB, mut3A, M.SssI, SunTag) or CRISPRoff (co-transfected with a gRNA-encoding plasmid). Successfully transfected cells were sorted based on GFP or BFP signal 3 days post-transfection (p.t.) using fluorescent activated cell sorting (FACS), GFP/BFP positive cells were cultured and harvested at days 3, 7, 14, 21, and 30 post transfection for methylation (EPIC, TMS and Pyrosequencing) and expression (Total RNAseq, mRNAseq and qPCR) analyses. Please check for more details under the “Samples” section and the “Treatment” column.


title: Boehmeria nivea (L.) Gaud. Ameliorates Oxidative stress-mediated Inflammatory Responses and Apoptosis in LPS/CSC-induced Chronic Obstructive Pulmonary Disease Mouse Model

city: Jeongeup-si

first: Ba-Wool

last: Lee

state: Jeollabuk-do

address: Korea Research Institute of Bioscience and Biotechnology, center 2

summary: Introduction: Boehmeria nivea (L.) Gaud. has traditionally been regarded as a functional food with applications in various inflammatory disorders. However, its role in chronic obstructive pulmonary disease (COPD) has not yet been clarified. Methods: In this study, the preventive efficacy of the ethyl acetate fraction of B. nivea (L.) Gaud. leaves (EA-BN) was evaluated in a COPD model established by intranasal instillation of lipopolysaccharide (LPS; 0.5 mg/kg body weight) and cigarette smoke condensate (CSC; 12.5 mg/kg body weight) in male C57BL/6N mice. The experimental groups received dexamethasone (3 mg/kg) as a positive control or EA-BN at doses of 200 mg/kg. Results: EA-BN administration significantly reduced T helper 1 cytokine levels and decreased macrophage and neutrophil counts in bronchoalveolar lavage fluid. Histological analyses revealed that EA-BN mitigated alveolar destruction and inflammatory infiltration, whereas pulmonary function tests demonstrated improvements in the FEV0.1/FVC ratio and lung elastance in the LPS/CSC-induced COPD. Additionally, EA-BN alleviated oxidative stress by promoting the nuclear translocation of Nrf2 and enhancing the expression of its downstream targets, HO-1 and NQO1, leading to a reduction in reactive oxygen species and nitric oxide production. EA-BN downregulated thioredoxin-interacting protein and NLRP3 inflammasome activation, thereby suppressing caspase-1 and IL-1β expression, and also attenuated apoptosis by modulating the Bax/Bcl-2/caspase-3 pathway. Discussion: Collectively, these findings suggest that EA-BN possesses antioxidant, anti-inflammatory, and anti-apoptotic properties, supporting its potential as a preventive agent against COPD.

overall_design: This study investigated transcriptomic changes in lung tissue using an LPS/CSC-induced COPD mouse model and evaluated the effect of EA-BN treatment. Male C57BL/6N mice were assigned to three groups for RNA-seq analysis: Normal control (NC; PBS intranasal instillation with vehicle), COPD (LPS/CSC intranasal instillation with vehicle), and EA-BN-H (LPS/CSC intranasal instillation with EA-BN 200 mg/kg). LPS (0.5 mg/kg) and CSC (12.5 mg/kg) were intranasally instilled under light anesthesia on days 1, 6, and 13. EA-BN (200 mg/kg; in 2% DMSO) or vehicle was administered orally once daily from days 1 to 14. Lung tissues were collected on day 15, and total RNA was extracted using TRIzol reagent. RNA quality was assessed prior to library preparation, and RNA-seq was performed to compare gene expression profiles among NC, COPD, and EA-BN-H groups.

first: Ji-Hye

last: Ha

first: Da-Hye

last: Yi

first: Ju-Hong

last: Kim

first: Seong-Hun

last: Jeong

first: Ju Hwan

first: Kyungsook

last: Jung

first: Hyung Jae

first: Ji-Young

last: Park

first: Woo Sik

first: Young-Bae

last: Ryu

first: Hyung-Jun

last: Kwon

first: Jong-Choon

first: In-Sik

last: Shin

first: In-Chul


title: Systemic comparison  of dCas9-based DNA methylation editing systems for specificity and stability [Bisulfite-Seq (reduced representation)_TMS1]

first: Maria

last: Needhamsen

first: Majid

last: Pahlevan Kakhki

first: Fatemeh

last: Rangani

first: Ewoud

last: Ewing

first: Chiara

last: Starvaggi Cucuzza

first: Galina

last: Zheleznyakova

first: Tejaswi

first: Ruxandra

first: Ioanna

first: Lara


title: ROR1-PI3K/AKT signaling drives adaptive resistance to cell cycle blockade in TP53 mutated ovarian cancer

city: Oulu

first: Daniela

last: Ungureanu

address: Aapistie 5A

department: Faculty of Biochemistry and Molecular Medicine

country: Finland

institute: University of Oulu

summary: We developed long-term resistant (lt-res, several months) pre-clinical models to adavosertib (ADA) and paclitaxel (PTX). We identified distinct transcriptomic and morphological changes in the ovarian cancer lt-res models. ADA resistance involves signaling pathway alterations that allow cells to maintain unchecked proliferation, while PTX resistance primarily stems from structural changes within the cell, affecting microtubules and drug efflux. Upregulation of receptor tyrosine kinases, such as ROR1, was observed in both ROR1-positive ADA and PTX lt-res models. Targeting ROR1 with zilovertamab-vedotin, a monoclonal antibody-drug conjugate, resulted in enhanced cytotoxicity, demonstrating a new approach against recurrent drug-resistant ovarian cancer.

overall_design: Single-cell RNA-sequencing profiling of untreated parental and short-term, intermediate-resistant and long-term resistant ovarian cancer cell lines. Resistant cell lines were established by gradual increase of PTX or ADA concentrations.

first: Frida

last: Rantanen

first: Alice

last: Dini

first: Harlan

last: Barker


title: Epigenetic and transcriptomic profiling of cultured mouse retinal progenitor cells

city: Ikoma

first: Kanae

last: Matsuda-Ito

state: 奈良県

address: 8916-5, Takayama-cho

institute: Nara Institute of Science and Techn

summary: Dynamic epigenetic changes guide retinal progenitor cells (RPCs) toward diverse neuronal subtypes and Müller glia during retinal development. However, the epigenetic mechanisms that maintain RPC proliferative and neurogenic potential throughout the final stages of retinal cell genesis remain poorly understood. Here, we integrate RNA sequencing and assay for transposase-accessible chromatin sequencing (ATAC-seq) to investigate how mouse RPC stemness is regulated. Our analysis reveals conserved chromatin accessibility and gene expression profiles in mouse RPCs throughout retinal cell genesis. Notably, the histone methyltransferase Setd8, which catalyzes H4K20 monomethylation, remains persistently expressed in RPCs but is barely detectable in adult Müller glia. Setd8 deletion in developing RPCs reduces proliferation, triggers apoptosis, and disrupts retinal laminar organization and ocular axis length. Additionally, Setd8 deficiency impairs the chromatin accessibility that is normally preserved in RPCs, leading to a partial acquisition of a transcriptomic profile associated with terminally differentiated cells. Our study indicates that Setd8 safeguards mouse RPC identity by maintaining RPC-specific chromatin accessibility, thereby ensuring proper retinal development.

overall_design: We used over 20,000 sorted retinal cells to construct a library for each sample. For library preparation, Nestin-EGFP-positive cells were FACS-isolated from retinas of wild-type Nestin-EGFP mice at E14 and E17, and Nes-Cre-YFP-positive cells were FACS-isolated from the retinas of Setd8 conditional knockout and control mice at P0.

first: Taito

last: Matsuda

first: Haruka

last: Sekiryu


title: REV-ERB-alpha and -beta coordinately regulate astrocyte reactivity and proteostatic function

first: Eric

last: Tycksen

overall_design: To investigate the role of REV-ERB-ɑ, REV-ERB-ɑ/-.Beta., or the DNA-binding domain (DBD) of REV-ERB-ɑ in the brain. We generated inducible global knockouts of REV-ERB-ɑ, REV-ERB-ɑ/-.Beta., or REV-ERB-ɑ DBD. Genes were knocked out at 2 months of age and mice were aged to 8-9 months before sacrifice. Brains were removed and RNA was extracted from the cortices and bulk RNA sequencing was performed to determine differentially expressed genes.

first: Collin

last: Nadarajah

first: Michelle

last: Li

first: Ibrahim

last: Saliu

first: Elsa

last: Quillin

first: Kevin

last: Boyer

first: Julie

last: Dimitry

first: Yinying (Cynthia

last: Chen

first: Melvin

last: King

first: Jiyeon

last: Lee

first: Patrick

last: Sheehan

first: Albert

last: Davis

first: Mitchell

last: Lazar

first: Guoyan

last: Zhao

first: Erik

last: Musiek


title: Transcriptome analysis of HSPC at 6 days of culture of non- or 20mGy-irradiated LT-HSC

city: Fontenay aux roses

first: federica

last: ferri

address: 18 route du panorama

institute: cea

summary: Mouse LT-HSC cells were obtained by cytometry sorting, irradiated or not with 20mGy using a GSRD1 (cesium source) and cultured for 6 days in stem cell maintenance medium. HSPCs from these cultures were sorted and RNA extracted for transcriptomic analysis.

overall_design: we assesed the differentially expressed genes in sorted HSPC at 6 days of culture of non- or 20mGy irradiated LT-HSC

first: Nathalie

last: Gault

first: Daniel

last: Lewandowski


title: Systemic comparison  of dCas9-based DNA methylation editing systems for specificity and stability [EPIC]

first: Maria

last: Needhamsen

first: Majid

last: Pahlevan Kakhki

first: Fatemeh

last: Rangani

first: Ewoud

last: Ewing

first: Chiara

last: Starvaggi Cucuzza

first: Galina

last: Zheleznyakova

first: Tejaswi

last: Venkata S Badam

last: Kalomoiri

first: Ruxandra

last: Covacu

first: Ioanna

last: Andreou

first: Lara

last: Kular

first: Maja

last: Jagodic


title: Molecular signatures of altered energy metabolism and circadian rhythm perturbations in a model of synucleinopathy

city: Aarhus

first: Lin

last: Lin

address: Høegh-Guldbergs Gade 10

department: Department of Biomedicine

country: Denmark

institute: Aarhus University

summary: A pathological role of alpha-synuclein (AS) aggregation in the nervous system is a recognized feature in Parkinson disease (PD) and related neurodegenerative conditions termed synucleinopathies. In order to characterize the cellular response in CNS to incipient and advanced AS aggregation, we applied spatial transcriptomics on brain sections derived from a mouse model at prodromal and symptomatic stages of pathology. Our spatially-resolved data point to unique perturbations in brain energy metabolism during the progression of AS pathology, such that there is an initial phase of hypermetabolism in disease-affected regions, which is followed by a profound decline leading to the symptomatic phase. This latter stage was also associated with drastic reduction in mRNA translation machinery, neuroinflammation and aberrant expression of molecular drivers controlling circadian rhythms. Collectively, these data offer novel opportunities in knowledge translation for mechanism-based drug discovery and potentially inform on biological markers reflecting disease progression in PD and related diseases.

overall_design: Transgenic M83 mice overexpressing human mutant A53T AS (Prnp-SNCA*A53T) were bilaterally injected with pre-fibrillar aggregates of murine AS. Control animals were injected with phosphate-buffered saline (PBS, n=2) as control. Brains were collected at Early-stage pathology (Day 45, n=3) and Symptomatic stage (Day 75, n=3)

first: Asad

last: Jan


title: NF-κB and STAT3 signaling uniquely stratifies survival in female glioblastoma patients

first: Jason

middle: Paul

last: Wong

state: MO

address: Neuroscience Research Building

department: Pediatrics

institute: Washington University in St. Louis

summary: Sex differences in glioblastoma (GBM) incidence, prognosis, and response to treatment are well established. However, the molecular mechanisms that drive these differences are less well understood. In a pan-cancer study, we previously reported that female patients exhibit a sex bias towards upregulated inflammatory signaling across many cancers. Additionally, upregulated nuclear factor-kappa B (NF-κB) and signal transducer and activator of transcription 3 (STAT3) signaling in GBM is associated with poor survival. Here, we report that only female GBM patients with higher expression of NF-κB- or IL6/JAK/STAT3-related genes have poorer survival compared to females with lower expression, a pattern not seen in male patients. Interestingly this sex difference was only evident in GBM tumors with wild-type epidermal growth factor receptor (EGFR). Using a mouse GBM model, we report that female GBM cells have similar stronger signatures in NF-κB and STAT3 signaling and exhibit a more robust response to manipulation of both pathways. Furthermore, female cells exhibited a stronger relationship between STAT3 activity and its sensitivity towards STAT3 inhibition. These results demonstrate that targeting NF-κB and STAT3 signaling in a sex-informed manner in GBM patients with wild-type EGFR tumors may improve patient response to treatment. Overall, this study highlights the mechanistic and clinical importance of analyzing data that is disaggregated by sex.

overall_design: RNA-sequencing (by BRB-seq) to profile multiple iterations (i.e. dervied from separate litters) of male and female Nf1-/- DNp53 transformed murine astrocytes.

first: Lloyd

last: Tripp

first: Robi

middle: D

last: Mitra

first: Joshua

middle: B

last: Rubin


title: Heritable ER stress impairs mitochondrial metabolism and leads to exhaustion of low-dose irradiated hematopoietic stem cells [RREMseqHSC]

first: federica

last: ferri

summary: How hematopoietic stem cells (HSC) respond to low levels of stress such as exposure to very low doses of radiation currently used in medicine, is largely unknown. Here, we show that 20mGy-irradiated HSC (20mGy-HSC) exhibit, when they proliferate, oxidative stress with increased mitochondrial Reactive Oxygen Species and metabolism together with mitochondrial Ca2+ overload. These mitochondrial defects are due to an immediate and sustained endoplasmic reticulum (ER) stress adapted by proliferative 20mGy-HSC through activation of the eIF2-ATF4 branch of the UPR. The ER stress is heritable and leads, in long-term quiescent 20mGy-HSC, to activation of the IRE1-Xbp1 branch of UPR, which fails to restore ER homeostasis resulting in HSC self-renewal deficiency and exhaustion. Finally, we show that this heritable ER stress leads to a global DNA hypomethylation, partially reverted by early inhibition of ER stress. Our studies illuminate how an adaptive ER stress response can lead to mitochondrial defects and HSC deficiency.

overall_design: DNA methylation profiling in HSC isolated from bone marrow of mice transplanted with sham or 20mGy-irradiated LSK, pre-treated or not with 4PBA

first: Federica

last: Ferri

first: Nathalie

last: Gault


title: Lack of synergy between AR targeted therapies and PARP inhibition in homologous recombination- proficient prostate cancer

city: Boston

first: Nicole

last: Traphagen

overall_design: RNA-seq profiling of LNCaP and 22RV1 cells treated with PARP inhibitors and AR inhibition

middle: A

first: Myles

last: Brown


title: Heritable ER stress impairs mitochondrial metabolism and leads to exhaustion of low-dose irradiated hematopoietic stem cells [ATACseqHSC]

overall_design: ATAC-seq in HSC isolated from bone marrow of mice transplanted with sham or 20mGy-irradiated LSK


title: Pathogenic tau in the mouse locus coeruleus produces noradrenergic hyperactivity and neuropsychiatric phenotypes reminiscent of prodromal Alzheimer’s disease

status: Public on Jan 12 2026

city: Atlanta

first: Anu

last: Korukonda

state: Georgia

address: 615 Michael St

institute: Emory University

summary: Alzheimer’s disease (AD), though defined as a cognitive disorder, often presents neuropsychiatric symptoms such as anxiety, depression, agitation and sleep disruptions years before the onset of frank memory impairment. A hallmark prodromal feature is the accumulation of hyperphosphorylated “pretangle” tau (pTau) in the locus coeruleus (LC), the brain’s primary source of norepinephrine (NE), prior to any other region. While clinical studies link LC tau burden to behavioral abnormalities, causal mechanisms remain unclear. We developed a translationally-relevant mouse model that recapitulates the ‘LC-first’ phenomenon observed in humans using cell type-specific viral expression of pathogenic P364S mutant human tau in LC neurons. Three months post-infusion, pTau accumulation coincided with anxiety- and compulsive-like behaviors and reduced sleep spindles without altering overall sleep architecture. Consistent with the behavioral phenotypes, electrophysiological recordings revealed significant increases in spontaneous and evoked LC activity, accompanied by astrocytic reactivity with no apparent neuronal death. Transcriptomic analysis identified upregulation of the pacemaker potassium/sodium channel Hcn2 in the LC, which may contribute to neuronal hyperexcitability. To further define molecular mechanisms linking pTau to behavioral and cellular phenotypes, we developed a cell type-specific proteomics approach, which revealed synaptic and metabolic alterations in LC neurons associated with tau pathology. Interestingly, early anxiety-like behaviors observed at 3 months diminished at later timepoints (6-9 months) and were replaced by anxiolytic phenotypes. These findings demonstrate that pTau triggers phenotypes reflective of LC-NE hyperactivity in the early stages of AD pathogenesis, laying the foundation for the development of LC-based disease-modifying targets to address neuropsychiatric manifestations.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for LC-mRNA (IP) for P364S mutant human tau-infused or EYFP-infused controls. The background strain is C57Bl/6 and the exact cross is: Th-cre (B6.Cg-7630403G23RikTg(Th-cre)1Tmd/J, The Jackson Laboratory, #008601) crossed with Slc6a2-eGFP/Rpl10a (B6;FVB-Tg(Slc6a2-eGFP/Rpl10a)JD1538Htz/J, The Jackson Laboratory, #031151).

first: David

last: Weinshenker