Pub Date : 2025-04-30DOI: 10.1016/j.gde.2025.102353
Amelie A Raz , Yukiko M Yamashita
Adult stem cells maintain tissue homeostasis through the production of differentiating cells. Considerable recent work has identified that stem cells themselves are replaceable through the process of dedifferentiation. The capacity and mechanisms of dedifferentiation vary widely among species and organ contexts. However, some core features are commonly present. In this review, we summarize ‘hallmarks’ of dedifferentiation, including mechanisms for maintenance of potency, sensation of loss, and migration, and review the current understanding of dedifferentiation as a true replacement mechanism.
{"title":"Rewinding the clock: mechanisms of dedifferentiation","authors":"Amelie A Raz , Yukiko M Yamashita","doi":"10.1016/j.gde.2025.102353","DOIUrl":"10.1016/j.gde.2025.102353","url":null,"abstract":"<div><div>Adult stem cells maintain tissue homeostasis through the production of differentiating cells. Considerable recent work has identified that stem cells themselves are replaceable through the process of dedifferentiation. The capacity and mechanisms of dedifferentiation vary widely among species and organ contexts. However, some core features are commonly present. In this review, we summarize ‘hallmarks’ of dedifferentiation, including mechanisms for maintenance of potency, sensation of loss, and migration, and review the current understanding of dedifferentiation as a true replacement mechanism.</div></div>","PeriodicalId":50606,"journal":{"name":"Current Opinion in Genetics & Development","volume":"93 ","pages":"Article 102353"},"PeriodicalIF":3.7,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143890918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-30DOI: 10.1016/j.gde.2025.102351
Melissa T Adams, Heinrich Jasper, Lluc Mosteiro
Partial reprogramming achieved by the transient expression of the transcription factors (TFs) Oct4, Sox2, Klf4 and C-Myc (abbreviated OSKM) can erase aging and damage features in cells, leading to increased healthspan, lifespan and tissue regeneration. Recent reports suggest that the mechanisms of partial reprogramming may share some similarities with natural dedifferentiation and regeneration. Both processes appear to involve the transient repression of somatic identity through the sequestration of somatic identity TFs to noncanonical sites, which are opened by the high expression of pioneer TFs, leading to transient dedifferentiation into a fetal-like state. Here, we review the reported benefits of partial reprogramming on tissue regeneration and propose a common mechanism of epigenetic remodeling with natural regeneration after tissue injury.
{"title":"Unlocking regeneration: how partial reprogramming resembles tissue healing","authors":"Melissa T Adams, Heinrich Jasper, Lluc Mosteiro","doi":"10.1016/j.gde.2025.102351","DOIUrl":"10.1016/j.gde.2025.102351","url":null,"abstract":"<div><div>Partial reprogramming achieved by the transient expression of the transcription factors (TFs) Oct4, Sox2, Klf4 and C-Myc (abbreviated OSKM) can erase aging and damage features in cells, leading to increased healthspan, lifespan and tissue regeneration. Recent reports suggest that the mechanisms of partial reprogramming may share some similarities with natural dedifferentiation and regeneration. Both processes appear to involve the transient repression of somatic identity through the sequestration of somatic identity TFs to noncanonical sites, which are opened by the high expression of pioneer TFs, leading to transient dedifferentiation into a fetal-like state. Here, we review the reported benefits of partial reprogramming on tissue regeneration and propose a common mechanism of epigenetic remodeling with natural regeneration after tissue injury.</div></div>","PeriodicalId":50606,"journal":{"name":"Current Opinion in Genetics & Development","volume":"93 ","pages":"Article 102351"},"PeriodicalIF":3.7,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143890916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-29DOI: 10.1016/j.gde.2025.102350
Yingwo Sun, Marc Vermulst
At first glance, biological systems appear to operate with remarkable precision and order. Yet, closer examination reveals that this perfection is an illusion, biological processes are inherently prone to errors. Here, we describe recent evidence that indicates that errors that occur during transcription play an important role in neurological diseases. These errors, though transient, can have lasting consequences when they generate mutant proteins with amyloid or prion-like properties. Such proteins can seed aggregation cascades, converting wild-type counterparts into misfolded conformations, ultimately leading to toxic deposits seen in diseases like Alzheimer’s and amyotrophic lateral sclerosis. These observations help to paint a fuller picture of the origins of neurodegenerative diseases in aging humans and suggest a unified mechanism by which they may arise.
{"title":"The hidden costs of imperfection: transcription errors in protein aggregation diseases","authors":"Yingwo Sun, Marc Vermulst","doi":"10.1016/j.gde.2025.102350","DOIUrl":"10.1016/j.gde.2025.102350","url":null,"abstract":"<div><div>At first glance, biological systems appear to operate with remarkable precision and order. Yet, closer examination reveals that this perfection is an illusion, biological processes are inherently prone to errors. Here, we describe recent evidence that indicates that errors that occur during transcription play an important role in neurological diseases. These errors, though transient, can have lasting consequences when they generate mutant proteins with amyloid or prion-like properties. Such proteins can seed aggregation cascades, converting wild-type counterparts into misfolded conformations, ultimately leading to toxic deposits seen in diseases like Alzheimer’s and amyotrophic lateral sclerosis. These observations help to paint a fuller picture of the origins of neurodegenerative diseases in aging humans and suggest a unified mechanism by which they may arise.</div></div>","PeriodicalId":50606,"journal":{"name":"Current Opinion in Genetics & Development","volume":"93 ","pages":"Article 102350"},"PeriodicalIF":3.7,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143881751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-25DOI: 10.1016/j.gde.2025.102348
Sung-Ya Lin , Mia T Levine
Telomeres are essential nucleoprotein structures that preserve our terminal DNA sequence and protect chromosome ends from fusion. Our vast knowledge of telomeres comes almost entirely from studies of healthy and diseased somatic cells. However, building evidence suggests that the molecules and mechanisms required for telomere integrity in somatic cells are insufficient to preserve telomere integrity during the sperm-to-embryo transition. Here, we review this growing body of work on telomere ‘paternal effects’, wherein zygotic telomere integrity is determined not by the genotype of the zygote but instead by the genotype of the father. Direct inheritance of sperm-specific proteins establishes paternal telomere epigenetic identity, while direct inheritance of sperm telomere length contributes to telomere length inheritance. Together, these investigations of telomere integrity through the sperm-to-embryo transition reveal potent paternal effects on zygotic telomere functions, with implications for human infertility.
{"title":"Paternal effects on telomere integrity during the sperm-to-embryo transition","authors":"Sung-Ya Lin , Mia T Levine","doi":"10.1016/j.gde.2025.102348","DOIUrl":"10.1016/j.gde.2025.102348","url":null,"abstract":"<div><div>Telomeres are essential nucleoprotein structures that preserve our terminal DNA sequence and protect chromosome ends from fusion. Our vast knowledge of telomeres comes almost entirely from studies of healthy and diseased somatic cells. However, building evidence suggests that the molecules and mechanisms required for telomere integrity in somatic cells are insufficient to preserve telomere integrity during the sperm-to-embryo transition. Here, we review this growing body of work on telomere ‘paternal effects’, wherein zygotic telomere integrity is determined not by the genotype of the zygote but instead by the genotype of the father. Direct inheritance of sperm-specific proteins establishes paternal telomere epigenetic identity, while direct inheritance of sperm telomere length contributes to telomere length inheritance. Together, these investigations of telomere integrity through the sperm-to-embryo transition reveal potent paternal effects on zygotic telomere functions, with implications for human infertility.</div></div>","PeriodicalId":50606,"journal":{"name":"Current Opinion in Genetics & Development","volume":"93 ","pages":"Article 102348"},"PeriodicalIF":3.7,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143868698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-16DOI: 10.1016/j.gde.2025.102349
Stefanie Williams, Robin Scott Hawley
The synaptonemal complex (SC) is structurally conserved across eukaryotes and is essential for a proper progression of meiosis. Despite this conservation, SC protein sequences diverge drastically. In this review, we explore findings on SC protein evolution, highlighting key differences and commonalities among lineages like the Caenorhabditis and the Drosophila genera. We further explore known cases where the SC and its proteins adopt novel functional roles and discuss why knowledge of these cases could be important for the study of canonical SC biology. The existing studies demonstrate that work on the evolutionary biology of SC proteins and functional studies in more diverse meiotic research organisms should play a major role in aiding our understanding of SC structure and functions.
{"title":"From conservation to adaptation: understanding the synaptonemal complex’s evolutionary dynamics","authors":"Stefanie Williams, Robin Scott Hawley","doi":"10.1016/j.gde.2025.102349","DOIUrl":"10.1016/j.gde.2025.102349","url":null,"abstract":"<div><div>The synaptonemal complex (SC) is structurally conserved across eukaryotes and is essential for a proper progression of meiosis. Despite this conservation, SC protein sequences diverge drastically. In this review, we explore findings on SC protein evolution, highlighting key differences and commonalities among lineages like the <em>Caenorhabditis</em> and the <em>Drosophila</em> genera. We further explore known cases where the SC and its proteins adopt novel functional roles and discuss why knowledge of these cases could be important for the study of canonical SC biology. The existing studies demonstrate that work on the evolutionary biology of SC proteins and functional studies in more diverse meiotic research organisms should play a major role in aiding our understanding of SC structure and functions.</div></div>","PeriodicalId":50606,"journal":{"name":"Current Opinion in Genetics & Development","volume":"93 ","pages":"Article 102349"},"PeriodicalIF":3.7,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143843881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-14DOI: 10.1016/j.gde.2025.102347
Tianyao Xiao, Elçin Ünal
The key to healthy offspring production lies in the accurate inheritance of components from progenitor germ cells during gametogenesis. Along with genetic material, precise regulation of organelle inheritance is vital for gamete health and embryonic development, especially in aged organisms, where organelle function declines and damage accumulates. In these cases, removing age-related organellar defects in precursor cells is crucial for successful reproduction. The single-celled organism Saccharomyces cerevisiae shares striking similarities with more complex organisms: like metazoan cells, yeast accumulate organelle damage with age, yet can still produce damage-free gametes with a reset lifespan. Recent studies show that organelles undergo significant reorganization during yeast gametogenesis, and similar remodeling occurs in metazoans, suggesting common strategies for maintaining gamete quality. This review summarizes organellar reorganization during gametogenesis in yeast and how it aids in clearing age-related cellular damage. We also explore organellar remodeling in multicellular organisms and discuss the potential mechanisms and biological benefits of meiotic organellar reshaping.
{"title":"Remodeling, compartmentalization, and degradation: a trifecta for organelle quality control during gametogenesis","authors":"Tianyao Xiao, Elçin Ünal","doi":"10.1016/j.gde.2025.102347","DOIUrl":"10.1016/j.gde.2025.102347","url":null,"abstract":"<div><div>The key to healthy offspring production lies in the accurate inheritance of components from progenitor germ cells during gametogenesis. Along with genetic material, precise regulation of organelle inheritance is vital for gamete health and embryonic development, especially in aged organisms, where organelle function declines and damage accumulates. In these cases, removing age-related organellar defects in precursor cells is crucial for successful reproduction. The single-celled organism <em>Saccharomyces cerevisiae</em> shares striking similarities with more complex organisms: like metazoan cells, yeast accumulate organelle damage with age, yet can still produce damage-free gametes with a reset lifespan. Recent studies show that organelles undergo significant reorganization during yeast gametogenesis, and similar remodeling occurs in metazoans, suggesting common strategies for maintaining gamete quality. This review summarizes organellar reorganization during gametogenesis in yeast and how it aids in clearing age-related cellular damage. We also explore organellar remodeling in multicellular organisms and discuss the potential mechanisms and biological benefits of meiotic organellar reshaping.</div></div>","PeriodicalId":50606,"journal":{"name":"Current Opinion in Genetics & Development","volume":"92 ","pages":"Article 102347"},"PeriodicalIF":3.7,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143829348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-09DOI: 10.1016/j.gde.2025.102346
Shreeya Bakshi, Lori L Isom
Alternative splicing of pre-mRNA generates multiple transcripts from a single gene, contributing to transcriptomic diversity. Alternative splicing can result in inclusion of poison exons (PEs), which contain a premature stop codons (PTC) that target transcripts for nonsense-mediated decay (NMD). PE-containing transcripts are prevalent in the brain, where they can play roles in fine-tuning mRNA and protein levels. Antisense, or splice-switching, oligonucleotides (ASOs/SSOs) are used to target PEs to reduce their inclusion and treat neurodevelopmental disorders. ASOs/SSOs address the genetic causes of disease and are precision therapies that can provide a cure rather than only address disease symptoms. This review explores the role of PEs in the brain, therapeutic targeting of PEs, and current challenges in our understanding of PEs.
{"title":"No more nonsense: evaluating poison exons as therapeutic targets in neurodevelopmental disorders","authors":"Shreeya Bakshi, Lori L Isom","doi":"10.1016/j.gde.2025.102346","DOIUrl":"10.1016/j.gde.2025.102346","url":null,"abstract":"<div><div>Alternative splicing of pre-mRNA generates multiple transcripts from a single gene, contributing to transcriptomic diversity. Alternative splicing can result in inclusion of poison exons (PEs), which contain a premature stop codons (PTC) that target transcripts for nonsense-mediated decay (NMD). PE-containing transcripts are prevalent in the brain, where they can play roles in fine-tuning mRNA and protein levels. Antisense, or splice-switching, oligonucleotides (ASOs/SSOs) are used to target PEs to reduce their inclusion and treat neurodevelopmental disorders. ASOs/SSOs address the genetic causes of disease and are precision therapies that can provide a cure rather than only address disease symptoms. This review explores the role of PEs in the brain, therapeutic targeting of PEs, and current challenges in our understanding of PEs.</div></div>","PeriodicalId":50606,"journal":{"name":"Current Opinion in Genetics & Development","volume":"92 ","pages":"Article 102346"},"PeriodicalIF":3.7,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143799968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-08DOI: 10.1016/j.gde.2025.102345
Chiara Beghѐ, Helena Harpham, Yasmine Barberic, Natalia Gromak
Neurodegenerative diseases are associated with the progressive loss of neurons. R-loops are non-canonical nucleic acid structures formed during transcription and composed of an RNA/DNA hybrid and a displaced single-stranded DNA. Whilst R-loops are important regulators of cellular processes, they are also associated with the pathologies of multiple disorders, including repeat expansion, motor neuron, inflammatory and ageing diseases. In this review, we discuss how R-loops contribute to pathological mechanisms that underpin neurodegeneration. We highlight the role of R-loops in several hallmarks of neurodegenerative disorders, including RNA and DNA defects, DNA damage, protein aggregation, inflammation, mitochondrial dysfunction, and neuronal cell death. We also discuss the potential role of R-loops as therapeutic targets for neurodegenerative disorders.
{"title":"R-loops in neurodegeneration","authors":"Chiara Beghѐ, Helena Harpham, Yasmine Barberic, Natalia Gromak","doi":"10.1016/j.gde.2025.102345","DOIUrl":"10.1016/j.gde.2025.102345","url":null,"abstract":"<div><div>Neurodegenerative diseases are associated with the progressive loss of neurons. R-loops are non-canonical nucleic acid structures formed during transcription and composed of an RNA/DNA hybrid and a displaced single-stranded DNA. Whilst R-loops are important regulators of cellular processes, they are also associated with the pathologies of multiple disorders, including repeat expansion, motor neuron, inflammatory and ageing diseases. In this review, we discuss how R-loops contribute to pathological mechanisms that underpin neurodegeneration. We highlight the role of R-loops in several hallmarks of neurodegenerative disorders, including RNA and DNA defects, DNA damage, protein aggregation, inflammation, mitochondrial dysfunction, and neuronal cell death. We also discuss the potential role of R-loops as therapeutic targets for neurodegenerative disorders.</div></div>","PeriodicalId":50606,"journal":{"name":"Current Opinion in Genetics & Development","volume":"92 ","pages":"Article 102345"},"PeriodicalIF":3.7,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143790942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-04-05DOI: 10.1016/j.gde.2025.102344
Louise Maillard , Pierre Bensidoun , Mounia Lagha
During the oocyte-to-embryo transition, the transcriptome and proteome are dramatically reshaped. This transition entails a shift from maternally inherited mRNAs to newly synthesized transcripts, produced during the zygotic genome activation (ZGA). Furthermore, a crucial transcription and translation selectivity is required for early embryonic development. Studies across various model organisms have revealed conserved cis- and trans-regulatory mechanisms dictating the regimes by which mRNA and proteins are produced during this critical phase. In this article, we highlight recent technological and conceptual advances that deepen our understanding of how the tuning of both transcription and translation evolves during ZGA.
{"title":"Reshaping transcription and translation dynamics during the awakening of the zygotic genome","authors":"Louise Maillard , Pierre Bensidoun , Mounia Lagha","doi":"10.1016/j.gde.2025.102344","DOIUrl":"10.1016/j.gde.2025.102344","url":null,"abstract":"<div><div>During the oocyte-to-embryo transition, the transcriptome and proteome are dramatically reshaped. This transition entails a shift from maternally inherited mRNAs to newly synthesized transcripts, produced during the zygotic genome activation (ZGA). Furthermore, a crucial transcription and translation selectivity is required for early embryonic development. Studies across various model organisms have revealed conserved <em>cis-</em> and <em>trans-</em>regulatory mechanisms dictating the regimes by which mRNA and proteins are produced during this critical phase. In this article, we highlight recent technological and conceptual advances that deepen our understanding of how the tuning of both transcription and translation evolves during ZGA.</div></div>","PeriodicalId":50606,"journal":{"name":"Current Opinion in Genetics & Development","volume":"92 ","pages":"Article 102344"},"PeriodicalIF":3.7,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143776585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-29DOI: 10.1016/j.gde.2025.102343
Sue Fletcher , Niall P Keegan , Rita Mejzini , Ianthe L Pitout
Accurate exon selection and processing of pre-messenger RNA are crucial for normal gene expression. Mutations that alter splicing disrupt pre-mRNA processing and can have diverse effects on transcript structure, making the consequences of many such mutations difficult to predict. While next-generation sequencing technologies have transformed genetic diagnosis for many patients, deep intronic variants generally evade detection and characterisation. Of all the known types of splicing mutations, the most elusive to predict are those that activate pseudoexons. Because transcripts that contain pseudoexons are otherwise generally intact, exclusion (or ‘skipping’) of the pseudoexon during processing of the pre-mRNA is likely to generate a normal, functional mRNA. Characterisation of pseudoexon mutations will open opportunities for the development of antisense oligonucleotide strategies to overcome these disease-causing mutations.
{"title":"To splice or not to splice: pseudoexons in neurological disease and opportunities for intervention","authors":"Sue Fletcher , Niall P Keegan , Rita Mejzini , Ianthe L Pitout","doi":"10.1016/j.gde.2025.102343","DOIUrl":"10.1016/j.gde.2025.102343","url":null,"abstract":"<div><div>Accurate exon selection and processing of pre-messenger RNA are crucial for normal gene expression. Mutations that alter splicing disrupt pre-mRNA processing and can have diverse effects on transcript structure, making the consequences of many such mutations difficult to predict. While next-generation sequencing technologies have transformed genetic diagnosis for many patients, deep intronic variants generally evade detection and characterisation. Of all the known types of splicing mutations, the most elusive to predict are those that activate pseudoexons. Because transcripts that contain pseudoexons are otherwise generally intact, exclusion (or ‘skipping’) of the pseudoexon during processing of the pre-mRNA is likely to generate a normal, functional mRNA. Characterisation of pseudoexon mutations will open opportunities for the development of antisense oligonucleotide strategies to overcome these disease-causing mutations.</div></div>","PeriodicalId":50606,"journal":{"name":"Current Opinion in Genetics & Development","volume":"92 ","pages":"Article 102343"},"PeriodicalIF":3.7,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143734631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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