BioEssaysPub Date : 2025-02-21DOI: 10.1002/bies.202400220
Yanfei Du, Chenhui Wang, Yu Zhang, Huiquan Liu
{"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}
BioEssaysPub Date : 2025-02-19DOI: 10.1002/bies.202400264
Anshul Sharma, Alok K Mishra
{"title":"Tumor-Associated Macrophages Write the Script of Cancer Obesity Paradox.","authors":"Anshul Sharma, Alok K Mishra","doi":"10.1002/bies.202400264","DOIUrl":"https://doi.org/10.1002/bies.202400264","url":null,"abstract":"<p><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>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":" ","pages":"e202400264"},"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}
BioEssaysPub Date : 2025-02-14DOI: 10.1002/bies.202400248
Hua Zhou, Xing Wang Deng
{"title":"Intron Retention, an Orchestrated Program of Gene Expression Regulation.","authors":"Hua Zhou, Xing Wang Deng","doi":"10.1002/bies.202400248","DOIUrl":"https://doi.org/10.1002/bies.202400248","url":null,"abstract":"<p><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>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":" ","pages":"e202400248"},"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}
BioEssaysPub Date : 2025-02-07DOI: 10.1002/bies.202400281
Lev G Nemchinov
{"title":"Selective Diversity in RNA Viruses: Do They Know How to Evolve? A Hypothesis.","authors":"Lev G Nemchinov","doi":"10.1002/bies.202400281","DOIUrl":"https://doi.org/10.1002/bies.202400281","url":null,"abstract":"<p><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":" ","pages":"e202400281"},"PeriodicalIF":3.2,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BioEssaysPub Date : 2025-02-03DOI: 10.1002/bies.202400257
Rebecca San Gil, Adam K Walker
{"title":"Unlocking Disease-Modifying Treatments for TDP-43-Mediated Neurodegeneration.","authors":"Rebecca San Gil, Adam K Walker","doi":"10.1002/bies.202400257","DOIUrl":"https://doi.org/10.1002/bies.202400257","url":null,"abstract":"<p><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":" ","pages":"e202400257"},"PeriodicalIF":3.2,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BioEssaysPub Date : 2025-01-20DOI: 10.1002/bies.202400232
Francisco Rodriguez-Algarra, Elliott Whittaker, Sandra Del Castillo Del Rio, Vardhman K Rakyan
{"title":"Assessing Human Ribosomal DNA Variation and Its Association With Phenotypic Outcomes.","authors":"Francisco Rodriguez-Algarra, Elliott Whittaker, Sandra Del Castillo Del Rio, Vardhman K Rakyan","doi":"10.1002/bies.202400232","DOIUrl":"https://doi.org/10.1002/bies.202400232","url":null,"abstract":"<p><p>Although genome-scale analyses have provided insights into the connection between genetic variability and complex human phenotypes, much trait variation is still not fully understood. Genetic variation within repetitive elements, such as the multi-copy, multi-locus ribosomal DNA (rDNA), has emerged as a potential contributor to trait variation. Whereas rDNA was long believed to be largely uniform within a species, recent studies have revealed substantial variability in the locus, both within and across individuals. This variation, which takes the form of copy number, structural arrangement, and sequence differences, has been found to be associated with human phenotypes. This review summarizes what is currently known about human rDNA variation, its causes, and its association with phenotypic outcomes, highlighting the technical challenges the field faces and the solutions proposed to address them. Finally, we suggest experimental approaches that can help clarify the elusive mechanisms underlying the phenotypic consequences of rDNA variation.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":" ","pages":"e202400232"},"PeriodicalIF":3.2,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000411","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}
BioEssaysPub Date : 2025-01-19DOI: 10.1002/bies.202400203
Isabel Reinisch, Sarah Enzenhofer, Andreas Prokesch
{"title":"Mechanisms of Lipid-Associated Macrophage Accrual in Metabolically Stressed Adipose Tissue.","authors":"Isabel Reinisch, Sarah Enzenhofer, Andreas Prokesch","doi":"10.1002/bies.202400203","DOIUrl":"https://doi.org/10.1002/bies.202400203","url":null,"abstract":"<p><p>Adipose tissue (AT) inflammation, a hallmark of the metabolic syndrome, is triggered by overburdened adipocytes sending out immune cell recruitment signals during obesity development. An AT immune landscape persistent throughout weight loss and regain constitutes an immune-obesogenic memory that hinders long-term weight loss management. Lipid-associated macrophages (LAMs) are emerging as major players in diseased, inflamed metabolic tissues and may be key contributors to an obesogenic memory in AT. Our previous study found that LAM abundance increases with weight loss via intermittent fasting (IF) in obese mice, which is driven by adipocyte p53 signalling. However, the specific signals causing LAM accumulation in AT under IF remain unknown. In this piece, we hypothesise on a range of adipocyte-secreted signals that can harbor immune-attractive features upon fasting/refeeding cycles. We highlight possible mechanisms including cell death signalling, matrikines, and other damage-associated molecular patterns (DAMPs), as well as adipo(-cyto)kines, lipid mediators, metabolites, extracellular vesicles, and epigenetic rewiring. Finally, we consider how advances in mechanisms of AT LAM recruitment gleaned from preclinical models might be translatable to long-term weight management in humans. Thus, we provide vantage points to study signals driving monocyte recruitment, polarisation towards LAMs, and LAM retention, to harness the therapeutic potential of modulating AT LAM levels by impacting the immune-obesogenic memory in metabolic disease.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":" ","pages":"e202400203"},"PeriodicalIF":3.2,"publicationDate":"2025-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000413","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}