BioEssaysPub Date : 2025-03-13DOI: 10.1002/bies.202400188
Verena Nadin Fritsch, Michael Hensel
{"title":"Experimental Approaches to Visualize Effector Protein Translocation During Host-Pathogen Interactions","authors":"Verena Nadin Fritsch, Michael Hensel","doi":"10.1002/bies.202400188","DOIUrl":"10.1002/bies.202400188","url":null,"abstract":"<p>Bacterial pathogens deliver effector proteins into host cells by deploying sophisticated secretion systems. This effector translocation during host-pathogen interactions is a prerequisite for the manipulation of host cells and organisms and is important for pathogenesis. Analyses of dynamics and kinetics of translocation, subcellular localization, and cellular targets of effector proteins lead to understanding the mode of action and function of effector proteins in host-pathogen interplay. This review provides an overview of biochemical and genetic tools that have been developed to study protein effector translocation qualitatively or quantitatively. After introducing the challenges of analyses of effector translocation during host-pathogen interaction, we describe various methods ranging from static visualization in fixed cells to dynamic live-cell imaging of effector protein translocation. We show the main findings enabled by the approaches, emphasize the advantages and limitations of the methods, describe recent approaches that allow real-time tracking of effector proteins in living cells on a single molecule level, and highlight open questions in the field to be addressed by application of new methods.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 4","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/bies.202400188","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613469","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}
BioEssaysPub Date : 2025-03-05DOI: 10.1002/bies.202400266
Patrick Wilmott, Leszek Lisowski
{"title":"AAV Genome Topology Decides ITR Secondary Structure","authors":"Patrick Wilmott, Leszek Lisowski","doi":"10.1002/bies.202400266","DOIUrl":"10.1002/bies.202400266","url":null,"abstract":"<div>\u0000 \u0000 <p>Intra-strand base pairing is possible when double-stranded DNA contains inverted repeats, but vanishingly improbable without so-called negative superhelicity. This superhelicity itself is conditional upon whether the molecule can retain torsional stress—a question of “topology.” This principle has been uncontroversial to biophysicists since the 1980s but has proven challenging for outsiders to grasp and retain. For those in AAV research, this constitutes a decades-long missed connection. AAV is one of a multitude of viruses bearing secondary-structure-forming elements on their termini. Its “inverted terminal repeats” (ITRs) can self-anneal into relatively large hammerhead structures on both ends of the dynamically structured genome and are central to numerous host interactions that drive the viral lifecycle. A standalone article such as this is therefore warranted to promote an understanding of these ideas in the AAV research community and highlight their significance in the basic biology of the virus and its vector gene delivery system.</p>\u0000 </div>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143566187","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 : 2025-03-03DOI: 10.1002/bies.202500004
Yuh-Ru Julie Lee, Bo Liu
{"title":"Phosphoregulation of Microtubule Assembly and Disassembly for Phragmoplast Expansion During Plant Cytokinesis","authors":"Yuh-Ru Julie Lee, Bo Liu","doi":"10.1002/bies.202500004","DOIUrl":"10.1002/bies.202500004","url":null,"abstract":"<div>\u0000 \u0000 <p>Plant cytokinesis results in the formation of the cell plate by the phragmoplast which contains dynamic microtubules serving as the track for the delivery of cell wall builders included in Golgi vesicles. During the centrifugal process of cell plate assembly, new microtubules are assembled and bundled at the leading edge to prepare for vesicle transport while older microtubules are disassembled at the lagging edge upon the completion of vesicle delivery. The turnover of phragmoplast microtubules in this process is thought to be regulated by phosphorylation of the key microtubule bundling factor MAP65. A recent study revealed a surprising role of the <i>α</i>-Aurora kinase, which is typically known for its role in governing the formation of the bipolar spindle apparatus, in phosphorylating the primary microtubule bundler MAP65-3 in Arabidopsis. This phosphorylation positively contributes to the expansion of the phragmoplast. The phragmoplast midzone is also the hub for other cytokinesis-important kinases. It is intriguing how these kinases are targeted and how they may crosstalk with each other to orchestrate the expansion of the phragmoplast.</p>\u0000 </div>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536640","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 : 2025-02-26DOI: 10.1002/bies.202400276
Tina Izard
{"title":"Environmental Toxicants 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":"<div>\u0000 \u0000 <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>\u0000 </div>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 5","pages":""},"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}
BioEssaysPub Date : 2025-02-26DOI: 10.1002/bies.202500020
Lorenz Adlung
{"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}
BioEssaysPub Date : 2025-02-25DOI: 10.1002/bies.202400202
Federica Mantica, Manuel Irimia
{"title":"Gene Duplication and Alternative Splicing as Evolutionary Drivers of Proteome Specialization","authors":"Federica Mantica, Manuel Irimia","doi":"10.1002/bies.202400202","DOIUrl":"10.1002/bies.202400202","url":null,"abstract":"<div>\u0000 \u0000 <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>\u0000 </div>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 5","pages":""},"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}
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":"10.1002/bies.202400220","url":null,"abstract":"<div>\u0000 \u0000 <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>\u0000 </div>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 5","pages":""},"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":"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}
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":"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}