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Why a Chloroplast Needs Its Own Genome Tethered to the Thylakoid Membrane—Co-Location for Redox Regulation 为什么叶绿体需要自己的基因组系在类囊体膜上进行氧化还原调控。
IF 3.3 3区 生物学
BioEssays Pub Date : 2026-08-06 DOI: 10.1002/bies.70170
John F. Allen
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引用次数: 0
Condensates on the Move: Midbody Remnants as Large, Translation-Competent Extracellular Vesicles 移动中的凝聚物:作为大的、具有翻译能力的细胞外囊泡的中间残体
IF 3.3 3区 生物学
BioEssays Pub Date : 2026-08-04 DOI: 10.1002/bies.70168
Ahna R. Skop
{"title":"Condensates on the Move: Midbody Remnants as Large, Translation-Competent Extracellular Vesicles","authors":"Ahna R. Skop","doi":"10.1002/bies.70168","DOIUrl":"https://doi.org/10.1002/bies.70168","url":null,"abstract":"<p>Recent work has expanded understanding of extracellular vesicle (EV) biology by identifying midbody remnants (MBRs) as large, translationally competent vesicles released during mitosis. MBRs contain ribosomes, mitochondria, translation factors, and selected mRNAs and small RNAs concentrated within a condensate‑like ribonucleoprotein core and can support protein synthesis after extracellular release. These features distinguish MBRs from more extensively studied exosomes and microvesicles yet also place them within a broader continuum of large EVs with organelle‑rich, cell‑like properties. This review summarizes current knowledge of MBR biogenesis, molecular organization, and translation competency; contrasts MBRs with canonical EVs and other large EVs; and discusses possible roles in development, tissue homeostasis, disease, and brain function. Particular emphasis is placed on outstanding mechanistic and physiological questions, including how MBR translation is regulated, which recipient cells interact with endogenous MBRs, and whether translation‑competent EVs offer practical advantages over existing EV platforms for therapeutic or biotechnological applications.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"48 8","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/bies.70168","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148667361","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}
引用次数: 0
Condensates on the Move: Midbody Remnants as Large, Translation-Competent Extracellular Vesicles 移动中的凝聚物:作为大的、具有翻译能力的细胞外囊泡的中间残体
IF 3.3 3区 生物学
BioEssays Pub Date : 2026-08-04 DOI: 10.1002/bies.70168
Ahna R. Skop
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引用次数: 0
Issue Information: BioEssays 8/2026 期刊信息:BioEssays 8/2026
IF 3.3 3区 生物学
BioEssays Pub Date : 2026-08-04 DOI: 10.1002/bies.70169
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引用次数: 0
Issue Information: BioEssays 8/2026 期刊信息:BioEssays 8/2026
IF 3.3 3区 生物学
BioEssays Pub Date : 2026-08-04 DOI: 10.1002/bies.70169
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引用次数: 0
Unique/Rapid Feedback Mechanisms of PGD2 and PGE2 as Local/Short-Lived Autacoids; Implications of Biased Activities by Their Metabolites PGD2和PGE2作为局部/短寿命类生物的独特/快速反馈机制它们的代谢物对偏倚活动的影响
IF 3.3 3区 生物学
BioEssays Pub Date : 2026-07-17 DOI: 10.1002/bies.70166
Hiromichi Fujino, Keijo Fukushima
{"title":"Unique/Rapid Feedback Mechanisms of PGD2 and PGE2 as Local/Short-Lived Autacoids; Implications of Biased Activities by Their Metabolites","authors":"Hiromichi Fujino,&nbsp;Keijo Fukushima","doi":"10.1002/bies.70166","DOIUrl":"https://doi.org/10.1002/bies.70166","url":null,"abstract":"<p>Prostanoids are involved in various physiological/pathophysiological functions, such as inflammation. Since persistent inflammation may cause chronic symptoms, their activation is very short and needs to be properly terminated. Due to structural similarities, some prostanoids and their metabolites may have ability to activate noncognate prostanoid receptors as biased agonists and/or blockers. However, the physiological roles of these biased activities remain unclear. This review mainly focused on prostaglandin (PG) E<sub>2</sub> and PGD<sub>2</sub> as well as their metabolites, and hypothesized that the physiological roles of their biased activities may be novel nongenomic immediate feedback systems strictly confined to local areas as autacoids. These nongenomic feedback systems completely differ from the genomic feedback systems used by endocrine hormones. Therefore, the biased activities of prostanoids may be newly defined and/or re-acknowledged as unique, rapid, and fine-tuned translation/transcription-free feedback systems which may be responsible for the roles of prostanoids in maintaining homeostasis as rapid-acting local-mediators, autacoids.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"48 7","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/bies.70166","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467603","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}
引用次数: 0
Engineering CAR-Tregs with Phage-Selected scFv Enables a New Paradigm for Immune Regulation 利用噬菌体选择的scFv来设计car - treg,为免疫调节提供了新的范例。
IF 3.3 3区 生物学
BioEssays Pub Date : 2026-07-15 DOI: 10.1002/bies.70164
Fatih Noyan, Matthias Hardtke-Wolenski
{"title":"Engineering CAR-Tregs with Phage-Selected scFv Enables a New Paradigm for Immune Regulation","authors":"Fatih Noyan,&nbsp;Matthias Hardtke-Wolenski","doi":"10.1002/bies.70164","DOIUrl":"10.1002/bies.70164","url":null,"abstract":"<p>Regulatory T cells (Tregs) are central to immune tolerance, yet antigen-specific cell therapies lag behind cytotoxic CAR-T approaches. Most CAR-Treg programs still use single-chain variable fragments (scFvs) derived from monoclonal antibodies optimized for effector function, a bias that may promote CAR clustering, tonic signaling, and lineage instability. Here, we propose a phage-first binder discovery framework for CAR-Tregs and state testable hypotheses linking phage-display selection pressures to scFv biophysical properties and Treg fate. We hypothesize that multi-parameter selection and counter-selection can enrich scFvs with moderate affinity, low polyspecificity, and improved framework stability, thereby lowering tonic signaling in defined backbone architectures and preserving FOXP3/TSDR stability under inflammatory stress. We outline a falsifiable two-phase roadmap—bench triage followed by mechanistic and preclinical validation to determine how scFv properties, expression level, and intracellular signaling domains define an optimal tonic window for durable immune regulation.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"48 7","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/bies.70164","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148454636","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}
引用次数: 0
Molecular Acrobats: How CHD Remodelers Shape the Genetic Playground to License Cell Identity 分子杂技:冠心病重塑者如何塑造基因游乐场以许可细胞身份。
IF 3.3 3区 生物学
BioEssays Pub Date : 2026-07-13 DOI: 10.1002/bies.70158
İsa Özdemir, Sarah J. Hainer
{"title":"Molecular Acrobats: How CHD Remodelers Shape the Genetic Playground to License Cell Identity","authors":"İsa Özdemir,&nbsp;Sarah J. Hainer","doi":"10.1002/bies.70158","DOIUrl":"10.1002/bies.70158","url":null,"abstract":"<p>In eukaryotes, DNA is not a naked repository of genetic information but is tightly wound around histone octamers to form nucleosomes. While this packaging solves the spatial problem of fitting 2 meters of DNA into a microscopic nucleus, it creates a massive accessibility problem for DNA-templated events, including transcription, replication, and DNA repair. Here, we review how the chromodomain helicase DNA-binding (CHD) family of ATP-dependent nucleosome remodelers act as the molecular acrobats of the chromatin accessibility landscape. We highlight that the three CHD subfamilies represent a developmental division of labor: subfamily I maintains pluripotent chromatin accessibility, subfamily II drives lineage commitment through chromatin closure, and subfamily III establishes tissue-specific enhancer and promoter accessibility during organogenesis. By dynamically transforming chromatin architecture through nucleosome sliding, spacing, and ejection, CHD remodelers license the transitions between cell states, ensuring that the epigenetic landscape is reshaped for the specific needs of a stem cell today and a differentiated cell type tomorrow. We discuss how disruption of this licensing, through mutation or loss of family members, leads to severe neurodevelopmental disorders, including CHARGE syndrome, autism spectrum disorder, and intellectual disability. We close by raising outstanding questions including how CHD activity is regulated, how co-expressed paralogs coordinate their activities, and whether CHD dysfunction can be therapeutically targeted.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"48 7","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/bies.70158","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148429774","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}
引用次数: 0
PHLPP is neither a Phosphatase nor a Tumor Suppressor PHLPP既不是磷酸酶也不是肿瘤抑制因子。
IF 3.3 3区 生物学
BioEssays Pub Date : 2026-07-12 DOI: 10.1002/bies.70165
Thomas A. Leonard
{"title":"PHLPP is neither a Phosphatase nor a Tumor Suppressor","authors":"Thomas A. Leonard","doi":"10.1002/bies.70165","DOIUrl":"10.1002/bies.70165","url":null,"abstract":"<p>PH domain leucine-rich repeat protein phosphatases 1 and 2 (PHLPP1/PHLPP2) have, for more than 20 years, been described as Akt phosphatases and tumor suppressor genes. Approximately 200 PubMed-indexed articles have been published on the topic, including efforts to pharmacologically inhibit PHLPP in disease settings. A recent study, however, presents evidence that PHLPP is actually a pseudophosphatase with no catalytic activity. These observations question its reported role in cancer. The designation of PHLPP1 and PHLPP2 as pseudophosphatases necessitates both a critical examination of the literature and new hypotheses for the biological function of these ancient proteins. Here, we review the emergence of PHLPP1 and PHLPP2 as cellular signal transducers, critically examine the evidence for their reported phosphatase activity and tumor suppressor functions, and propose steps to elucidate their biological functions.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"48 7","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/bies.70165","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148429725","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}
引用次数: 0
Decoding the Hot-Mitochondrion Paradox 破解热线粒体悖论。
IF 3.3 3区 生物学
BioEssays Pub Date : 2026-07-09 DOI: 10.1002/bies.70159
Peyman Fahimi, Michael Lynch, Chérif F. Matta
{"title":"Decoding the Hot-Mitochondrion Paradox","authors":"Peyman Fahimi,&nbsp;Michael Lynch,&nbsp;Chérif F. Matta","doi":"10.1002/bies.70159","DOIUrl":"10.1002/bies.70159","url":null,"abstract":"<p>In a 2018 paper and a subsequent article published in 2023, researchers reported that mitochondria maintain temperatures 10°C–15°C higher than the surrounding cytoplasm—a finding that deviates by five to six orders of magnitude from theoretical predictions based on Fourier's law of heat conduction. In 2022, we proposed a solution to this apparent paradox. In the present perspective, we build upon that framework and introduce new ideas to further unravel how a biological membrane—whether of an organelle or a whole cell—can become significantly warmer than its environment. We propose that ion-translocating proteins embedded in the inner mitochondrial membrane (IMM) can be modeled as ratchet engines, introducing a novel, previously overlooked mode of heat transfer. This mechanism, coupled with localized heat release during the cyclical dehydration-translocation-hydration of ions through membrane proteins, may generate transient but substantial temperature spikes. The cumulative thermal occupancy of these microscopic events across the three-dimensional surface of the IMM can account for the elevated temperatures detected by molecular probes.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"48 7","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/bies.70159","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148410692","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}
引用次数: 0
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