The mastery of fire transformed human evolution through advantages spanning diet, behavior, physiology, and ecology. While these benefits are well established, here we highlight a previously overlooked cost — and selective pressure — unique to humans: high-temperature burn injury. Unlike other species, humans and their hominin ancestors have faced increased lifetime risk of burns, which we argue has driven genetic adaptation. Drawing on comparative genomic evidence across primates, we suggest that genes associated with burn injury response — relating to wound healing and inflammation — show signs of accelerated evolution in humans. We propose that recurrent exposure to burns acted as a selective force in our lineage, helping to explain both beneficial adaptations and paradoxical maladaptive responses to severe injury. By framing burns as an evolutionary pressure, the Burn Selection Hypothesis invites a re-evaluation of how fire shaped human biology and offers new perspectives for understanding both the evolutionary past and modern burn care.
{"title":"Burn Selection: How Fire Injury Shaped Human Evolution","authors":"Joshua Cuddihy, Yuemin Li, Isobel Fisher, Zoltan Takats, Dominic Friston, Declan Collins, Marcela Vizcaychipi, Matteo Fumagalli, Istvan Nagy, Armand Leroi","doi":"10.1002/bies.70109","DOIUrl":"10.1002/bies.70109","url":null,"abstract":"<p>The mastery of fire transformed human evolution through advantages spanning diet, behavior, physiology, and ecology. While these benefits are well established, here we highlight a previously overlooked cost — and selective pressure — unique to humans: high-temperature burn injury. Unlike other species, humans and their hominin ancestors have faced increased lifetime risk of burns, which we argue has driven genetic adaptation. Drawing on comparative genomic evidence across primates, we suggest that genes associated with burn injury response — relating to wound healing and inflammation — show signs of accelerated evolution in humans. We propose that recurrent exposure to burns acted as a selective force in our lineage, helping to explain both beneficial adaptations and paradoxical maladaptive responses to severe injury. By framing burns as an evolutionary pressure, the <i>Burn Selection Hypothesis</i> invites a re-evaluation of how fire shaped human biology and offers new perspectives for understanding both the evolutionary past and modern burn care.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"48 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12873521/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146117954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
D. Kayo, S.K. Uehara, M.R. Royan, and S. Kanda, “Emerging Perspectives on Gonadotropin Regulation in Vertebrates Revealed by the Discovery of FSH-RH in Teleosts,” Bioessays 47 (2025): e70066. http://doi.org/10.1002/bies.70066.
{"title":"Erratum \"Emerging Perspectives on Gonadotropin Regulation in Vertebrates Revealed by the Discovery of FSH-RH in Teleosts\"","authors":"","doi":"10.1002/bies.70111","DOIUrl":"10.1002/bies.70111","url":null,"abstract":"<p>D. Kayo, S.K. Uehara, M.R. Royan, and S. Kanda, “Emerging Perspectives on Gonadotropin Regulation in Vertebrates Revealed by the Discovery of FSH-RH in Teleosts,” <i>Bioessays</i> 47 (2025): e70066. http://doi.org/10.1002/bies.70066.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"48 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12862110/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146099681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stem cell populations employ cell-intrinsic and niche-mediated mechanisms to preserve long-term self-renewal and regenerative potential. We propose that tumor-initiating cells (TICs) hijack this developmental circuitry to sustain their growth and establish an early immunosuppressive microenvironment during malignant progression. Recent work implicates CXCR4+ tissue-resident macrophages (TRMs) in the mammary gland as a central orchestrator of this process. Conserved CXCL12/CXCR4-AKT-β-catenin signaling links CXCR4+ TRM support of normal mammary stem cells to TIC maintenance, underscoring how developmental niches are exploited in malignancy. During tumorigenesis, aberrant CXCL12 production from tumor-associated fibroblasts promotes the expansion of CXCR4+ TRMs, while CXCR4 signaling enhances ALDH1A2-dependent retinoic acid production, which induces regulatory T cells and thereby suppresses anti-tumor immunity at the earliest stages of tumor development. From this perspective, early immune evasion is not only a hallmark of cancer but also a therapeutic window. Targeting TRMs early in cancer development could delay, or even prevent, malignant initiation. More broadly, we propose that TIC–niche crosstalk constitutes a tractable vulnerability, and that incorporating TRM-directed interventions alongside conventional and immune-based therapies may shift the balance toward durable tumor control.
{"title":"Macrophages in the Mammary Gland Stem Cell Niche: A Double-Edged Sword in Tissue Regeneration and Tumor Initiation","authors":"Eunmi Lee, Yibin Kang","doi":"10.1002/bies.70108","DOIUrl":"10.1002/bies.70108","url":null,"abstract":"<div>\u0000 \u0000 <p>Stem cell populations employ cell-intrinsic and niche-mediated mechanisms to preserve long-term self-renewal and regenerative potential. We propose that tumor-initiating cells (TICs) hijack this developmental circuitry to sustain their growth and establish an early immunosuppressive microenvironment during malignant progression. Recent work implicates CXCR4<sup>+</sup> tissue-resident macrophages (TRMs) in the mammary gland as a central orchestrator of this process. Conserved CXCL12/CXCR4-AKT-β-catenin signaling links CXCR4<sup>+</sup> TRM support of normal mammary stem cells to TIC maintenance, underscoring how developmental niches are exploited in malignancy. During tumorigenesis, aberrant CXCL12 production from tumor-associated fibroblasts promotes the expansion of CXCR4<sup>+</sup> TRMs, while CXCR4 signaling enhances ALDH1A2-dependent retinoic acid production, which induces regulatory T cells and thereby suppresses anti-tumor immunity at the earliest stages of tumor development. From this perspective, early immune evasion is not only a hallmark of cancer but also a therapeutic window. Targeting TRMs early in cancer development could delay, or even prevent, malignant initiation. More broadly, we propose that TIC–niche crosstalk constitutes a tractable vulnerability, and that incorporating TRM-directed interventions alongside conventional and immune-based therapies may shift the balance toward durable tumor control.</p>\u0000 </div>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"48 2","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146099682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Debashish Bhattacharya, Shrinivas Nandi, Erin E. Chille, Miriam Arroyo, Timothy G. Stephens
We review recent multi-omics analyses of the coral heat stress response to explore the generality of the Oxidative Theory of Coral Bleaching (OTCB), which posits that algal symbiont release is the final act of defense by the coral host to survive alga-derived oxidative stress. The OTCB is particularly relevant given that ocean warming, which is accelerating under climate change, has proven devastating for corals, leading to the bleaching phenotype and widespread reef loss. Multi-omics results, in combination with other data, such as genome-wide association studies, support the idea that coral bleaching is a multifactorial response that reflects a wide array of causes and effects and is population-specific under most conditions, with coral ploidy and genotype being critical to bleaching sensitivity. This perspective leverages the location, algal and prokaryotic microbiome, and host genotype-specific aspects of coral resilience to promote a new “personal genomics” approach to coral conservation, analogous to that used in human health.
{"title":"The Host Coral Bleaching Response Viewed Through the Lens of Multi-Omics","authors":"Debashish Bhattacharya, Shrinivas Nandi, Erin E. Chille, Miriam Arroyo, Timothy G. Stephens","doi":"10.1002/bies.70110","DOIUrl":"10.1002/bies.70110","url":null,"abstract":"<p>We review recent multi-omics analyses of the coral heat stress response to explore the generality of the Oxidative Theory of Coral Bleaching (OTCB), which posits that algal symbiont release is the final act of defense by the coral host to survive alga-derived oxidative stress. The OTCB is particularly relevant given that ocean warming, which is accelerating under climate change, has proven devastating for corals, leading to the bleaching phenotype and widespread reef loss. Multi-omics results, in combination with other data, such as genome-wide association studies, support the idea that coral bleaching is a multifactorial response that reflects a wide array of causes and effects and is population-specific under most conditions, with coral ploidy and genotype being critical to bleaching sensitivity. This perspective leverages the location, algal and prokaryotic microbiome, and host genotype-specific aspects of coral resilience to promote a new “personal genomics” approach to coral conservation, analogous to that used in human health.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"48 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12835581/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146050287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p>Originally, I planned to share these thoughts under the heading ‘Brainless animals still sleep’, but the insights are deeper than that. Still, a recent study showing that cnidarians, ‘lowly’ animals with neural networks but without brains, such as jellyfish and sea anemones, exhibit sleep, is a good place to start [<span>1</span>]. Thus, sleep actually evolved before a centralized nervous system, which had already become clear with the discovery of sleep-like states in jellyfish almost 10 years ago [<span>2</span>]. The latest, more specific, findings bolster a theory that sleep evolved, at least in part, to protect the DNA in individual nerve cells, helping to repair damage that builds up while animals are awake. So, what are these specific findings? It has been known for over a decade that sleep is critical for maintaining neuronal genomic integrity, as it reduces DNA damage, which normally accumulates in nerve cells of (in)vertebrates (e.g., flies and mice) during wakefulness. This stems from, among other things, higher metabolic activity and associated reactive oxygen species (ROS). Therefore, one of the benefits of sleep, and probably its oldest, is protecting neurons from accumulating DNA damage. The jellyfish model, <i>Cassiopea andromeda</i>, sleeps at night, while the sea anemone model, <i>Nematostella vectensis</i>, sleeps at dawn. But indeed, in both cases, sleep deprivation and mutagens increased neuronal DNA damage and sleep pressure, while sleep, both spontaneous and induced, improved genome stability. As an author of [<span>1</span>], Lior Appelbaum, states: “Neurons are very precious”, “they don't divide, so you need to keep them intact” [<span>3</span>]. Which brings us to the deeper question: why don't neurons (normally) divide anymore?</p><p>At the dawn of metazoan evolution, multicellularity and differentiation towards nerve cells allowed further encoding of the state of the world, including its history. This introduced concepts such as critical periods during embryogenesis, which allowed neural networks to start monitoring different parts of the body. Such mirroring evolved into a full representation of the body in the central nervous systems of ever more complex animals. Alongside this, the development of highly dynamic connections with varying strengths between ever-increasing numbers of neurons enabled the storage of exponentially growing amounts of information about the environment these bodies inhabit. In vertebrates, a single neuron can have between 10<sup>3</sup> and 10<sup>4</sup> synaptic connections. Thus, while we can easily replace dedicated cells such as muscle, skin, liver, or blood cells, neurons are exceptional because the information they help to encode is eroded upon their loss. As such, they will become ‘irreplaceable’. The new results with cnidarians demonstrate that such a threshold is reached surprisingly quickly.</p><p>This all fits nicely with an informative recent review about “signaling roles for
{"title":"The Thing About Neurons","authors":"Dave Speijer","doi":"10.1002/bies.70113","DOIUrl":"10.1002/bies.70113","url":null,"abstract":"<p>Originally, I planned to share these thoughts under the heading ‘Brainless animals still sleep’, but the insights are deeper than that. Still, a recent study showing that cnidarians, ‘lowly’ animals with neural networks but without brains, such as jellyfish and sea anemones, exhibit sleep, is a good place to start [<span>1</span>]. Thus, sleep actually evolved before a centralized nervous system, which had already become clear with the discovery of sleep-like states in jellyfish almost 10 years ago [<span>2</span>]. The latest, more specific, findings bolster a theory that sleep evolved, at least in part, to protect the DNA in individual nerve cells, helping to repair damage that builds up while animals are awake. So, what are these specific findings? It has been known for over a decade that sleep is critical for maintaining neuronal genomic integrity, as it reduces DNA damage, which normally accumulates in nerve cells of (in)vertebrates (e.g., flies and mice) during wakefulness. This stems from, among other things, higher metabolic activity and associated reactive oxygen species (ROS). Therefore, one of the benefits of sleep, and probably its oldest, is protecting neurons from accumulating DNA damage. The jellyfish model, <i>Cassiopea andromeda</i>, sleeps at night, while the sea anemone model, <i>Nematostella vectensis</i>, sleeps at dawn. But indeed, in both cases, sleep deprivation and mutagens increased neuronal DNA damage and sleep pressure, while sleep, both spontaneous and induced, improved genome stability. As an author of [<span>1</span>], Lior Appelbaum, states: “Neurons are very precious”, “they don't divide, so you need to keep them intact” [<span>3</span>]. Which brings us to the deeper question: why don't neurons (normally) divide anymore?</p><p>At the dawn of metazoan evolution, multicellularity and differentiation towards nerve cells allowed further encoding of the state of the world, including its history. This introduced concepts such as critical periods during embryogenesis, which allowed neural networks to start monitoring different parts of the body. Such mirroring evolved into a full representation of the body in the central nervous systems of ever more complex animals. Alongside this, the development of highly dynamic connections with varying strengths between ever-increasing numbers of neurons enabled the storage of exponentially growing amounts of information about the environment these bodies inhabit. In vertebrates, a single neuron can have between 10<sup>3</sup> and 10<sup>4</sup> synaptic connections. Thus, while we can easily replace dedicated cells such as muscle, skin, liver, or blood cells, neurons are exceptional because the information they help to encode is eroded upon their loss. As such, they will become ‘irreplaceable’. The new results with cnidarians demonstrate that such a threshold is reached surprisingly quickly.</p><p>This all fits nicely with an informative recent review about “signaling roles for ","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"48 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/bies.70113","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146050376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The cover image is based on the article Where, When, and How? Integrating Spatiotemporal Cues in Cell Division by Luca Cirillo et al., https://doi.org/10.1002/bies.70093.
封面图片来源于文章《Where， When, and How?》整合时空线索在细胞分裂由Luca Cirillo等人，https://doi.org/10.1002/bies.70093。
{"title":"BioEssays 1/2026","authors":"","doi":"10.1002/bies.70106","DOIUrl":"https://doi.org/10.1002/bies.70106","url":null,"abstract":"<p>The cover image is based on the article <i>Where, When, and How? Integrating Spatiotemporal Cues in Cell Division</i> by Luca Cirillo et al., https://doi.org/10.1002/bies.70093.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"48 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/bies.70106","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146099399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The Hippo signaling pathway plays a key role in organ size control in normal development and tumorigenesis. While many components of this pathway are well understood, its upstream regulation remains unclear. Among the most enigmatic upstream regulators are the protocadherins Dachsous and Fat. These transmembrane proteins regulate a growth-promoting complex composed of the atypical myosin Dachs, the adaptor protein Dlish, and the palmitoyltransferase Approximated (together termed the core complex). We propose that by default the core complex promotes growth and that Dachsous and Fat, which previously have been thought to act antagonistically, can also function synergistically to repress core complex function and therefore restrict growth. Understanding the molecular mechanisms underlying Dachsous-Fat signaling offers insight into how multicellular organisms precisely control organ size.
{"title":"Fat and Dachsous Signaling—Controlling Growth Requires Both Competition and Cooperation","authors":"Hitoshi Matakatsu, Richard G. Fehon","doi":"10.1002/bies.70103","DOIUrl":"10.1002/bies.70103","url":null,"abstract":"<p>The Hippo signaling pathway plays a key role in organ size control in normal development and tumorigenesis. While many components of this pathway are well understood, its upstream regulation remains unclear. Among the most enigmatic upstream regulators are the protocadherins Dachsous and Fat. These transmembrane proteins regulate a growth-promoting complex composed of the atypical myosin Dachs, the adaptor protein Dlish, and the palmitoyltransferase Approximated (together termed the core complex). We propose that by default the core complex promotes growth and that Dachsous and Fat, which previously have been thought to act antagonistically, can also function synergistically to repress core complex function and therefore restrict growth. Understanding the molecular mechanisms underlying Dachsous-Fat signaling offers insight into how multicellular organisms precisely control organ size.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"48 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12828244/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146028487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Life on Earth has evolved as a series of evolutionary transitions, during which lower-level units merged to form a new and more complex higher-level entity. Besides few canonical examples, many life forms exist for which it remains unclear whether or not they are about to complete the transition. This paucity of mechanistic understanding is likely due to an overemphasis on few model systems and a lack of criteria to compare disparate biological units. Here, we aim at filling this gap by proposing a new framework to classify different forms of biological organization, which considers two fundamental aspects: (i) the physiological component and (ii) the evolutionary component. Categorizing different biological units according to whether and how these aspects are represented yields six types of structural organization. Our framework allows to compare different organizational forms, and, in this way, provide insight into the evolutionary processes giving rise to these arrangements.
{"title":"A New Classification Framework to Understand Evolutionary Transitions in Individuality","authors":"Saskia Wilmsen, Christian Kost","doi":"10.1002/bies.70098","DOIUrl":"10.1002/bies.70098","url":null,"abstract":"<p>Life on Earth has evolved as a series of evolutionary transitions, during which lower-level units merged to form a new and more complex higher-level entity. Besides few canonical examples, many life forms exist for which it remains unclear whether or not they are about to complete the transition. This paucity of mechanistic understanding is likely due to an overemphasis on few model systems and a lack of criteria to compare disparate biological units. Here, we aim at filling this gap by proposing a new framework to classify different forms of biological organization, which considers two fundamental aspects: (i) the physiological component and (ii) the evolutionary component. Categorizing different biological units according to whether and how these aspects are represented yields six types of structural organization. Our framework allows to compare different organizational forms, and, in this way, provide insight into the evolutionary processes giving rise to these arrangements.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"48 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12828248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146028558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In eukaryotic cells, genomic DNA is packaged into chromatin, restricting the access of regulatory proteins and thus regulating key processes such as transcription, replication, recombination, and the repair of DNA. Barrier-to-autointegration factor (BAF) plays key roles in organizing chromatin architecture and nuclear functions. BAF bridges DNA segments and connects them to Lamin A/C and inner nuclear membrane proteins containing the LEM domain, ensuring proper chromatin organization and nuclear envelope assembly and repair. Over the last three decades, multiple structural studies have revealed that BAF dimerizes to bind DNA and shapes higher-order chromatin structure. In this review, we summarize the structural features of BAF in complexes with its binding partners and explore how these interactions contribute to maintaining nuclear integrity and regulating genome function.
{"title":"Nucleosome Bundling by Barrier-to-Autointegration Factor: Implications for Its Diverse Functions","authors":"Naoki Horikoshi, Hitoshi Kurumizaka","doi":"10.1002/bies.70104","DOIUrl":"10.1002/bies.70104","url":null,"abstract":"<div>\u0000 \u0000 <p>In eukaryotic cells, genomic DNA is packaged into chromatin, restricting the access of regulatory proteins and thus regulating key processes such as transcription, replication, recombination, and the repair of DNA. Barrier-to-autointegration factor (BAF) plays key roles in organizing chromatin architecture and nuclear functions. BAF bridges DNA segments and connects them to Lamin A/C and inner nuclear membrane proteins containing the LEM domain, ensuring proper chromatin organization and nuclear envelope assembly and repair. Over the last three decades, multiple structural studies have revealed that BAF dimerizes to bind DNA and shapes higher-order chromatin structure. In this review, we summarize the structural features of BAF in complexes with its binding partners and explore how these interactions contribute to maintaining nuclear integrity and regulating genome function.</p>\u0000 </div>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"48 1","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146028541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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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