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Scaling life as an interspecies hallmark of aging 缩放生命是物种间衰老的标志
IF 10.5 1区 生物学
Genes & development Pub Date : 2025-07-15 DOI: 10.1101/gad.353113.125
Itamar Harel
{"title":"Scaling life as an interspecies hallmark of aging","authors":"Itamar Harel","doi":"10.1101/gad.353113.125","DOIUrl":"https://doi.org/10.1101/gad.353113.125","url":null,"abstract":"Across species, the “pace of life”—encompassing development, reproduction, and senescence—varies widely, yet the molecular mechanisms that regulate these interspecies trajectories of aging remain elusive. Even among vertebrates, a 1000-fold difference in life span is observed between species, ranging from several months in the turquoise killifish to half a millennium in the Greenland shark. As a relatively “young” area of investigation, aging research lacks the unifying conceptual frameworks that anchor more established disciplines, such as neuroscience. Therefore, current theories, which in some cases provide contradicting predictions, rely heavily on experimental data to mature. These contradictions not only define key outstanding questions but also illuminate fertile ground for transformative research.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":"3 1","pages":""},"PeriodicalIF":10.5,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144639722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A noncanonical Pol III-dependent, Microprocessor-independent biogenesis pathway generates a germline-enriched miRNA family 一个非规范的依赖于Pol iii，不依赖于微处理器的生物发生途径产生了一个种系富集的miRNA家族
IF 10.5 1区 生物学
Genes & development Pub Date : 2025-07-14 DOI: 10.1101/gad.352481.124
Rima M. Sakhawala, Reyhaneh Tirgar, Karl-Frédéric Vieux, Dustin Haskell, Guoyun Yu, Anna Zinovyeva, Katherine McJunkin
{"title":"A noncanonical Pol III-dependent, Microprocessor-independent biogenesis pathway generates a germline-enriched miRNA family","authors":"Rima M. Sakhawala, Reyhaneh Tirgar, Karl-Frédéric Vieux, Dustin Haskell, Guoyun Yu, Anna Zinovyeva, Katherine McJunkin","doi":"10.1101/gad.352481.124","DOIUrl":"https://doi.org/10.1101/gad.352481.124","url":null,"abstract":"MicroRNAs (miRNAs) are short RNAs that post-transcriptionally regulate gene expression. In canonical miRNA biogenesis, primary miRNAs are transcribed from intergenic loci or intronic regions by RNA polymerase II and sequentially cleaved by the Microprocessor complex and Dicer, and the resulting mature miRNAs are loaded into Argonaute to repress target mRNAs. A minority of miRNAs are generated via noncanonical biogenesis pathways that bypass the Microprocessor complex and/or Dicer. Here, we describe a new Pol III-dependent, Microprocessor-independent, and Dicer-dependent biogenesis pathway exemplified by the <em>mir-1829</em> family in <em>Caenorhabditis elegans</em>. Although the <em>mir-1829</em> family loci reside in intronic regions of protein-coding genes, we show that the miRNAs are derived from independent Pol III transcripts. Unlike other Pol III-dependent miRNAs, the <em>mir-1829</em> family small RNAs are the dominant species derived from their loci rather than fragments of a larger functional noncoding RNA. These germline-enriched miRNAs are loaded in multiple miRNA Argonautes, including the recently characterized germline Argonaute ALG-5, which we demonstrated is repressive when tethered to a reporter transcript. We extend these findings, identifying additional Pol III transcribed and noncanonical small RNAs in <em>C. elegans</em> and human data sets, including human miR-4521. These young, noncanonical miRNAs may represent an early snapshot in the evolution of de novo miRNA genes.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":"220 2 1","pages":""},"PeriodicalIF":10.5,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144629611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Cancer mortality and senescence: Is redox therapy an option? 癌症死亡率和衰老：氧化还原治疗是一种选择吗？
IF 10.5 1区 生物学
Genes & development Pub Date : 2025-07-14 DOI: 10.1101/gad.353129.125
Shan Kuang, Manojit M. Swamynathan, Lloyd C. Trotman
{"title":"Cancer mortality and senescence: Is redox therapy an option?","authors":"Shan Kuang, Manojit M. Swamynathan, Lloyd C. Trotman","doi":"10.1101/gad.353129.125","DOIUrl":"https://doi.org/10.1101/gad.353129.125","url":null,"abstract":"Patient genomics and mouse functional genetics have revealed that senescence is a barrier to metastatic progression of prostate cancer. Many efforts focus on eliminating senescent cells, whereas others aim to elucidate distinct characteristics that set them apart from normal and aging cells. Here, we discuss how exploration of the redox state of senescent cells could help define new markers and pro-oxidant vulnerabilities, drawing analogy to what is known about the redox sensitivity of proliferating cancer cells.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":"17 1","pages":""},"PeriodicalIF":10.5,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144629612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
C. elegans cognitive decline with age: more than just wiggling forward and backward 秀丽隐杆线虫的认知能力随着年龄的增长而下降：不仅仅是向前和向后摆动
IF 10.5 1区 生物学
Genes & development Pub Date : 2025-07-11 DOI: 10.1101/gad.353115.125
Titas Sengupta, Coleen T. Murphy
{"title":"C. elegans cognitive decline with age: more than just wiggling forward and backward","authors":"Titas Sengupta, Coleen T. Murphy","doi":"10.1101/gad.353115.125","DOIUrl":"https://doi.org/10.1101/gad.353115.125","url":null,"abstract":"<em>Caenorhabditis elegans</em> has been at the forefront of research on mechanisms of age-related decline for the past 30 years. Despite its popularity in longevity research, <em>C. elegans</em> is underappreciated for its potential to study complex behaviors and the progressive decline in these functions with age. Using assays of learning and memory, we have identified genetic pathways that regulate these behaviors and identified new mechanisms to boost these functions with age in both worms and mice. Because <em>C. elegans</em> is so highly conserved, some of these recently described mechanisms may be good targets to prevent human cognitive decline with age.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":"22 1","pages":""},"PeriodicalIF":10.5,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144611027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Beyond the usual suspects: expanding aging research from classic models to really cool critters 超越通常的怀疑：将衰老研究从经典模型扩展到非常酷的动物
IF 10.5 1区 生物学
Genes & development Pub Date : 2025-07-11 DOI: 10.1101/gad.353124.125
Amy Walker
{"title":"Beyond the usual suspects: expanding aging research from classic models to really cool critters","authors":"Amy Walker","doi":"10.1101/gad.353124.125","DOIUrl":"https://doi.org/10.1101/gad.353124.125","url":null,"abstract":"Model organisms such as yeast, worms, flies, and mice were key to discovering genes and other factors controlling life span and directly improved our understanding of human aging. Today, genomic tools allow study of a broader range of species, including those with short or long life spans, closely related species with different aging rates, or differences in interspecies aging. Models such as killifish, bats, and ants have much to teach us about human aging. They also reveal a flexible biological toolkit that species can use when evolutionary pressures drive rebalancing of growth, reproduction, or resilience with age-related decline.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":"12 1","pages":""},"PeriodicalIF":10.5,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144611025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Telomeres at the nexus of aging, tumor suppression, and inflammation: toward an understanding beyond senescence 端粒在衰老、肿瘤抑制和炎症的关系：走向超越衰老的理解
IF 10.5 1区 生物学
Genes & development Pub Date : 2025-07-11 DOI: 10.1101/gad.353122.125
Samuel I. Bloom, Jan Karlseder
{"title":"Telomeres at the nexus of aging, tumor suppression, and inflammation: toward an understanding beyond senescence","authors":"Samuel I. Bloom, Jan Karlseder","doi":"10.1101/gad.353122.125","DOIUrl":"https://doi.org/10.1101/gad.353122.125","url":null,"abstract":"Aging is the greatest risk factor for most diseases. We propose that aging manifests as disease as a function of tumor-suppressive capabilities. Adequate tumor suppression results in cell death or an accumulation of damaged cells leading to inflammation and tissue dysfunction that underlies diseases such as cardiovascular disease, neurodegenerative diseases, or type 2 diabetes. Conversely, inadequate tumor suppression leads to cancer. Telomeres are central to this process because they oppose hyperproliferation that is required for cancer initiation by enforcing two potent tumor suppressor mechanisms: senescence and crisis. Although senescent cells promote age-related diseases via inflammatory signaling, crisis cells have lost the p53 and RB pathways, have more unstable genomes, and harbor shorter telomeres, all of which could increase inflammation to a greater degree than is seen in senescence. This model emphasizes the intimate relationship between aging, telomeres, tumor suppression, and inflammation and suggests that crisis cells may represent an unexplored driver of inflammation in advanced age.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":"97 1","pages":""},"PeriodicalIF":10.5,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144611028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Mitochondria dysfunction: cause or consequence of physiologic aging? 线粒体功能障碍：生理性衰老的原因还是结果？
IF 10.5 1区 生物学
Genes & development Pub Date : 2025-07-11 DOI: 10.1101/gad.353106.125
G.R. Scott Budinger, Navdeep S. Chandel
{"title":"Mitochondria dysfunction: cause or consequence of physiologic aging?","authors":"G.R. Scott Budinger, Navdeep S. Chandel","doi":"10.1101/gad.353106.125","DOIUrl":"https://doi.org/10.1101/gad.353106.125","url":null,"abstract":"Mitochondria are no longer viewed solely as ATP- or metabolite-generating organelles but as key regulators of cellular signaling that shape physiologic aging. Contrary to earlier theories linking aging to mitochondrial DNA mutations and oxidative damage, current evidence shows that these factors do not causally limit physiologic aging. Instead, an evolving literature links age-related loss of mitochondrial signaling and function to important physiologic changes of aging. Moreover, mild inhibition of mitochondrial respiratory function with drugs like metformin promote health span. These findings open new paths for pharmacologically reprogramming mitochondrial signaling to extend healthy aging.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":"6 1","pages":""},"PeriodicalIF":10.5,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144611026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The interplay between senescence, inflammation, and the immune system 衰老、炎症和免疫系统之间的相互作用
IF 10.5 1区 生物学
Genes & development Pub Date : 2025-07-11 DOI: 10.1101/gad.353125.125
Jesús Gil
{"title":"The interplay between senescence, inflammation, and the immune system","authors":"Jesús Gil","doi":"10.1101/gad.353125.125","DOIUrl":"https://doi.org/10.1101/gad.353125.125","url":null,"abstract":"The past 40 years have witnessed significant progress in aging research. Although aging was once considered a stochastic process, it is now understood to be regulated by pathways and processes that can be dissected with modern cellular and molecular biology approaches. The aberrant accumulation of cells undergoing cellular senescence and an increase in chronic, sterile inflammation are two of those aging hallmarks. Here we discuss how these processes are connected and how the relationship between senescent cells and the immune system dictates the extent of inflammatory processes contributing to age-related dysfunction and disease.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":"11 1","pages":""},"PeriodicalIF":10.5,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144611253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Studying ovarian aging and its health impacts: modern tools and approaches 研究卵巢老化及其对健康的影响：现代工具和方法
IF 10.5 1区 生物学
Genes & development Pub Date : 2025-07-10 DOI: 10.1101/gad.352732.125
Bérénice A. Benayoun, Alison Kochersberger, Jennifer L. Garrison
{"title":"Studying ovarian aging and its health impacts: modern tools and approaches","authors":"Bérénice A. Benayoun, Alison Kochersberger, Jennifer L. Garrison","doi":"10.1101/gad.352732.125","DOIUrl":"https://doi.org/10.1101/gad.352732.125","url":null,"abstract":"Ovarian aging is a critical yet understudied driver of systemic aging in female bodies, with profound implications for female health and longevity. Despite its significance, we still know little about ovarian aging and its systemic effects on aging trajectories. With new efforts over the past few years, interest in the field has been growing and there is momentum to address these questions. This review highlights the importance of leveraging modern tools and approaches to better understand ovarian aging and its impact on health span. Specifically, we believe it will be useful for both aging researchers looking to go into research on ovarian aging and reproductive researchers looking to adopt more modern toolkit. We focus on menopause—a key marker of ovarian aging—as a lens through which to examine the current state of the field, identify limitations in existing research, and outline goals for future progress. By emphasizing cutting-edge techniques and emerging models, we seek to illuminate new pathways for research that could lead to improved strategies for managing ovarian aging and enhancing overall female health.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":"22 1","pages":""},"PeriodicalIF":10.5,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144593971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
SUMO2 promotes histone pre-mRNA processing by stabilizing histone locus body interactions and facilitating U7 snRNP assembly SUMO2通过稳定组蛋白位点体相互作用和促进U7 snRNP组装来促进组蛋白pre-mRNA加工
IF 10.5 1区 生物学
Genes & development Pub Date : 2025-07-10 DOI: 10.1101/gad.352728.125
Shuying He, Pin Lyu, Marnie W. Skinner, Anthony Desotell, Brendan Foley, Chance M. McCaig, Wei Wang, Jiang Qian, Liang Tong, William F. Marzluff, Michael J. Matunis
{"title":"SUMO2 promotes histone pre-mRNA processing by stabilizing histone locus body interactions and facilitating U7 snRNP assembly","authors":"Shuying He, Pin Lyu, Marnie W. Skinner, Anthony Desotell, Brendan Foley, Chance M. McCaig, Wei Wang, Jiang Qian, Liang Tong, William F. Marzluff, Michael J. Matunis","doi":"10.1101/gad.352728.125","DOIUrl":"https://doi.org/10.1101/gad.352728.125","url":null,"abstract":"Histone mRNAs are the only nonpolyadenylated mRNAs in eukaryotic cells and require specialized processing in the histone locus body (HLB), a nuclear body where essential processing factors, including the U7 snRNP, are concentrated. Recent studies have revealed that misregulation of histone pre-mRNA processing can lead to polyadenylation of histone mRNAs and disruption of histone protein homeostasis. Despite links to human disease, the factors contributing to polyadenylation of histone mRNAs and the mechanisms underlying HLB assembly and U7 snRNP biogenesis remain unclear. Here, we report novel functions of the small ubiquitin-related modifier 2 (SUMO2) in promoting histone pre-mRNA processing. Using a SUMO2 knockout osteosarcoma cell line, we identified a defect in 3′ end cleavage and a global increase in histone mRNA polyadenylation. Subsequent analysis of HLBs revealed increased dynamics and reduced levels of the U7 snRNP complex. By overexpressing the U7 snRNP-specific components Lsm11 and U7 snRNA, we rescued U7 snRNP levels and processing defects in SUMO2 knockout cells. Through analysis of Lsm11, we identified a SUMO-interacting motif in its N terminus required for efficient formation of U7 snRNP. Collectively, we demonstrated that SUMO2 promotes histone pre-mRNA 3′ end processing by stabilizing HLB interactions and facilitating U7 snRNP assembly.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":"93 1","pages":""},"PeriodicalIF":10.5,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144593973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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