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The proximity interactome of PML isoforms I and II under fatty acid stress 脂肪酸胁迫下PML异构体I和II的邻近相互作用。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-20 DOI: 10.1002/1873-3468.15081
Jordan Thompson, François-Michel Boisvert, Jayme Salsman, Dominique Lévesque, Graham Dellaire, Neale D. Ridgway
{"title":"The proximity interactome of PML isoforms I and II under fatty acid stress","authors":"Jordan Thompson,&nbsp;François-Michel Boisvert,&nbsp;Jayme Salsman,&nbsp;Dominique Lévesque,&nbsp;Graham Dellaire,&nbsp;Neale D. Ridgway","doi":"10.1002/1873-3468.15081","DOIUrl":"10.1002/1873-3468.15081","url":null,"abstract":"<p>Promyelocytic leukemia (PML) protein forms the scaffold for PML nuclear bodies (PML NB) that reorganize into Lipid-Associated PML Structures (LAPS) under fatty acid stress. We determined how the fatty acid oleate alters the interactome of PMLI or PMLII by expressing fusions with the ascorbate peroxidase APEX2 in U2OS cells. The resultant interactome included ESCRT and COPII transport protein nodes. Proximity ligation assay (PLA) revealed that COPII proteins SEC23B, SEC24A and USO1 preferentially associated with PML NBs. Nuclear localization of USO1, but not SEC23B and SEC24A, was reduced in PML knockout cells and restored by PMLII expression. Thus, proximity-labelling methods identified COPII transport protein interactions with PML NBs that are disrupted by fatty acid stress.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 5","pages":"682-699"},"PeriodicalIF":3.5,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.15081","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Transcription as a double-edged sword in genome maintenance 转录是基因组维持中的一把双刃剑。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-20 DOI: 10.1002/1873-3468.15080
Jian Ouyang
{"title":"Transcription as a double-edged sword in genome maintenance","authors":"Jian Ouyang","doi":"10.1002/1873-3468.15080","DOIUrl":"10.1002/1873-3468.15080","url":null,"abstract":"<p>Genome maintenance is essential for the integrity of the genetic blueprint, of which only a small fraction is transcribed in higher eukaryotes. DNA lesions occurring in the transcribed genome trigger transcription pausing and transcription-coupled DNA repair. There are two major transcription-coupled DNA repair pathways. The transcription-coupled nucleotide excision repair (TC-NER) pathway has been well studied for decades, while the transcription-coupled homologous recombination repair (TC-HR) pathway has recently gained attention. Importantly, recent studies have uncovered crucial roles of RNA transcripts in TC-HR, opening exciting directions for future research. Transcription also plays pivotal roles in regulating the stability of highly specialized genomic structures such as telomeres, centromeres, and fragile sites. Despite their positive function in genome maintenance, transcription and RNA transcripts can also be the sources of genomic instability, especially when colliding with DNA replication and forming unscheduled pathological RNA:DNA hybrids (R-loops), respectively. Pathological R-loops can result from transcriptional stress, which may be induced by transcription dysregulation. Future investigation into the interplay between transcription and DNA repair will reveal novel molecular bases for genome maintenance and transcriptional stress-associated genomic instability, providing therapeutic targets for human disease intervention.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 2","pages":"147-156"},"PeriodicalIF":3.5,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.15080","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Transcription-coupled repair – mechanisms of action, regulation, and associated human disorders 转录偶联修复-作用机制，调节，和相关的人类疾病。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-20 DOI: 10.1002/1873-3468.15073
Yuka Nakazawa, Yasuyoshi Oka, Tomoko Matsunaga, Tomoo Ogi
{"title":"Transcription-coupled repair – mechanisms of action, regulation, and associated human disorders","authors":"Yuka Nakazawa,&nbsp;Yasuyoshi Oka,&nbsp;Tomoko Matsunaga,&nbsp;Tomoo Ogi","doi":"10.1002/1873-3468.15073","DOIUrl":"10.1002/1873-3468.15073","url":null,"abstract":"<p>The transcription-coupled repair (TCR) pathway resolves transcription-blocking DNA lesions to maintain cellular function and prevent transcriptional arrest. Stalled RNA polymerase II (RNAPII) triggers repair mechanisms, including RNAPII ubiquitination, which recruit UVSSA and TFIIH. Defects in TCR-associated genes cause disorders like Cockayne syndrome, UV-sensitive syndrome, xeroderma pigmentosum, and recently defined AMeDS. TCR safeguards transcription, linking its failure to neurodegeneration and disease phenotypes.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 2","pages":"166-167"},"PeriodicalIF":3.5,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11771657/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Temperature adaptation of yeast phospholipid molecular species at the acyl chain positional level 酵母磷脂分子物种在酰基链位置水平上的温度适应性。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-13 DOI: 10.1002/1873-3468.15060
Celine Kelso, Alan T. Maccarone, Anton I. P. M. de Kroon, Todd W. Mitchell, Mike F. Renne
{"title":"Temperature adaptation of yeast phospholipid molecular species at the acyl chain positional level","authors":"Celine Kelso,&nbsp;Alan T. Maccarone,&nbsp;Anton I. P. M. de Kroon,&nbsp;Todd W. Mitchell,&nbsp;Mike F. Renne","doi":"10.1002/1873-3468.15060","DOIUrl":"10.1002/1873-3468.15060","url":null,"abstract":"<p>Yeast is a poikilothermic organism and adapts its lipid composition to the environmental temperature to maintain membrane physical properties. Studies addressing temperature-dependent adaptation of the lipidome have described changes in the phospholipid composition at the level of sum composition (e.g. PC 32:1) and molecular composition (e.g. PC 16:0_16:1). However, there is little information at the level of positional isomers (e.g. PC 16:0/16:1 versus PC 16:1/16:0). Here, we used collision- and ozone-induced dissociation (CID/OzID) mass spectrometry to investigate homeoviscous adaptation of PC, PE and PS to determine the phospholipid acyl chains at the <i>sn</i>-1 and <i>sn</i>-2 position. Our data establish the <i>sn</i>-molecular species composition of PC, PE and PS in the lipidome of yeast cultured at different temperatures.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 4","pages":"530-544"},"PeriodicalIF":3.5,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.15060","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142823966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
RETRACTION: Theaflavins Retard Human Breast Cancer Cell Migration by Inhibiting NF-κB via p53-ROS Cross-talk 返回：茶黄素通过 p53-ROS 交叉对话抑制 NF-κB 从而延缓人类乳腺癌细胞的迁移。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-13 DOI: 10.1002/1873-3468.15076
{"title":"RETRACTION: Theaflavins Retard Human Breast Cancer Cell Migration by Inhibiting NF-κB via p53-ROS Cross-talk","authors":"","doi":"10.1002/1873-3468.15076","DOIUrl":"10.1002/1873-3468.15076","url":null,"abstract":"<p><b>RETRACTION:</b> A. Adhikary, S. Mohanty, L. Lahiry, D. S. Hossain, S. Chakraborty and T. Das, “Theaflavins Retard Human Breast Cancer Cell Migration by Inhibiting NF-κB via p53-ROS Cross-talk,” <i>FEBS Letters</i> 584, no. 1 (2010): 7-14, https://doi.org/10.1016/j.febslet.2009.10.081.</p><p>The above article, published online on 31 October 2009 in Wiley Online Library (wileyonlinelibrary.com), has been published by agreement between the journal Editor-in-Chief, Michael Brunner; FEBS Press; and John Wiley and Sons Ltd. The retraction has been agreed due to partial duplication of micrographs observed in Figure 2C and the unexpected similarity of curves presented in 3C. Additionally, the blot against histone H1 in figure 4D (bottom-left panel) is a stretched duplication of the blot against alpha-actin in figure 3F (right-hand panel). Further, duplications have been observed between the MCF-7 p53 bands presented in Figures 1D and the p53 bands in Figure 3F; the alpha actin bands shown in Figure 3F and the Histone H1 bands in Figure 4D; and the alpha actin bands presented in Figures 3E and 4D. The authors provided some supporting data and an explanation, but the editors found them unsatisfactory. Due to the extent and nature of these concerns, the editors consider the results and conclusions of this article to be invalid. The authors disagree with the retraction.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 4","pages":"596"},"PeriodicalIF":3.5,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.15076","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142823962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Suppression of amber stop codons impairs pathogenicity in Salmonella 琥珀色终止密码子的抑制削弱了沙门氏菌的致病性。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-12 DOI: 10.1002/1873-3468.15075
Zhihui Lyu, Cierra Wilson, Prajita Paul, Jiqiang Ling
{"title":"Suppression of amber stop codons impairs pathogenicity in Salmonella","authors":"Zhihui Lyu,&nbsp;Cierra Wilson,&nbsp;Prajita Paul,&nbsp;Jiqiang Ling","doi":"10.1002/1873-3468.15075","DOIUrl":"10.1002/1873-3468.15075","url":null,"abstract":"<p>Translation terminates at UAG (amber), UGA (opal), and UAA (ochre) stop codons. In nature, readthrough of stop codons can be substantially enhanced by suppressor tRNAs. Stop-codon suppression also provides powerful tools in synthetic biology and disease treatment. How stop-codon suppression affects bacterial pathogenesis is poorly understood. Here, we show that suppression of UAG codons, but not UGA or UAA codons, attenuates expression of <i>Salmonella</i> Pathogenicity Island 1 (SPI-1) genes, which are required for virulence. Consistently, amber suppression abolishes <i>Salmonella</i> infection of macrophages. Systematic genetic and biochemical analyses further show that amber suppression decreases the activity, but not the level, of the master SPI-1 regulator HilD. Our work thus demonstrates an unexpected selectivity of stop codons in regulating <i>Salmonella</i> virulence.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 4","pages":"476-487"},"PeriodicalIF":3.5,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.15075","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
The immunological interface: dendritic cells as key regulators in metabolic dysfunction-associated steatotic liver disease. 免疫界面：树突状细胞作为代谢功能障碍相关脂肪变性肝病的关键调节因子。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-12 DOI: 10.1002/1873-3468.15072
Camilla Klaimi, WanTing Kong, Camille Blériot, Joel T Haas
{"title":"The immunological interface: dendritic cells as key regulators in metabolic dysfunction-associated steatotic liver disease.","authors":"Camilla Klaimi, WanTing Kong, Camille Blériot, Joel T Haas","doi":"10.1002/1873-3468.15072","DOIUrl":"https://doi.org/10.1002/1873-3468.15072","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) refers to a broad spectrum of conditions associating fat accumulation in the liver (steatosis) with varying degrees of inflammation (hepatitis) and fibrosis, which can progress to cirrhosis and potentially cancer (hepatocellular carcinoma). The first stages of these diseases are reversible and the immune system, together with metabolic factors (obesity, insulin resistance, Western diet, etc.), can influence the disease trajectory leading to progression or regression. Dendritic cells are professional antigen-presenting cells that constantly sense environmental stimuli and orchestrate immune responses. Herein, we discuss the existing literature on the heterogeneity of dendritic cell lineages, states, and functions, to provide a comprehensive overview of how liver dendritic cells influence the onset and evolution of MASLD.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Transcriptional regulation of basophil-specific protease genes by C/EBPα, GATA2, TGF-β signaling, and epigenetic mechanisms C/EBPα、GATA2、TGF-β信号通路和表观遗传机制对嗜碱性粒细胞特异性蛋白酶基因的转录调控
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-11 DOI: 10.1002/1873-3468.15069
Ryotaro Tojima, Kazuki Nagata, Naoto Ito, Kenta Ishii, Takahiro Arai, Tomoka Ito, Kazumi Kasakura, Chiharu Nishiyama
{"title":"Transcriptional regulation of basophil-specific protease genes by C/EBPα, GATA2, TGF-β signaling, and epigenetic mechanisms","authors":"Ryotaro Tojima,&nbsp;Kazuki Nagata,&nbsp;Naoto Ito,&nbsp;Kenta Ishii,&nbsp;Takahiro Arai,&nbsp;Tomoka Ito,&nbsp;Kazumi Kasakura,&nbsp;Chiharu Nishiyama","doi":"10.1002/1873-3468.15069","DOIUrl":"10.1002/1873-3468.15069","url":null,"abstract":"<p>Basophils and mast cells (MCs) play an important role in immune responses against allergens and parasitic infection. To elucidate the mechanisms that determine the commitment between basophils and mast cell (MCs), transcription factors and epigenetic modifications regulating the gene expression of basophil-specific enzymes, Mcpt8 and Mcpt11, were analyzed using bone marrow-derived (BM) cells containing basophils and MCs. Knockdown (KD) and overexpression experiments revealed that the transcription factor C/EBPα positively regulated the gene expression of <i>Mcpt8</i> and <i>Prss34</i> (encoding Mcpt11). <i>Cebpa</i>, <i>Mcpt8</i>, and <i>Prss34</i> mRNAs levels were upregulated by histone deacetylases and downregulated by DNA methyltransferases. <i>Gata2</i> KD significantly reduced the mRNA levels of <i>Mcpt8</i> and <i>Prss34</i>, while TGF-β treatment increased those of <i>Mcpt8</i> and <i>Prss34</i>. These results show that basophil-specific protease genes were transactivated by C/EBPα, GATA2, and TGF-β signaling and modified with epigenetic regulation.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 5","pages":"777-786"},"PeriodicalIF":3.5,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.15069","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Covalent labeling of the Arabidopsis plasma membrane H+-ATPase reveals 3D conformational changes involving the C-terminal regulatory domain 拟南芥质膜H+- atp酶的共价标记揭示了涉及c端调控域的三维构象变化。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-03 DOI: 10.1002/1873-3468.15067
Matthew R. Blackburn, Thao T. Nguyen, Sophia E. Patton, Jordan M. Bartosiak, Michael R. Sussman
{"title":"Covalent labeling of the Arabidopsis plasma membrane H+-ATPase reveals 3D conformational changes involving the C-terminal regulatory domain","authors":"Matthew R. Blackburn,&nbsp;Thao T. Nguyen,&nbsp;Sophia E. Patton,&nbsp;Jordan M. Bartosiak,&nbsp;Michael R. Sussman","doi":"10.1002/1873-3468.15067","DOIUrl":"10.1002/1873-3468.15067","url":null,"abstract":"<p>The plasma membrane proton pump is the primary energy transducing, electrogenic ion pump of the plasma membrane in plants and fungi. Compared to its fungal counterpart, the plant plasma membrane proton pump's regulatory C-terminal domain (CTD) contains an additional regulatory segment that links multiple sensory pathways regulating plant cell length through phosphorylation and recruitment of regulatory 14-3-3 proteins. However, a complete structural model of a plant proton pump is lacking. Here, we performed covalent labeling with mass spectrometric analysis (CL-MS) on the <i>Arabidopsis</i> pump AHA2 to identify potential interactions between the CTD and the catalytic domains. Our results suggest that autoinhibition in the plant enzyme is much more structurally complex than in the fungal enzyme.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 4","pages":"545-558"},"PeriodicalIF":3.5,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142767610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
p12 isoform-2 is a regulatory subunit of human DNA polymerase delta and is dysregulated in various cancers p12亚型-2是人类DNA聚合酶delta的调控亚基，在多种癌症中失调。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2024-12-03 DOI: 10.1002/1873-3468.15070
Jugal Kishor Sahu, Shweta Thakur, Ipsita Subhadarsini, Narottam Acharya
{"title":"p12 isoform-2 is a regulatory subunit of human DNA polymerase delta and is dysregulated in various cancers","authors":"Jugal Kishor Sahu,&nbsp;Shweta Thakur,&nbsp;Ipsita Subhadarsini,&nbsp;Narottam Acharya","doi":"10.1002/1873-3468.15070","DOIUrl":"10.1002/1873-3468.15070","url":null,"abstract":"<p>Dysregulation of human DNA polymerase delta (Polδ) subunits is associated with genome instability and pathological disorders. Genome databases suggest the expression of several spliced variants of subunits which may alter Polδ function. Here, we analyzed the protein-encoding variants of the Polδ subunit p12 and their association with cancer. p12 isoform-2 (p12*) encodes a 79 aa protein with a C-terminal tail distinct from the previously characterized p12. Like p12, p12* dimerizes and interacts with p125 and p50 subunits and is thus an integral component of Polδ. Further, we observed dysregulated p12* expression in low-grade glioma, renal, thyroid, and pancreatic carcinomas. This study identifies a previously unrecognized Polδ complex and highlights a possible regulatory role of p12 variants in cellular phenotypes.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"598 24","pages":"3087-3104"},"PeriodicalIF":3.5,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142767616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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