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Identification of sex-biased MiRNA markers informative of heat-past events

BMC Genomics 2025年第1期26卷 1-17页

作者： van Gelderen, Tosca A. Montfort, Jerome Álvarez-Dios, José Antonio Piferrer, Francesc Bobe, Julien Ribas, Laia Institut de Ciències del Mar Consejo Superior de Investigaciones Científicas (ICM-CSIC) Barcelona 08003 Spain PhD Program in Genetics Autonomous University of Barcelona Bellaterra 08193 Spain INRAE Laboratoire de Physiologie et Génomique des Poissons Rennes France Departamento de Matemática Aplicada Facultad de Matemáticas Universidad de Santiago de Compostela Santiago de Compostela 15781 Spain

Elevated temperatures during early developmental stages play a pivotal role in the fate of the adult sexual phenotype of fish populations, usually leading to male-skewed sex ratios. This is the case with European sea bass (Dicentrarchus labrax), one of the most important species in the European aquaculture industry. To unveil informative markers of the past thermal events, we investigated changes in the miRNome within the gonads of this species. Consequently, we exposed European sea bass to elevated temperatures (21ºC) during early development (from 7 to 68 days post fertilization). After one-year post-heat treatment growing at natural temperature, a miRNA-sequencing analysis was conducted in the ovaries and testes of juvenile fish. The examination of miRNA expression levels identified three and twelve miRNAs in ovaries and testes, respectively, reflecting past thermal events. To assess the evolutionary conservation of these identified miRNAs in gonads, we cross-referenced our data with miRNome public information from ovaries and testes in nine additional fish species from the FishmiRNA database. This analysis uncovered 33 potential sex-biased markers present in at least five studied species along the evolutionary timeline. For instance, miR-155, miR-429, and miR-140 were consistently female-skewed, while miR-143, miR-499, and miR-135b-3p were consistently male-skewed. In addition, among these markers, three conserved sex-skewed miRNAs proved to be informative regarding past thermal events in the ovaries (e.g., miR-192-5p, miR-146a-5p and miR-143-3p) and four in the testes (miR-129-5p, miR-724-5p, miR-143-3p, and miR-223-3p). Notably, miR-223-3p was conserved female-skewed, but showed upregulation in males exposed to high temperature, and miR-143-3p was inhibited in both heated females and males. These miRNAs could serve as markers of heat-induced masculinization. This research broadens the inventory of sex-specific miRNAs across evolution in fish, and elucidates th

关键词： Climate change European sea bass Evolution Fish High temperature

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Genomic data processing with GenomeFlow

arXiv

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arXiv 2025年

作者： Park, Junseok Maury, Eduardo A. Oh, Changhoon Shin, Donghoon Denisko, Danielle Lee, Eunjung Alice Division of Genetics and Genomics Boston Children’s Hospital 3 Blackfan Circle BostonMA United States Department of Pediatrics Harvard Medical School 25 Shattuck St BostonMA United States Bioinformatics Integrative Genomics Program Harvard/MIT MD-PHD Program Harvard Medical School BostonMA United States Program in Medical and Population Genetics Broad Institute of MIT and Harvard CambridgeMA United States Graduate School of Information Yonsei University 50 Yonsei-ro Seodaemun-gu Seoul Korea Republic of Department of Human Centered Design and Engineering University of Washington SeattleWA United States Department of Biomedical Informatics Harvard Medical School BostonMA United States

Advances in genome sequencing technologies generate massive amounts of sequence data that are increasingly analyzed and shared through public repositories. On-demand infrastructure services on cloud computing platforms enable the processing of such large-scale genomic sequence data in distributed processing environments with a significant reduction in analysis time. However, parallel processing on cloud computing platforms presents many challenges to researchers, even skillful bioinformaticians. In particular, it is difficult to design a computing architecture optimized to reduce the cost of computing and disk storage as genomic data analysis pipelines often employ many heterogeneous tools with different resource requirements. To address these issues, we developed GenomeFlow, a tool for automated development of computing architecture and resource optimization on Google Cloud Platform, which allows users to process a large number of samples at minimal cost. We outline multiple use cases of GenomeFlow demonstrating its utility to significantly reduce computing time and cost associated with analyzing genomic and transcriptomic data from hundreds to tens of thousands of samples from several consortia. Here, we describe a step-by-step protocol on how to use GenomeFlow for a common genomic data processing task. We introduce this example protocol geared toward a bioinformatician with little experience in cloud computing. © 2025, CC BY.

关键词： Cloud platforms

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CIWARS: A Web Server for Antibiotic Resistance Surveillance Using Longitudinal Metagenomic Data

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Journal of Molecular Biology 2025年

作者： Emon, Muhit Islam Cheung, Yat Fei Stoll, James Rumi, Monjura Afrin Brown, Connor Choi, Joung Min Moumi, Nazifa Ahmed Ahmed, Shafayat Song, Haoqiu Sein, Justin Yao, Shunyu Khan, Ahmad Gupta, Suraj Kulkarni, Rutwik Butt, Ali Vikesland, Peter Pruden, Amy Zhang, Liqing Department of Computer Science Virginia Tech Blacksburg 24060 VA United States Fralin Life Science Institute Virginia Tech Blacksburg 24060 VA United States Department of Civil and Environmental Engineering Virginia Tech Blacksburg 24060 VA United States The Interdisciplinary PhD Program in Genetics Bioinformatics and Computational Biology Virginia Tech Blacksburg 24060 VA United States

The rise of antibiotic resistance (AR) poses a substantial threat to human and animal health, food security, and economic stability. Wastewater-based surveillance (WBS) has emerged as a powerful strategy for population-level AR monitoring, providing valuable data to guide public health and policy decisions. Metagenomic sequencing is especially promising, as it can yield comprehensive profiles of antibiotic resistance genes (ARGs) and other genes relevant to AR in a single run. However, online analytical platforms to facilitate analysis of longitudinal metagenomic data are lacking. To address this, we introduce CyberInfrastructure for Waterborne Antibiotic Resistance Surveillance (CIWARS), a web server configured for characterizing key AR trends from longitudinal metagenomic WBS data. CIWARS offers comprehensive profiling of ARGs and taxonomic profiling of pathogen-associated bacterial taxonomic groups, identifies potential associations of ARGs with mobile genetic elements (MGEs) and pathogen-containing taxa, and assesses resistome risk based on the co-occurrence of ARGs, MGEs, and pathogen-like sequences. Additionally, it detects anomalous AR indicators over time, aiding in identifying potential events of concern, such as the emergence of resistant strains or outbreaks. Through interactive temporal data visualization, CIWARS enables AR monitoring and can serve as a tool to inform effective and timely interventions to mitigate the spread and transmission of AR. Here, CIWARS is demonstrated using longitudinal metagenomic data from a wastewater treatment plant (WWTP) influent and effluent, but it can be extended to any environment. CIWARS provides a valuable tool to support global efforts to combat the evolution and spread of AR, while also guiding agricultural and public health efforts aimed at optimizing antibiotic use. The web server is freely available at https://***/. © 2025 Elsevier Ltd

关键词： anomaly detection antibiotic resistance (AR) AR indicator profiling longitudinal metagenomics wastewater-based surveillance

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TRIM52 maintains cellular fitness and is under tight proteolytic control by multiple giant E3 ligases

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Nature Communications 2025年第1期16卷 1-19页

作者： Shulkina, Alexandra Hacker, Kathrin Ehrmann, Julian F. Budroni, Valentina Mandlbauer, Ariane Bock, Johannes Grabarczyk, Daniel B. Edobor, Genevieve Cochella, Luisa Clausen, Tim Versteeg, Gijs A. Max Perutz Labs Vienna Biocenter Campus (VBC) Dr.-Bohr-Gasse 9 Vienna 1030 Austria University of Vienna Center for Molecular Biology Department of Microbiology Immunobiology and Genetics Dr.-Bohr-Gasse 9 Vienna 1030 Austria Vienna Biocenter PhD Program a Doctoral School of the University of Vienna and the Medical University of Vienna Vienna 1030 Austria Research Institute of Molecular Pathology (IMP) Vienna BioCenter (VBC) Vienna Austria Department of Molecular Biology and Genetics Johns Hopkins School of Medicine Baltimore 21205 MD United States Medical University of Vienna Vienna BioCenter (VBC) Vienna Austria Department of Biological Chemistry and Molecular Pharmacology Harvard Medical School Boston 02115 MA United States Program in Cellular and Molecular Medicine Boston Children’s Hospital Boston 02115 MA United States

Tripartite motif 52 (TRIM52) exhibits strong positive selection in humans, yet is lost in many other mammals. In contrast to what one would expect for such a non-conserved factor, TRIM52 loss compromises cell fitness. We set out to determine the cellular function of TRIM52. Genetic and proteomic analyses revealed TRIM52 physically and functionally interacts with the DNA repair machinery. Our data suggest that TRIM52 limits topoisomerase 2 adducts, thereby preventing cell-cycle arrest. Consistent with a fitness-promoting function, TRIM52 is upregulated in various cancers, prompting us to investigate its regulatory pathways. We found TRIM52 to be targeted for ultra-rapid proteasomal degradation by the giant E3 ubiquitin ligases BIRC6, HUWE1, and UBR4/KCMF1. BIRC6 mono-ubiquitinates TRIM52, with subsequent extension by UBR4/KCMF1. These findings suggest a role for TRIM52 in maintaining genome integrity, and regulation of its own abundance through multi-ligase degradation. © The Author(s) 2025.

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Multi-site investigation of gut microbiota in CDKL5 deficiency disorder mouse models: Targeting dysbiosis to improve neurological outcomes

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Cell Reports 2025年第4期44卷 115546页

作者： Damiani, Francesca Giuliano, Maria Grazia Cornuti, Sara Putignano, Elena Tognozzi, Andrea Suckow, Vanessa Kalscheuer, Vera M. Pizzorusso, Tommaso Tognini, Paola Laboratory of Biology BIO@SNS Scuola Normale Superiore Piazza dei Cavalieri 7 Pisa 56126 Italy Health Science Interdisciplinary Center Sant'Anna School of Advanced Studies Piazza Martiri della Libertà 33 Pisa 56127 Italy Institute of Neuroscience National Research Council Via G. Moruzzi 1 Pisa 56124 Italy PhD Program in Clinical and Translational Science University of Pisa Via Savi 10 Pisa 56126 Italy Max Planck Institute for Molecular Genetics Ihnestraße 63 Berlin 14195 Germany

Cyclin-dependent kinase-like 5 (CDKL5) deficiency disorder (CDD) is a rare neurodevelopmental disorder often associated with gastrointestinal (GI) issues and subclinical immune dysregulation, suggesting a link to the gut microbiota. We analyze the fecal microbiota composition in two CDKL5 knockout (KO) mouse models at postnatal days (P) 25, 32 (youth), and 70 (adulthood), revealing significant microbial imbalances, particularly during juvenile stages. To investigate the role of the intestinal microbiota in CDD and assess causality, we administer antibiotics, which lead to improved visual cortical responses and reduce hyperactivity. Additionally, microglia morphology changes, indicative of altered surveillance and activation states, are reversed. Strikingly, fecal transplantation from CDKL5 KO to wild-type (WT) recipient mice successfully transfers both visual response deficits and hyperactive behavior. These findings show that gut microbiota alterations contribute to the severity of neurological symptoms in CDD, shedding light on the interplay between microbiota, microglia, and neurodevelopmental outcomes. © 2025

关键词： antibiotics CDKL5 CP: Microbiology CP: Neuroscience dysbiosis fecal transplantation gut microbiota gut-brain axis microglia neurodevelopmental disorder

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Fate and state transitions during human blood vessel organoid development

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Cell 2025年

作者： Nikolova, Marina T. He, Zhisong Seimiya, Makiko Jonsson, Gustav Cao, Wuji Okuda, Ryo Wimmer, Reiner A. Okamoto, Ryoko Penninger, Josef M. Camp, J. Gray Treutlein, Barbara Department of Biosystems Science and Engineering ETH Zurich Basel Switzerland Institute of Molecular Biotechnology of the Austrian Academy of Sciences Vienna Austria Vienna BioCenter PhD Program Doctoral School of the University of Vienna and Medical University of Vienna Vienna 1030 Austria Roche Pharma Research and Early Development Roche Innovation Center Basel Switzerland Department of Medical Genetics Life Science Institute University of British Columbia Vancouver V6T 1Z3 BC Canada Department of Laboratory Medicine Medical University of Vienna Vienna Austria Helmholtz Centre for Infection Research Braunschweig Germany Institute of Human Biology Roche Pharma Research and Early Development Roche Innovation Center Basel Basel Switzerland Biozentrum University of Basel Basel Switzerland

Human blood vessel organoids (hBVOs) have emerged as a system to model human vascular development and disease. Here, we use single-cell multi-omics together with genetic and signaling pathway perturbations to reconstruct hBVO development. Mesodermal progenitors bifurcate into endothelial and mural fates in vitro, and xenografted BVOs acquire definitive arteriovenous endothelial cell specification. We infer a gene regulatory network and use single-cell genetic perturbations to identify transcription factors (TFs) and receptors involved in cell fate specification, including a role for MECOM in endothelial and mural specification. We assess the potential of BVOs to generate organotypic states, identify TFs lacking expression in hBVOs, and find that induced LEF1 overexpression increases brain vasculature specificity. Finally, we map vascular disease-associated genes to hBVO cell states and analyze an hBVO model of diabetes. Altogether, we provide a comprehensive cell state atlas of hBVO development and illuminate the power and limitation of hBVOs for translational research. © 2025 The Authors

关键词： arteriovenous specification human blood vessel organoid human development organoid cell atlas single-cell genomics single-cell perturbation screen

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Discovering nanoparticle corona ligands for liver macrophage capture

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Nature Nanotechnology 2025年 1-12页

作者： Bram Bussin Marshall G. G. MacDuff Sara Ahmed Wayne Ngo Jamie L. Y. Wu Zachary P. Lin Benjamin Stordy Zahra Sepahi Jason Moffat Warren C. W. Chan Adrian Granda Farias Department of Laboratory Medicine and Pathobiology University of Toronto Toronto Ontario Canada Institute of Biomedical Engineering University of Toronto Toronto Ontario Canada Terrence Donnelly Centre for Cellular and Biomolecular Research University of Toronto Toronto Ontario Canada Department of Molecular Genetics University of Toronto Toronto Ontario Canada MD/PhD Program University of Toronto Toronto Ontario Canada Gladstone Institutes San Francisco CA USA California Institute for Quantitative Biosciences University of California Berkeley Berkeley CA USA Innovative Genomics Institute University of California Berkeley Berkeley CA USA Program in Genetics and Genome Biology The Hospital for Sick Children Toronto Ontario Canada School of Chemistry Chemical Engineering and Biotechnology Nanyang Technological University Singapore Singapore

Liver macrophages capture circulating nanoparticles and reduce their delivery to target organs. Serum proteins adsorb to the nanoparticle surface after administration. However, the adsorbed serum proteins and their cognate cell receptors for removing nanoparticles from the bloodstream have not been linked. Here we use a multi-omics strategy to identify the adsorbed serum proteins binding to specific liver macrophage receptors. We discovered six absorbed serum proteins that bind to two liver macrophage receptors. Nanoparticle physicochemical properties can affect the degree of the six serum proteins adsorbing to the surface, the probability of binding to cell receptors and whether the liver removes the nanoparticle from circulation. Identifying the six adsorbed proteins allowed us to engineer decoy nanoparticles that prime the liver to take up fewer therapeutic nanoparticles, enabling more nanoparticles for targeting extrahepatic tissues. Elucidating the molecular interactions governing the nanoparticle journey in vivo will enable us to control nanoparticle delivery to diseased tissues.

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TNF MicrosatelUtes in patients with systemic lupus erythemathosus

TNF MicrosatelUtes in patients with systemic lupus erythemat...

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The 8th International Congress on SLE

作者： Oliveira C.B. Rassi D.M. Wastowski I.J. Sim■es A.L Mendes-Junior C.T. Donadi E.A. (MSc) Program of Basic and Applied Immunology (PhD) Division of Clinical Immunology of the Department of Medicine (MSc) Program of Basic and Applied Immunology (MD PhD) Department of Genetics-Faculty of Medicine of Ribeino Preto University of So Paulo Brazil (PhD) Division of Clinical Immunology of the Department of Medicine (MD PhD) Program of Basic and Applied Immunology Division of Clinical Immunology of the Department of Medicine

Introduction:Systemic lupus erythemathosus(SLE)is a chronic inflammatory autoimmune disease of unknown etiology,characterized by autoantibody production that affects multiple organs and ***, immunological,genetic and ... 详细信息

关键词： TNF MicrosatelUtes in patients with systemic lupus erythemathosus

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Surgical menopause enhances hippocampal amyloidogenesis following global cerebral ischemia

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Journal of Sport and Health Science 2014年第3期3卷 206-216页

作者： Erin L.Scott Quan-Guang Zhang Yan Dong Dong Han Rui-Min Wang Ratna K.Vadlamudi Darrell W.Brann University System of Georgia MD/PhD Program Georgia Regents University Institute of Molecular Medicine and Genetics.Georgia Regents University Department of Obstetrics and Gynecology.University of Texas Health Science Center at San Antonio

Background： Prematurely menopausal women have a doubled lifetime risk of dementia and a 5-fold increased risk of mortality from neuro- logical disorders, but the molecular mechanisms underlying these risks remain unclear. We hypothesized that ischemia-induced amyloidogenesis may be enhanced in the hippocampus following prolonged loss of ovarian 17β-estradiol （E2）, which could contribute to these phenomena. Methods： The current study used a rat model of premature surgical menopause （10-week bilateral ovariectomy） with E2 therapy either initiated immediately （short-term E2 deprivation （STED）） or delayed to the end of the ovariectomy period （long-term E2 deprivation （LTED））. One week after continuous, subcutaneous E2 therapy, we subjected animals to 10-min global cerebral ischemia （GCI） to assess the effect of LTED on ischemia-induced amyloidogenesis in the hippocampal CA1. Results： The present study revealed that while hippocampal β-amyloid （Aβ） is not typically enhanced following GCI, there is a rapid, robust elevation of endogenous Aβ in LTED females after GCI. In STED females, we observed that GCI attenuates and E2 maintains A Disintegrin and Metalloprotease 10 （ADAM 10） expression in the hippocampal CA1, and concurrently, GCI increases and E2 decreases BACE1 levels in the same region. Intriguingly, however, we observed a loss of E2 regulation of ADAM 10, ADAM 17, and BACE 1 levels in the hippocampal CA I of LTED females, which provides mechanistic evidence for the enhanced post-ischemic Aβ load following LTED. We also observed loss of E2 regulation of tau hyperphosphorylation in LTED females subjected to GCI. Conclusion： Collectively, these studies partially explain the enhanced risk of dementia and mortality from neurological disorders seen in prematurely menopausal women and support timely initiation of E2 therapy to yield maximum neurological benefit.

关键词： Amyloid Dementia Estrogen Ischemia Surgical menopause

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Targeting multiple signaling pathways:the new approach to acute myeloid leukemia therapy

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Signal Transduction and Targeted Therapy 2021年第1期6卷 41-69页

作者： Jenna LCarter Katie Hege Jay Yang Hasini AKalpage Yongwei Su Holly Edwards Maik Hüttemann Jeffrey WTaub Yubin Ge Cancer Biology Graduate Program Wayne State University School of MedicineDetroitMIUSA MD/PhD Program Wayne State University School of MedicineDetroitMIUSA Department of Oncology Wayne State University School of MedicineDetroitMIUSA Molecular Therapeutics Program Barbara Ann Karmanos Cancer InstituteWayne State University School of MedicineDetroitMIUSA Center for Molecular Medicine and Genetics Wayne State University School of MedicineDetroitMIUSA National Engineering Laboratory for AIDS Vaccine Key Laboratory for Molecular Enzymology and EngineeringThe Ministry of EducationSchool of Life SciencesJilin UniversityChangchunChina Division of Pediatric Hematology/Oncology Children’s Hospital of MichiganDetroitMIUSA Department of Pediatrics Wayne State University School of MedicineDetroitMIUSA

Acute myeloid leukemia(AML)is the most common form of acute leukemia in adults and the second most common form of acute leukemia in *** this,very little improvement in survival rates has been achieved over the past few *** is partially due to the heterogeneity of AML and the need for more targeted therapeutics than the traditional cytotoxic chemotherapies that have been a mainstay in therapy for the past 50 *** the past 20 years,research has been diversifying the approach to treating AML by investigating molecular pathways uniquely relevant to AML cell proliferation and *** we review the development of novel therapeutics in targeting apoptosis,receptor tyrosine kinase(RTK)signaling,hedgehog(HH)pathway,mitochondrial function,DNA repair,and c-Myc *** has been an impressive effort into better understanding the diversity of AML cell characteristics and here we highlight important preclinical studies that have supported therapeutic development and continue to promote new ways to target AML *** addition,we describe clinical investigations that have led to FDA approval of new targeted AML therapies and ongoing clinical trials of novel therapies targeting AML survival *** also describe the complexity of targeting leukemia stem cells(LSCs)as an approach to addressing relapse and remission in AML and targetable pathways that are unique to LSC *** comprehensive review details what we currently understand about the signaling pathways that support AML cell survival and the exceptional ways in which we disrupt them.

关键词： myeloid approach approval

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