{"title":"Multiomics reveals that triacylglycerol mobilization helps drive recovery from mitochondrial stress","authors":"","doi":"10.1038/s41556-024-01603-8","DOIUrl":"https://doi.org/10.1038/s41556-024-01603-8","url":null,"abstract":"We devised a multiomics strategy to identify metabolic pathways used by yeast to surmount mitochondrial stress. Strains capable of recovery relied on triacylglycerol mobilization to provide acyl groups for nascent cardiolipin biosynthesis during mitochondrial biogenesis. We further linked multiple proteins to this mobilization phenotype, including essential lipases in both yeast and mammalian model systems.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"74 1","pages":""},"PeriodicalIF":21.3,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143026721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Mitochondrial protein import stress","authors":"Nikolaus Pfanner, Fabian den Brave, Thomas Becker","doi":"10.1038/s41556-024-01590-w","DOIUrl":"https://doi.org/10.1038/s41556-024-01590-w","url":null,"abstract":"<p>Mitochondria have to import a large number of precursor proteins from the cytosol. Chaperones keep these proteins in a largely unfolded state and guide them to the mitochondrial import sites. Premature folding, mitochondrial stress and import defects can cause clogging of import sites and accumulation of non-imported precursors, representing a critical burden for cellular proteostasis. Here we discuss how cells respond to mitochondrial protein import stress by regenerating clogged import sites and inducing stress responses. The mitochondrial protein import machinery has a dual role by serving as sensor for detecting mitochondrial dysfunction and inducing stress-response pathways. The production of chaperones that fold or sequester precursor proteins in deposits is induced and the proteasomal activity is increased to remove the excess precursor proteins. Together, these pathways reveal how mitochondria are tightly integrated into a cellular proteostasis and stress response network to maintain cell viability.</p>","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"32 1","pages":""},"PeriodicalIF":21.3,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142991965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Tripotency in human pancreas","authors":"Stylianos Lefkopoulos","doi":"10.1038/s41556-024-01601-w","DOIUrl":"10.1038/s41556-024-01601-w","url":null,"abstract":"","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"27 1","pages":"4-4"},"PeriodicalIF":17.3,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142986736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Adapting to improve the author experience","authors":"","doi":"10.1038/s41556-024-01596-4","DOIUrl":"10.1038/s41556-024-01596-4","url":null,"abstract":"Here we discuss approaches to refine our editorial processes.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"27 1","pages":"1-1"},"PeriodicalIF":17.3,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41556-024-01596-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142986742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Chaperoning RNA into granules","authors":"Daryl J. V. David","doi":"10.1038/s41556-024-01602-9","DOIUrl":"10.1038/s41556-024-01602-9","url":null,"abstract":"","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"27 1","pages":"4-4"},"PeriodicalIF":17.3,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142986738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Mitotic lethality prevents inflammation","authors":"Christian Zierhut, Andreas Villunger","doi":"10.1038/s41556-024-01529-1","DOIUrl":"10.1038/s41556-024-01529-1","url":null,"abstract":"A study now finds that, after DNA damage, DNA repair by homologous recombination drives non-immunogenic cell death during mitosis. Loss of homologous recombination allows cells to pass through mitosis, but drives interphase death and inflammation. This suggests a dichotomy between immunogenic and non-immunogenic cell-death modes, with biomedical potential.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"27 1","pages":"7-8"},"PeriodicalIF":17.3,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142974576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Radoslaw Szmyd, Sienna Casolin, Lucy French, Anna G. Manjón, Melanie Walter, Léa Cavalli, Christopher B. Nelson, Scott G. Page, Andrew Dhawan, Eric Hau, Hilda A. Pickett, Harriet E. Gee, Anthony J. Cesare
{"title":"Homologous recombination promotes non-immunogenic mitotic cell death upon DNA damage","authors":"Radoslaw Szmyd, Sienna Casolin, Lucy French, Anna G. Manjón, Melanie Walter, Léa Cavalli, Christopher B. Nelson, Scott G. Page, Andrew Dhawan, Eric Hau, Hilda A. Pickett, Harriet E. Gee, Anthony J. Cesare","doi":"10.1038/s41556-024-01557-x","DOIUrl":"10.1038/s41556-024-01557-x","url":null,"abstract":"Double-strand breaks (DSBs) can initiate mitotic catastrophe, a complex oncosuppressive phenomenon characterized by cell death during or after cell division. Here we unveil how cell cycle-regulated DSB repair guides disparate cell death outcomes through single-cell analysis of extended live imaging. Following DSB induction in S or G2, passage of unresolved homologous recombination intermediates into mitosis promotes non-immunogenic intrinsic apoptosis in the immediate attempt at cell division. Conversely, non-homologous end joining, microhomology-mediated end joining and single-strand annealing cooperate to enable damaged G1 cells to complete the first cell cycle with an aberrant cell division at the cost of delayed extrinsic lethality and interferon production. Targeting non-homologous end joining, microhomology-mediated end joining or single-strand annealing promotes mitotic death, while suppressing mitotic death enhances interferon production. Together the data indicate that a temporal repair hierarchy, coupled with cumulative DSB load, serves as a reliable predictor of mitotic catastrophe outcomes following genome damage. In this pathway, homologous recombination suppresses interferon production by promoting mitotic lethality. Szmyd et al. show that DNA repair pathways impact whether cells with DNA lesions arrest in mitosis. The formation of homologous recombination-driven double Holliday junctions elicits mitotic cell death and suppresses inflammatory signalling.","PeriodicalId":18977,"journal":{"name":"Nature Cell Biology","volume":"27 1","pages":"59-72"},"PeriodicalIF":17.3,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41556-024-01557-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142968247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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