Lineage plasticity drives treatment resistance in lung adenocarcinoma (LUAD) as cancer cells adopt new identities. In this issue of Genes & Development, Fort and colleagues (doi:10.1101/gad.352742.125) report HNF4α as a key regulator of hybrid identity states and tumor progression in NKX2-1-positive LUAD. Using murine and human models, they show that HNF4α promotes gastrointestinal/liver-like programs and suppresses pulmonary identity by modulating cell identity-specific binding of NKX2-1. In addition, RAS/MEK signaling was implicated in maintenance of this hybrid identity state by regulating NKX2-1 chromatin binding in LUAD. These findings nominate HNF4α as a driver of LUAD plasticity and a potential therapeutic target to overcome resistance.
{"title":"Lineage rewiring in lung adenocarcinoma via HNF4α and NKX2-1 dynamics","authors":"Alice Feng, Alena Yermalovich, Matthew Meyerson","doi":"10.1101/gad.353142.125","DOIUrl":"https://doi.org/10.1101/gad.353142.125","url":null,"abstract":"Lineage plasticity drives treatment resistance in lung adenocarcinoma (LUAD) as cancer cells adopt new identities. In this issue of <em>Genes & Development</em>, Fort and colleagues (doi:10.1101/gad.352742.125) report HNF4α as a key regulator of hybrid identity states and tumor progression in NKX2-1-positive LUAD. Using murine and human models, they show that HNF4α promotes gastrointestinal/liver-like programs and suppresses pulmonary identity by modulating cell identity-specific binding of NKX2-1. In addition, RAS/MEK signaling was implicated in maintenance of this hybrid identity state by regulating NKX2-1 chromatin binding in LUAD. These findings nominate HNF4α as a driver of LUAD plasticity and a potential therapeutic target to overcome resistance.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":"33 1","pages":""},"PeriodicalIF":10.5,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144701925","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}
Although vertebrates share a similar body plan, different vertebrate species can develop at very different rates. In recent years, there has been an increasing appreciation of the fact that protein stability regulates the pace of differentiation. For example, global differences in protein stability may help explain why humans develop more slowly than mice. Mechanisms controlling the stability of particular proteins are also likely to play a role. In keeping with this idea, in this issue of Genes & Development, Meijer and colleagues (doi:10.1101/gad.352909.125) report that cells must keep tight control over the stability of the Notch1 intracellular domain (NICD) to tune developmental timing in the context of human somitogenesis.
{"title":"Speed of life: tuning the ticktock of the segmentation clock","authors":"Sally Lowell","doi":"10.1101/gad.353096.125","DOIUrl":"https://doi.org/10.1101/gad.353096.125","url":null,"abstract":"Although vertebrates share a similar body plan, different vertebrate species can develop at very different rates. In recent years, there has been an increasing appreciation of the fact that protein stability regulates the pace of differentiation. For example, global differences in protein stability may help explain why humans develop more slowly than mice. Mechanisms controlling the stability of particular proteins are also likely to play a role. In keeping with this idea, in this issue of <em>Genes & Development</em>, Meijer and colleagues (doi:10.1101/gad.352909.125) report that cells must keep tight control over the stability of the Notch1 intracellular domain (NICD) to tune developmental timing in the context of human somitogenesis.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":"10 1","pages":""},"PeriodicalIF":10.5,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144652095","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}
Rachel E. Turn, Keren I. Hilgendorf, Carl T. Johnson, Kyuho Han, Mohammad Ovais Aziz-Zanjani, Samuel Swails Bollinger, Pablo Domizi, Ran Cheng, Atefeh Rabiee, Yingdi Zhu, Zewen Jiang, Anushweta Asthana, Janos Demeter, Katrin J. Svensson, Michael C. Bassik, Peter K. Jackson
In response to excess nutrients, white adipose tissue expands by both generating new adipocytes and upregulating lipogenesis in existing adipocytes. Here, we performed a genome-wide functional CRISPR screen to identify regulators of adipogenesis in the mouse 3T3-L1 preadipocyte model. In this pooled screening strategy, we used FACS to isolate populations based on lipid content, gating for fluorescence intensity of lipophilic fluorescent BODIPY dye. Additionally, we categorized whether the gene functions primarily during mitotic clonal expansion, lipogenesis, or both. We found that translation initiation and ubiquitin-dependent protein stability regulators drive both adipogenic fate change and lipogenesis. We further supported these findings with proteomics, demonstrating that essential changes in protein reprogramming can drive or inhibit 3T3-L1 adipogenesis independent of transcription. Furthermore, we demonstrated that specific branches of the hypusination pathway, a conserved regulator of translation initiation, are critical for translating adipogenic inducers of mitotic clonal expansion and that the neddylation/ubiquitin pathway modulates insulin sensitivity during lipogenesis.
{"title":"A genome-wide, CRISPR-based screen reveals new requirements for translation initiation and ubiquitination in driving adipogenic fate change","authors":"Rachel E. Turn, Keren I. Hilgendorf, Carl T. Johnson, Kyuho Han, \u0000Mohammad Ovais Aziz-Zanjani, Samuel Swails Bollinger, Pablo Domizi, Ran Cheng, Atefeh Rabiee, Yingdi Zhu, Zewen Jiang, Anushweta Asthana, Janos Demeter, Katrin J. Svensson, Michael C. Bassik, Peter K. Jackson","doi":"10.1101/gad.352779.125","DOIUrl":"https://doi.org/10.1101/gad.352779.125","url":null,"abstract":"In response to excess nutrients, white adipose tissue expands by both generating new adipocytes and upregulating lipogenesis in existing adipocytes. Here, we performed a genome-wide functional CRISPR screen to identify regulators of adipogenesis in the mouse 3T3-L1 preadipocyte model. In this pooled screening strategy, we used FACS to isolate populations based on lipid content, gating for fluorescence intensity of lipophilic fluorescent BODIPY dye. Additionally, we categorized whether the gene functions primarily during mitotic clonal expansion, lipogenesis, or both. We found that translation initiation and ubiquitin-dependent protein stability regulators drive both adipogenic fate change and lipogenesis. We further supported these findings with proteomics, demonstrating that essential changes in protein reprogramming can drive or inhibit 3T3-L1 adipogenesis independent of transcription. Furthermore, we demonstrated that specific branches of the hypusination pathway, a conserved regulator of translation initiation, are critical for translating adipogenic inducers of mitotic clonal expansion and that the neddylation/ubiquitin pathway modulates insulin sensitivity during lipogenesis.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":"73 1","pages":""},"PeriodicalIF":10.5,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144652094","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}
Cellular senescence plays a dual role in tissue biology by promoting tumor suppression and wound healing when transient but driving inflammation, fibrosis, and age-related disease when persistent. The growing recognition that senescent cell clearance can reverse these pathologies has catalyzed efforts to develop therapeutics that preferentially kill senescent cells (also known as “senolytics”). However, clinical translation from bench to bedside remains challenging due to senescent state heterogeneity, limited biomarkers, off-target toxicities, and the frailty of aged patients. Small molecule senolytics, although promising, often lack defined mechanisms of action and pose safety concerns that may constrain their use in older adults. Emerging precision approaches, including those that exploit surface markers and leverage engineered immune therapies, offer a rational and potentially more selective path forward. Here we highlight recent advances in senescence profiling and targeted clearance strategies, emphasizing the need for therapies designed with both biological complexity and the needs of aging populations in mind.
{"title":"Killing wisely: precision senolytics in the age of frailty","authors":"Valentin J.A. Barthet, Scott W. Lowe","doi":"10.1101/gad.353134.125","DOIUrl":"https://doi.org/10.1101/gad.353134.125","url":null,"abstract":"Cellular senescence plays a dual role in tissue biology by promoting tumor suppression and wound healing when transient but driving inflammation, fibrosis, and age-related disease when persistent. The growing recognition that senescent cell clearance can reverse these pathologies has catalyzed efforts to develop therapeutics that preferentially kill senescent cells (also known as “senolytics”). However, clinical translation from bench to bedside remains challenging due to senescent state heterogeneity, limited biomarkers, off-target toxicities, and the frailty of aged patients. Small molecule senolytics, although promising, often lack defined mechanisms of action and pose safety concerns that may constrain their use in older adults. Emerging precision approaches, including those that exploit surface markers and leverage engineered immune therapies, offer a rational and potentially more selective path forward. Here we highlight recent advances in senescence profiling and targeted clearance strategies, emphasizing the need for therapies designed with both biological complexity and the needs of aging populations in mind.","PeriodicalId":12591,"journal":{"name":"Genes & development","volume":"76 1","pages":""},"PeriodicalIF":10.5,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144639725","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}
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.
{"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}
Rima M. Sakhawala, Reyhaneh Tirgar, Karl-Frédéric Vieux, Dustin Haskell, Guoyun Yu, Anna Zinovyeva, Katherine McJunkin
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 mir-1829 family in Caenorhabditis elegans. Although the mir-1829 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 mir-1829 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 C. elegans 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.
{"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}
Shan Kuang, Manojit M. Swamynathan, Lloyd C. Trotman
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.
{"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}
Caenorhabditis elegans has been at the forefront of research on mechanisms of age-related decline for the past 30 years. Despite its popularity in longevity research, C. elegans 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 C. elegans is so highly conserved, some of these recently described mechanisms may be good targets to prevent human cognitive decline with age.
{"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}
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.
{"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}
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.
{"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}
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