Seminars in cell & developmental biology最新文献

{"title":"Diverse genetic conflicts mediated by molecular mimicry and computational approaches to detect them","authors":"","doi":"10.1016/j.semcdb.2024.07.001","DOIUrl":"10.1016/j.semcdb.2024.07.001","url":null,"abstract":"<div><p>In genetic conflicts between intergenomic and selfish elements, driver and killer elements achieve biased survival, replication, or transmission over sensitive and targeted elements through a wide range of molecular mechanisms, including mimicry. Driving mechanisms manifest at all organismal levels, from the biased propagation of individual genes, as demonstrated by transposable elements, to the biased transmission of genomes, as illustrated by viruses, to the biased transmission of cell lineages, as in cancer. Targeted genomes are vulnerable to molecular mimicry through the conserved motifs they use for their own signaling and regulation. Mimicking these motifs enables an intergenomic or selfish element to control core target processes, and can occur at the sequence, structure, or functional level. Molecular mimicry was first appreciated as an important phenomenon more than twenty years ago. Modern genomics technologies, databases, and machine learning approaches offer tremendous potential to study the distribution of molecular mimicry across genetic conflicts in nature. Here, we explore the theoretical expectations for molecular mimicry between conflicting genomes, the trends in molecular mimicry mechanisms across known genetic conflicts, and outline how new examples can be gleaned from population genomic datasets. We discuss how mimics involving short sequence-based motifs or gene duplications can evolve convergently from new mutations<em>.</em> Whereas, processes that involve divergent domains or fully-folded structures occur among genomes by horizontal gene transfer. These trends are largely based on a small number of organisms and should be reevaluated in a general, phylogenetically independent framework. Currently, publicly available databases can be mined for genotypes driving non-Mendelian inheritance patterns, epistatic interactions, and convergent protein structures. A subset of these conflicting elements may be molecular mimics. We propose approaches for detecting genetic conflict and molecular mimicry from these datasets.</p></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1084952124000557/pdfft?md5=d2592468bfb577ff0aef406716dc2946&pid=1-s2.0-S1084952124000557-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141856430","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}

{"title":"From the cauldron of conflict: Endogenous gene regulation by piRNA and other modes of adaptation enabled by selfish transposable elements","authors":"Justin P. Blumenstiel","doi":"10.1016/j.semcdb.2024.05.001","DOIUrl":"10.1016/j.semcdb.2024.05.001","url":null,"abstract":"<div><p>Transposable elements (TEs) provide a prime example of genetic conflict because they can proliferate in genomes and populations even if they harm the host. However, numerous studies have shown that TEs, though typically harmful, can also provide fuel for adaptation. This is because they code functional sequences that can be useful for the host in which they reside. In this review, I summarize the \"how\" and \"why\" of adaptation enabled by the genetic conflict between TEs and hosts. In addition, focusing on mechanisms of TE control by small piwi-interacting RNAs (piRNAs), I highlight an indirect form of adaptation enabled by conflict. In this case, mechanisms of host defense that regulate TEs have been redeployed for endogenous gene regulation. I propose that the genetic conflict released by meiosis in early eukaryotes may have been important because, among other reasons, it spurred evolutionary innovation on multiple interwoven trajectories - on the part of hosts and also embedded genetic parasites. This form of evolution may function as a complexity generating engine that was a critical player in eukaryotic evolution.</p></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":7.3,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141186135","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}

{"title":"WHO elements – A new category of selfish genetic elements at the borderline between homing elements and transposable elements","authors":"Matthieu Osborne,&nbsp;Athaliah Fubara,&nbsp;Eoin Ó Cinnéide,&nbsp;Aisling Y. Coughlan,&nbsp;Kenneth H. Wolfe","doi":"10.1016/j.semcdb.2024.04.001","DOIUrl":"10.1016/j.semcdb.2024.04.001","url":null,"abstract":"<div><p>Homing genetic elements are a form of selfish DNA that inserts into a specific target site in the genome and spreads through the population by a process of biased inheritance. Two well-known types of homing element, called inteins and homing introns, were discovered decades ago. In this review we describe WHO elements, a newly discovered type of homing element that constitutes a distinct third category but is rare, having been found only in a few yeast species so far. WHO elements are inferred to spread using the same molecular homing mechanism as inteins and introns: they encode a site-specific endonuclease that cleaves the genome at the target site, making a DNA break that is subsequently repaired by copying the element. For most WHO elements, the target site is in the glycolytic gene <em>FBA1</em>. WHO elements differ from inteins and homing introns in two fundamental ways: they do not interrupt their host gene (<em>FBA1</em>), and they occur in clusters. The clusters were formed by successive integrations of different WHO elements into the <em>FBA1</em> locus, the result of an ‘arms race’ between the endonuclease and its target site. We also describe one family of WHO elements (WHO10) that is no longer specifically associated with the <em>FBA1</em> locus and instead appears to have become transposable, inserting at random genomic sites in <em>Torulaspora globosa</em> with up to 26 copies per strain. The WHO family of elements is therefore at the borderline between homing genetic elements and transposable elements.</p></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":7.3,"publicationDate":"2024-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1084952124000326/pdfft?md5=ca5197c79a4967a06b53c679ce8a49e9&pid=1-s2.0-S1084952124000326-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140774912","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}

{"title":"Out with the old, in with the new: Meiotic driving of sex chromosome evolution","authors":"Callie M. Swanepoel,&nbsp;Jacob L. Mueller","doi":"10.1016/j.semcdb.2024.04.004","DOIUrl":"10.1016/j.semcdb.2024.04.004","url":null,"abstract":"<div><p>Chromosomal regions with meiotic drivers exhibit biased transmission (&gt; 50 %) over their competing homologous chromosomal region. These regions often have two prominent genetic features: suppressed meiotic crossing over and rapidly evolving multicopy gene families. Heteromorphic sex chromosomes (e.g., XY) often share these two genetic features with chromosomal regions exhibiting meiotic drive. Here, we discuss parallels between meiotic drive and sex chromosome evolution, how the divergence of heteromorphic sex chromosomes can be influenced by meiotic drive, experimental approaches to study meiotic drive on sex chromosomes, and meiotic drive in traditional and non-traditional model organisms with high-quality genome assemblies. The newly available diversity of high-quality sex chromosome sequences allows us to revisit conventional models of sex chromosome evolution through the lens of meiotic drive.</p></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":7.3,"publicationDate":"2024-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140759524","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}

{"title":"Cover image of cell death and resilience in health and disease","authors":"Hadley Hanson ,&nbsp;Jane Feng","doi":"10.1016/j.semcdb.2024.04.003","DOIUrl":"https://doi.org/10.1016/j.semcdb.2024.04.003","url":null,"abstract":"","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":7.3,"publicationDate":"2024-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S108495212400034X/pdfft?md5=7421370082880d496827b62ff687887a&pid=1-s2.0-S108495212400034X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140557848","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}

{"title":"Mitochondrial control of lymphocyte homeostasis","authors":"Yavuz F. Yazicioglu ,&nbsp;Robert J. Mitchell ,&nbsp;Alexander J. Clarke","doi":"10.1016/j.semcdb.2024.03.002","DOIUrl":"https://doi.org/10.1016/j.semcdb.2024.03.002","url":null,"abstract":"<div><p>Mitochondria play a multitude of essential roles within mammalian cells, and understanding how they control immunity is an emerging area of study. Lymphocytes, as integral cellular components of the adaptive immune system, rely on mitochondria for their function, and mitochondria can dynamically instruct their differentiation and activation by undergoing rapid and profound remodelling. Energy homeostasis and ATP production are often considered the primary functions of mitochondria in immune cells; however, their importance extends across a spectrum of other molecular processes, including regulation of redox balance, signalling pathways, and biosynthesis. In this review, we explore the dynamic landscape of mitochondrial homeostasis in T and B cells, and discuss how mitochondrial disorders compromise adaptive immunity.</p></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":7.3,"publicationDate":"2024-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1084952124000314/pdfft?md5=60e9f6a11ceaf2027bd611227bfb6eb1&pid=1-s2.0-S1084952124000314-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140545736","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}

{"title":"Genetic conflicts in budding yeast: The 2μ plasmid as a model selfish element","authors":"Michelle Hays","doi":"10.1016/j.semcdb.2024.04.002","DOIUrl":"https://doi.org/10.1016/j.semcdb.2024.04.002","url":null,"abstract":"<div><p>Antagonistic coevolution, arising from genetic conflict, can drive rapid evolution and biological innovation. Conflict can arise both between organisms and within genomes. This review focuses on budding yeasts as a model system for exploring intra- and inter-genomic genetic conflict, highlighting in particular the 2-micron (2μ) plasmid as a model selfish element. The 2μ is found widely in laboratory strains and industrial isolates of <em>Saccharomyces cerevisiae</em> and has long been known to cause host fitness defects. Nevertheless, the plasmid is frequently ignored in the context of genetic, fitness, and evolution studies. Here, I make a case for further exploring the evolutionary impact of the 2μ plasmid as well as other selfish elements of budding yeasts, discuss recent advances, and, finally, future directions for the field.</p></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":7.3,"publicationDate":"2024-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140539220","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}

{"title":"Symbiotic symphony: Understanding host-microbiota dialogues in a spatial context","authors":"Soumi Chatterjee ,&nbsp;Steven T. Leach ,&nbsp;Kei Lui ,&nbsp;Archita Mishra","doi":"10.1016/j.semcdb.2024.03.001","DOIUrl":"https://doi.org/10.1016/j.semcdb.2024.03.001","url":null,"abstract":"<div><p>Modern precision sequencing techniques have established humans as a holobiont that live in symbiosis with the microbiome. Microbes play an active role throughout the life of a human ranging from metabolism and immunity to disease tolerance. Hence, it is of utmost significance to study the eukaryotic host in conjunction with the microbial antigens to obtain a complete picture of the host-microbiome crosstalk. Previous attempts at profiling host-microbiome interactions have been either superficial or been attempted to catalogue eukaryotic transcriptomic profile and microbial communities in isolation. Additionally, the nature of such immune-microbial interactions is not random but spatially organised. Hence, for a holistic clinical understanding of the interplay between hosts and microbiota, it's imperative to concurrently analyze both microbial and host genetic information, ensuring the preservation of their spatial integrity. Capturing these interactions as a snapshot in time at their site of action has the potential to transform our understanding of how microbes impact human health. In examining early-life microbial impacts, the limited presence of communities compels analysis within reduced biomass frameworks. However, with the advent of spatial transcriptomics we can address this challenge and expand our horizons of understanding these interactions in detail. In the long run, simultaneous spatial profiling of host-microbiome dialogues can have enormous clinical implications especially in gaining mechanistic insights into the disease prognosis of localised infections and inflammation. This review addresses the lacunae in host-microbiome research and highlights the importance of profiling them together to map their interactions while preserving their spatial context.</p></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":7.3,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140338770","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}

{"title":"Mitochondrial dynamics: Regulating cell metabolism, homoeostasis, health and disease","authors":"Karoline D. Raven ,&nbsp;Ronan Kapetanovic","doi":"10.1016/j.semcdb.2024.02.002","DOIUrl":"https://doi.org/10.1016/j.semcdb.2024.02.002","url":null,"abstract":"","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":7.3,"publicationDate":"2024-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140163042","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}

{"title":"The interplay between mitochondrial dynamics and autophagy: From a key homeostatic mechanism to a driver of pathology","authors":"Alice Lacombe ,&nbsp;Luca Scorrano","doi":"10.1016/j.semcdb.2024.02.001","DOIUrl":"https://doi.org/10.1016/j.semcdb.2024.02.001","url":null,"abstract":"<div><p>The complex relationship between mitochondrial dynamics and autophagy illustrates how two cellular housekeeping processes are intimately linked, illuminating fundamental principles of cellular homeostasis and shedding light on disparate pathological conditions including several neurodegenerative disorders. Here we review the basic tenets of mitochondrial dynamics i.e., the concerted balance between fusion and fission of the organelle, and its interplay with macroautophagy and selective mitochondrial autophagy, also dubbed mitophagy, in the maintenance of mitochondrial quality control and ultimately in cell viability. We illustrate how conditions of altered mitochondrial dynamics reverberate on autophagy and vice versa. Finally, we illustrate how altered interplay between these two key cellular processes participates in the pathogenesis of human disorders affecting multiple organs and systems.</p></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":7.3,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1084952124000223/pdfft?md5=40242cc4361ea0b7c371f277046e0a49&pid=1-s2.0-S1084952124000223-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140000282","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}