BioEssays最新文献

{"title":"Environmental and Their Disruption of Integrin Signaling in Lipid Rafts.","authors":"Tina Izard","doi":"10.1002/bies.202400276","DOIUrl":"10.1002/bies.202400276","url":null,"abstract":"<p><p>Talin, a key integrin activator, is essential for cellular adhesion, signal transduction, and mechanical stability. Its transition between autoinhibited and active conformations allows dynamic regulation of adhesion in response to environmental cues. Cholesterol-rich membrane microdomains, such as lipid rafts, organize and stabilize signaling platforms, influencing talin and integrin conformational states. Cholesterol is a switch modulating talin activation, integrin binding, and adhesion. Environmental pollutants, including heavy metals and air toxins, disrupt cholesterol homeostasis, destabilize lipid rafts, and interfere with talin-integrin interactions. These disruptions impair adhesion, tissue repair, and signaling fidelity, contributing to atherosclerosis and cancer metastasis. Understanding talin's interaction with cholesterol-rich domains offers critical insights into adhesion regulation and reveals the broader impact of environmental toxicants on cellular function. This framework emphasizes the importance of membrane composition, particularly cholesterol, in mediating the effects of environmental stressors and suggests potential therapeutic interventions.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":" ","pages":"e202400276"},"PeriodicalIF":3.2,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514745","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}

{"title":"The LAM Is Not Enough–An Idea to Watch Regarding Adipose Tissue Macrophages and Their Disease Relevance","authors":"Lorenz Adlung","doi":"10.1002/bies.202500020","DOIUrl":"10.1002/bies.202500020","url":null,"abstract":"","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 4","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514746","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}

{"title":"Gene Duplication and Alternative Splicing as Evolutionary Drivers of Proteome Specialization.","authors":"Federica Mantica, Manuel Irimia","doi":"10.1002/bies.202400202","DOIUrl":"https://doi.org/10.1002/bies.202400202","url":null,"abstract":"<p><p>Animals comprise hundreds of cell types, each with specialized biological functions. However, many genes expressed in each cell type belong to widely conserved gene families with ancestrally ubiquitous expression. This raises a paradox: how have these genes evolved to shape cell type-specific traits without compromising their ancestral function in all other cells? This can be achieved through gene duplication and the origin of regulated, alternatively spliced exons, which generate new related proteins in the form of paralogous genes and alternative isoforms, respectively. Here, we explore how such new related proteins can contribute to the evolution of specific cell types while preserving broader ancestral roles. Specifically, we separately classify possible expression and functional fates for new related proteins and discuss their interplays and evolutionary likelihood. Our primary hypothesis is that expression specialization, mostly coupled with functional specialization, is the predominant fate for both paralogous genes and alternative isoforms throughout animal evolution.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":" ","pages":"e202400202"},"PeriodicalIF":3.2,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143490768","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}

{"title":"Issue Information: BioEssays 3/2025","authors":"","doi":"10.1002/bies.202570003","DOIUrl":"https://doi.org/10.1002/bies.202570003","url":null,"abstract":"","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 3","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/bies.202570003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143475468","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}

{"title":"Evolutionary Origins and Adaptive Significance of A-to-I RNA Editing in Animals and Fungi.","authors":"Yanfei Du, Chenhui Wang, Yu Zhang, Huiquan Liu","doi":"10.1002/bies.202400220","DOIUrl":"https://doi.org/10.1002/bies.202400220","url":null,"abstract":"<p><p>Adenosine-to-inosine (A-to-I) RNA editing, capable of protein recoding, has evolved independently in animals and fungi. This study proposes adaptive hypotheses regarding its origins and phenotypic significance, suggesting that A-to-I editing enhances adaptability by alleviating genetic trade-offs. In metazoans, its emergence may have been driven by a development-defense trade-off associated with transposable element activation during the evolution of multicellularity. Late Devonian cooling and End-Permian warming are hypothesized to have driven the emergence of extensive A-to-I recoding in coleoid nervous systems and Sordariomycete sexual fruiting bodies, respectively. These adaptations may have influenced key evolutionary innovations, including the evolution of metazoan nervous systems, coleoid intelligence, and shell loss, and fungal sexual reproductive structures. Additionally, extensive A-to-I recoding is proposed to facilitate accelerated development and specific life-history strategies in both animals and fungi. This paper provides new perspectives on the evolutionary forces shaping A-to-I RNA editing and its role in phenotypic diversity across taxa.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":" ","pages":"e202400220"},"PeriodicalIF":3.2,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467036","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}

{"title":"Tumor-Associated Macrophages Write the Script of Cancer Obesity Paradox","authors":"Anshul Sharma,&nbsp;Alok K. Mishra","doi":"10.1002/bies.202400264","DOIUrl":"10.1002/bies.202400264","url":null,"abstract":"<div>\u0000 \u0000 <p>Obesity paradoxically advances cancer progression while enhancing certain immunotherapies, like anti-PD-1/PD-L1. Bader et al. discovered that obesity-driven factors increase PD-1 on tumor-associated macrophages (TAMs), suppressing anti-tumor responses. Remarkably, anti-PD-1 therapy reverses this metabolic dysfunction, boosting immune checkpoint blockade (ICB) effectiveness by reactivating PD-1+ TAMs.</p>\u0000 </div>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 4","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143447904","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}

{"title":"Intron Retention, an Orchestrated Program of Gene Expression Regulation","authors":"Hua Zhou,&nbsp;Xing Wang Deng","doi":"10.1002/bies.202400248","DOIUrl":"10.1002/bies.202400248","url":null,"abstract":"<div>\u0000 \u0000 <p>Intron retention (IR), a well-conserved form of alternative splicing, is widespread among eukaryotic organisms. It serves as an orchestrated program for regulating gene expression. A previously reported role of IR is to induce intron-retained transcript (IRT) degradation via the nonsense-mediated mRNA decay (NMD) pathway, resulting in the downregulation of gene expression. However, accumulating evidence indicates that most IRTs are detained in the nucleus, and thus, IR can downregulate gene expression through the storage of IRTs in the nucleus. Although the importance of IRTs in gene expression regulation is well established, the detailed mechanisms remain unclear. Here, we propose a potential model to explain how IRTs are retained in the nucleus and respond to environmental changes or developmental transitions. Plenty of future studies are still ahead of us to fully dissect the biological function of IR and the underlying mechanisms.</p>\u0000 </div>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 4","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143413341","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}

{"title":"Safeguarding Scientific Accuracy in a Rapidly Changing World","authors":"Dave Speijer","doi":"10.1002/bies.202500016","DOIUrl":"10.1002/bies.202500016","url":null,"abstract":"&lt;p&gt;Recently, I have become more aware of the fact that scientific mores are changing when it comes to publishing results or theories. After a period of increased rigor (no more “unpublished results” in papers, please), the rules seem to be relaxing somewhat. One example: referring to papers that have not undergone peer review (yet). Preprint repositories, such as bioRxiv, were around from the nineties but they really multiplied and got intensely used from about 2010 onward. To be honest, I have one manuscript, reflecting unfinished business, in such a repository myself. It has been there since 2013 and was, to my surprise, quoted on several occasions. I would still hesitate to do so myself and I will explain why.&lt;/p&gt;&lt;p&gt;Current Biology is an excellent journal with, for example, high-quality reviews that are a joy to read. Recently, I encountered a great paper about the evolutionary arms race with defense systems and anti-defense systems constantly evolving in prokaryotes on the one hand and phages and plasmids on the other [&lt;span&gt;1&lt;/span&gt;]. While perusing it, I stumbled upon a surprising fact: more than 5% (6 out of 103) of the references were to non-peer reviewed manuscripts on bioRxiv (deposited in 2023 and 2024). This example illustrates a pronounced development over the last decade: the use of preprints in such manner is now widely accepted [&lt;span&gt;2&lt;/span&gt;]. The positive aspects seem clear. Researchers can get rapid feedback and community review, as well as hasten dissemination, and all this in open access form. In mathematics, meeting abstracts and preprints are even standard and encouraged by major journals (the actual publication process is almost an afterthought). On the minus side stands the possible loss of one of the safeguards of scientific quality: peer review. However, on balance, the fact that the preprint is publicly available and is clearly identified as still having to undergo peer scrutiny, does help in neutralizing the potential harm of sub-standard research.&lt;/p&gt;&lt;p&gt;Indeed, the quality of the process of peer review itself could be under pressure. At the risk of anecdotal misrepresentation, I have the strong impression of seeing more mistakes in published articles nowadays as compared to a few decades before. This could just reflect a greater “publish or perish” pressure, as well as ever more complicated techniques and algorithms associated with massively increased datasets. However, rapidly evolving new areas of expertise, time pressures, and the “courtesy” basis of relatively unrewarded reviewing seem to be taking their toll. I will give just one example of an error that should have been spotted before publication, having to do with one of my own hobbyhorses, the mitochondrial electron transport chain (ETC). A highly interesting PNAS perspective looks at how modern-day ETCs could tell us something about how the earliest stages of evolution might have harnessed the potential available in electrochemical gradients [&lt;span&gt;3&lt;/span&gt;","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 4","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/bies.202500016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381585","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}

{"title":"Selective Diversity in RNA Viruses: Do They Know How to Evolve? A Hypothesis","authors":"Lev G. Nemchinov","doi":"10.1002/bies.202400281","DOIUrl":"10.1002/bies.202400281","url":null,"abstract":"<p>Genetic diversity of viral populations is almost unanimously attributed to the build-up of random mutations along with accidental recombination events. This passive role of viruses in the selection of viable genotypes is widely acknowledged. According to the hypothesis presented here, populations of steady-state error copies of a master viral sequence would have a dominant mutant rather than a random pool of heterogeneous viral genomes with changes scattered uniformly without any preferential distribution. It would let viruses face the selection stage of host surveillance having a preceding set of potential survivors or “guard” genomes among an ordinary cloud of random quasispecies.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 4","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/bies.202400281","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143363664","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}

{"title":"Unlocking Disease-Modifying Treatments for TDP-43-Mediated Neurodegeneration","authors":"Rebecca San Gil,&nbsp;Adam K. Walker","doi":"10.1002/bies.202400257","DOIUrl":"10.1002/bies.202400257","url":null,"abstract":"<p>Neurons degenerate in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), causing progressive and inevitably fatal neurological decline. The best therapeutic strategies target underlying disease mediators, but after decades of intensive research, the causes of these neurodegenerative diseases remain elusive. Recently, coordinated activities of large consortia, increasing open access to large datasets, new methods such as cryo-transmission electron microscopy, and advancements in high-resolution omics technologies have offered new insights into the biology of disease that bring us closer to understanding mechanisms of neurodegeneration. In particular, improved understanding of the roles of the key pathological protein TAR DNA binding protein 43 (TDP-43) in disease has revealed intriguing new opportunities that provide hope for better diagnostic tools and effective treatments for ALS and FTD.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 4","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/bies.202400257","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122172","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}