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TBK1 activity regulates the directionality of axonal transport of signalling endosomes. TBK1活性调节信号内体轴突运输的方向性。
IF 3.1 2区 生物学
Life Science Alliance Pub Date : 2026-02-04 Print Date: 2026-04-01 DOI: 10.26508/lsa.202503527
David Villarroel-Campos, Jose Norberto S Vargas, Martin Wallace, Kai Sun, James N Sleigh, Pietro Fratta, Giampietro Schiavo
{"title":"TBK1 activity regulates the directionality of axonal transport of signalling endosomes.","authors":"David Villarroel-Campos, Jose Norberto S Vargas, Martin Wallace, Kai Sun, James N Sleigh, Pietro Fratta, Giampietro Schiavo","doi":"10.26508/lsa.202503527","DOIUrl":"10.26508/lsa.202503527","url":null,"abstract":"<p><p>The polarised and complex morphology of neurons poses massive challenges for efficient cargo delivery between the axon and soma, a process termed axonal transport. We have previously shown that the retrograde axonal transport of pro-survival, neurotrophic signalling endosomes relies on Rab7 in motor neurons, and that their trafficking is impaired in the early stages of amyotrophic lateral sclerosis (ALS) pathogenesis. Here, we report the effect of Rab7 phosphorylation on the transport of these signalling endosomes. We show that the ALS-linked kinase TBK1 phosphorylates Rab7 at S72 in neurons, altering its binding to cytoplasmic dynein adaptors. Accordingly, both TBK1 knockdown and the expression of a loss-of-function Rab7 mutant (S72E) induce aberrant bidirectional movement of signalling endosomes without modifying neuronal polarity or endosomal sorting. This alteration is specific for signalling endosomes, as axonal transport of lysosomes and mitochondria remains unaffected. We have therefore discovered a new TBK1 function that ensures the unidirectional transport of signalling endosomes, suggesting that reduced TBK1 activity determines retrograde transport dysfunctions and long-range signalling impairments.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12872394/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146119412","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}
引用次数: 0
Syk activation during FcγR-mediated phagocytosis involves Syk palmitoylation and desulfenylation. 在fc γ r介导的吞噬过程中,Syk的激活涉及Syk棕榈酰化和去硫化。
IF 3.1 2区 生物学
Life Science Alliance Pub Date : 2026-02-04 Print Date: 2026-04-01 DOI: 10.26508/lsa.202503500
Maxime Jansen, Jean-Marc Strub, Laurent Chaloin, Peter Coopman, Bruno Beaumelle
{"title":"Syk activation during FcγR-mediated phagocytosis involves Syk palmitoylation and desulfenylation.","authors":"Maxime Jansen, Jean-Marc Strub, Laurent Chaloin, Peter Coopman, Bruno Beaumelle","doi":"10.26508/lsa.202503500","DOIUrl":"10.26508/lsa.202503500","url":null,"abstract":"<p><p>The Syk tyrosine kinase acts downstream of several immune receptors such as the FcγR. Syk owns two SH2 domains that interact with biphosphorylated ITAMs of the FcγR upon phagocytosis. This results in the activation of Syk by autophosphorylation, triggering phosphorylation of several downstream targets, F-actin polymerization, and phagocytosis of the IgG-opsonized target. We found that Syk is S-acylated upon phagocytosis by macrophages. Palmitoylation is performed on a single Syk-Cys by the DHHC5 enzyme that specifically associates with Syk upon phagocytosis. Syk palmitoylation is important for Syk localization to the phagocytic cup, phosphorylation, and phagocytosis. We observed that another Syk-Cys residue, within a redox motif, is modified by sulfenylation. Nevertheless, Syk desulfenylation seems to occur during phagocytosis, when H<sub>2</sub>O<sub>2</sub> production at the cup decreases, after 3.5 min of phagocytosis. Molecular dynamics studies indicated that desulfenylation increased the exposure of a loop within the Syk interdomain B. This could facilitate phosphorylation of key Syk-Tyr residues by upstream kinases. We thus propose an updated model for Syk activation during FcγR-mediated phagocytosis that involves both Syk palmitoylation and desulfenylation.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12872395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146119434","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}
引用次数: 0
Repeated proliferative events ameliorate age-associated accumulation of DNA damage in HSPCs. 重复增殖事件可改善HSPCs中与年龄相关的DNA损伤积累。
IF 3.1 2区 生物学
Life Science Alliance Pub Date : 2026-01-29 Print Date: 2026-04-01 DOI: 10.26508/lsa.202503337
Shubham Haribhau Mehatre, Harsh Agrawal, Irene Mariam Roy, Sarah Schouteden, Satish Khurana
{"title":"Repeated proliferative events ameliorate age-associated accumulation of DNA damage in HSPCs.","authors":"Shubham Haribhau Mehatre, Harsh Agrawal, Irene Mariam Roy, Sarah Schouteden, Satish Khurana","doi":"10.26508/lsa.202503337","DOIUrl":"10.26508/lsa.202503337","url":null,"abstract":"<p><p>Upon aging, hematopoietic stem cells show accumulation of DNA damage that has been causally linked with their functional decline, with debatable role of proliferative events. In this study, we sought to enquire the effect of increased proliferation rate in hematopoietic stem and progenitor cells (HSPCs) on hematopoietic aging. Multiple rounds of blood withdrawals were performed during adult life to maintain a higher proliferation rate in HSPC population in mice. Our experiments showed little effect of increased proliferation on age-associated functional decline in the hematopoietic system. However, we noted a decrease in the double-strand breaks accumulated with age after the serial bleeding regimen. Analysis of scRNA-Seq data from mouse and human HSPCs showed enrichment of DNA damage response pathways. Importantly, we demonstrate that the induction of HSPC proliferation in aged mice was sufficient to activate the DNA damage response in vivo and decrease the load of double-strand breaks. Hence, these results show that repeated blood withdrawals equivalent to clinical blood donation clear DNA damages without impacting the functioning of HSPCs.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12861689/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146086353","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}
引用次数: 0
wgbstools: a computational suite for DNA methylation sequencing data analysis. wgbstools:用于DNA甲基化测序数据分析的计算套件。
IF 3.1 2区 生物学
Life Science Alliance Pub Date : 2026-01-29 Print Date: 2026-04-01 DOI: 10.26508/lsa.202503514
Netanel Loyfer, Jonathan Rosenski, Tommy Kaplan
{"title":"<i>wgbstools</i>: a computational suite for DNA methylation sequencing data analysis.","authors":"Netanel Loyfer, Jonathan Rosenski, Tommy Kaplan","doi":"10.26508/lsa.202503514","DOIUrl":"10.26508/lsa.202503514","url":null,"abstract":"<p><p>Next-generation methylation-aware sequencing of DNA sheds light on the fundamental role of methylation in cellular function in health and disease, increasing the number of covered CpG sites from hundreds of thousands in previous array-based approaches to tens of millions across the whole genome. While array-based approaches are limited to single-CpG resolution, next-generation sequencing allows for a more detailed, single-molecule fragment-level analysis; however, existing tools to fully use this capability are not yet well developed. Here, we present <i>wgbstools</i>, an extensive computational suite tailored for methylation sequencing data. <i>wgbstools</i> allows fast access and ultracompact anonymized representation of high-throughput methylome data, obtained through various library preparation and sequencing methods, with a custom epiread file format achieving a compression factor of over 100x from the input BAM file. In addition, <i>wgbstools</i> contains state-of-the-art algorithms for genomic segmentation, biomarker identification, genetic and epigenetic data integration, and more. <i>wgbstools</i> offers fragment-level analysis and informative visualizations, across multiple genomic regions and samples.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12861688/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146086318","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}
引用次数: 0
TEAD-independent mechanisms of YAP function in cardiomyocyte cell cycle reentry. YAP功能在心肌细胞周期再进入中的不依赖于tead的机制。
IF 3.1 2区 生物学
Life Science Alliance Pub Date : 2026-01-23 Print Date: 2026-04-01 DOI: 10.26508/lsa.202503496
Bing Xie, Jeffrey Steimle, Vaibhav Deshmukh, Lin Liu, Chang-Ru Tsai, Todd R Heallen, Wyatt Paltzer, Yuka Morikawa, Fansen Meng, Jun Wang, James F Martin
{"title":"TEAD-independent mechanisms of YAP function in cardiomyocyte cell cycle reentry.","authors":"Bing Xie, Jeffrey Steimle, Vaibhav Deshmukh, Lin Liu, Chang-Ru Tsai, Todd R Heallen, Wyatt Paltzer, Yuka Morikawa, Fansen Meng, Jun Wang, James F Martin","doi":"10.26508/lsa.202503496","DOIUrl":"10.26508/lsa.202503496","url":null,"abstract":"<p><p>Adult mammalian hearts exhibit limited regenerative capacity because of the restricted renewal of cardiomyocytes. Recent studies reveal that mammalian hearts exhibit transient regenerative potential within a short time frame after birth, suggesting a regulatory mechanism that prevents adult hearts from initiating a regenerative response to cardiac injury. Here, we discovered that an active form of YAP, named YAP6SA, which is not inhibited by the Hippo signaling pathway and does not interact with TEADs, induces cardiomyocyte cell cycle reentry. In addition, YAP6SA interacts with scaffold protein MPDZ to regulate Rho GTPases and promote cell cycle progression in cardiomyocytes (CMs). Importantly, YAP6SA overexpression is well tolerated in mammalian hearts. These findings provide new insights into YAP function in cardiomyocytes.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12830084/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146041034","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}
引用次数: 0
Notch signaling stabilizes lengths of motile cilia in multiciliated cells in the lung. Notch信号稳定肺多纤毛细胞的运动纤毛长度。
IF 3.1 2区 生物学
Life Science Alliance Pub Date : 2026-01-22 Print Date: 2026-03-01 DOI: 10.26508/lsa.202503268
Neenu Joy, Aditya Deshpande, Sai Manoz Lingamallu, Vasam Manjveekar Prabantu, Chakenalli N Naveenkumar, Kumaraswamy Bharathkumar, Sukanya Bhat, Zabdiel Alvarado-Martinez, Alessandra Livraghi-Butrico, James S Hagood, Richard C Boucher, Daniel Lafkas, Kevin M Byrd, Shridhar Narayanan, Radha K Shandil, Arjun Guha
{"title":"Notch signaling stabilizes lengths of motile cilia in multiciliated cells in the lung.","authors":"Neenu Joy, Aditya Deshpande, Sai Manoz Lingamallu, Vasam Manjveekar Prabantu, Chakenalli N Naveenkumar, Kumaraswamy Bharathkumar, Sukanya Bhat, Zabdiel Alvarado-Martinez, Alessandra Livraghi-Butrico, James S Hagood, Richard C Boucher, Daniel Lafkas, Kevin M Byrd, Shridhar Narayanan, Radha K Shandil, Arjun Guha","doi":"10.26508/lsa.202503268","DOIUrl":"10.26508/lsa.202503268","url":null,"abstract":"<p><p>Airway multiciliated cells (MCs) maintain respiratory health by clearing mucus and trapped particles through coordinated ciliary beating. Although ciliary length progressively decreases along the proximal-distal (P-D) axis of the tracheobronchial tree, the mechanisms that maintain this gradient remain unclear. We show that canonical Notch signaling in MCs stabilizes ciliary length across airway regions. Inhibition of Notch signaling shortens tracheal cilia, lengthens distal airway cilia, abolishes the P-D gradient in ciliary length, and induces region-specific changes in gene expression. To assess how environmental factors influence this regulation, we examined germ-free mice and a model of <i>Mycobacterium tuberculosis</i> (<i>M. tb</i>) infection. Germ-free conditions did not alter ciliary architecture, whereas <i>M. tb</i> infection led to elongation of distal airway cilia accompanied by down-regulation of Notch signaling. These findings identify Notch signaling as a key homeostatic regulator that maintains ciliary length and preserves the P-D gradient in airway multiciliated cells.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 3","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12827581/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146029766","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}
引用次数: 0
Targeted recruitment of USP15 enhances CTLA4 surface levels and restricts its degradation. 靶向募集USP15提高CTLA4表面水平,限制其降解。
IF 2.9 2区 生物学
Life Science Alliance Pub Date : 2026-01-22 Print Date: 2026-04-01 DOI: 10.26508/lsa.202503563
Francesca Querques, Victoria Ciampani, Pei Yee Tey, Victoria D Kutilek, Elma Kadic, Michael J Clague, Sylvie Urbé
{"title":"Targeted recruitment of USP15 enhances CTLA4 surface levels and restricts its degradation.","authors":"Francesca Querques, Victoria Ciampani, Pei Yee Tey, Victoria D Kutilek, Elma Kadic, Michael J Clague, Sylvie Urbé","doi":"10.26508/lsa.202503563","DOIUrl":"10.26508/lsa.202503563","url":null,"abstract":"<p><p>Induced protein proximity offers powerful new routes to modulate protein fate. Whereas proteolysis-targeting chimeras (PROTACs) promote degradation through E3 ligase recruitment, the converse principle, targeted protein stabilisation or enhancement via deubiquitylase (DUB) recruitment, is only beginning to emerge. The immune checkpoint receptor CTLA4, whose deficiency causes severe autoimmunity, undergoes rapid ubiquitin-dependent lysosomal degradation, making it one of the most short-lived transmembrane proteins. Using an inducible \"RapTag\" system, which brings together tagged proteins through rapalog-mediated FKBP-FRB dimerisation, we show that enforced proximity to the broad-specificity DUB USP15 markedly increases total and cell surface CTLA4 levels. Controlled expression of WT or catalytically inactive USP15 in isogenic cell lines revealed a clear requirement for DUB activity. The elevation of CTLA4 at the plasma membrane exceeded that of the total cellular pool, consistent with a diversion from ubiquitin-driven lysosomal sorting towards recycling. This easily adaptable platform enables systematic testing of DUB-substrate combinations that informs rational Enhancement Targeting Chimera (ENTAC) design for downstream drug discovery efforts and targeted protein rescue in therapeutic contexts.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 4","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12827578/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146030028","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}
引用次数: 0
Amyloid-β fibrils accumulated in preeclamptic placentas suppress cytotrophoblast syncytialization. 在子痫前期胎盘中积累的淀粉样蛋白-β原纤维抑制细胞滋养细胞合胞。
IF 2.9 2区 生物学
Life Science Alliance Pub Date : 2026-01-20 Print Date: 2026-04-01 DOI: 10.26508/lsa.202503453
Kaho Nishioka, Midori Ikezaki, Naoyuki Iwahashi, Miyu Arakawa, Momo Fukushima, Noa Mori, Mika Mizoguchi, Yuko Horiuchi-Tanizaki, Megumi Fujino, Takami Tomiyama, Yoshito Ihara, Kenji Uchimura, Kazuhiko Ino, Kazuchika Nishitsuji
{"title":"Amyloid-β fibrils accumulated in preeclamptic placentas suppress cytotrophoblast syncytialization.","authors":"Kaho Nishioka, Midori Ikezaki, Naoyuki Iwahashi, Miyu Arakawa, Momo Fukushima, Noa Mori, Mika Mizoguchi, Yuko Horiuchi-Tanizaki, Megumi Fujino, Takami Tomiyama, Yoshito Ihara, Kenji Uchimura, Kazuhiko Ino, Kazuchika Nishitsuji","doi":"10.26508/lsa.202503453","DOIUrl":"10.26508/lsa.202503453","url":null,"abstract":"<p><p>Cerebral deposition of fibrillar amyloid-β (Aβ) is a pathological hallmark of Alzheimer's disease. Although Aβ is present in human placentas and accumulates in preeclamptic placentas characterized by poor placentation, the production and role of Aβ in the human placenta remain unclear. Because hypoxia in mid-to-late pregnancy is a risk for preeclampsia, we found that levels of hypoxia-inducible factor 1-α and β-secretase (BACE-1) increased concurrently with placental Aβ deposition in late-stage preeclamptic placentas. We also found that a human cytotrophoblast (CTB) model, BeWo cells, actually produced Aβ species and that hypoxia increased Aβ production and BACE-1 protein levels. Aβ42 fibrils inhibited CTB syncytialization, a critical step in maintaining pregnancy, by inducing loss of membrane localization of cell-cell adhesion molecules. Primary human CTBs confirmed these observations. Taken together, our results suggest that increased Aβ production in CTBs by hypoxia may lead to the formation of Aβ fibrils, which inhibit syncytiotrophoblast formation and are detrimental to pregnancy. Thus, our results reveal the novel role of Aβ fibrils in the pathogenesis of preeclampsia.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 4","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12819053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146011121","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}
引用次数: 0
Apicortin defines the Plasmodium apical conoid body but is dispensable for the parasite life cycle. 皮质素决定了疟原虫的顶锥体,但在寄生虫的生命周期中是不可缺少的。
IF 3.1 2区 生物学
Life Science Alliance Pub Date : 2026-01-16 Print Date: 2026-04-01 DOI: 10.26508/lsa.202503522
Mohammad Zeeshan, Akancha Mishra, Sarah L Pashley, Robert Markus, Declan Brady, Anthony A Holder, Carolyn Moores, Rita Tewari
{"title":"Apicortin defines the <i>Plasmodium</i> apical conoid body but is dispensable for the parasite life cycle.","authors":"Mohammad Zeeshan, Akancha Mishra, Sarah L Pashley, Robert Markus, Declan Brady, Anthony A Holder, Carolyn Moores, Rita Tewari","doi":"10.26508/lsa.202503522","DOIUrl":"10.26508/lsa.202503522","url":null,"abstract":"<p><p>Apicomplexan parasites such as <i>Plasmodium</i> spp. and <i>Toxoplasma gondii</i> possess unique tubulin-based structures, including subpellicular microtubules and apical polar rings, which are essential for parasite motility, host cell invasion, and replication. Apicortin, a microtubule-associated protein, contains a doublecortin (DC) domain and a partial <u>t</u>ubulin <u>p</u>olymerization-<u>p</u>romoting <u>p</u>rotein (TPPP) domain, both implicated in microtubule binding and stabilization. How tubulin-based structures are maintained is poorly understood, but it may involve Apicortin, so far found only in apicomplexans and the placozoan <i>Trichoplax adhaerens</i> Here, we investigated the location and function of Apicortin in <i>Plasmodium berghei</i> Live-cell imaging of a transgenic parasite line expressing GFP-tagged Apicortin showed its location at the apical end of invasive parasite stages within the mosquito vector. Super-resolution and expansion microscopy revealed that Apicortin forms a distinct ringlike structure in the apical complex region at the apical end. However, deletion of the Apicortin gene had no effect on parasite development, indicating that this protein is not essential. This suggests that there may be redundancy or compensatory functions in the mechanisms that stabilize the apical complex.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 4","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12811414/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145989848","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}
引用次数: 0
Deconstruction by C. thermocellum-from microbe mediated to dynamic redistribution of cellulosomes. C. thermocell的解构——从微生物介导到纤维素的动态再分配。
IF 3.1 2区 生物学
Life Science Alliance Pub Date : 2026-01-16 Print Date: 2026-03-01 DOI: 10.26508/lsa.202503239
John M Yarbrough, Neal N Hengge, Qi Xu, Samantha J Ziegler, Daehwan Chung, Shu Huang, Sarah Moraïs, Itzhak Mizrahi, Edward A Bayer, Yannick J Bomble
{"title":"Deconstruction by <i>C. thermocellum</i>-from microbe mediated to dynamic redistribution of cellulosomes.","authors":"John M Yarbrough, Neal N Hengge, Qi Xu, Samantha J Ziegler, Daehwan Chung, Shu Huang, Sarah Moraïs, Itzhak Mizrahi, Edward A Bayer, Yannick J Bomble","doi":"10.26508/lsa.202503239","DOIUrl":"10.26508/lsa.202503239","url":null,"abstract":"<p><p><i>Clostridium thermocellum</i> is one of the most efficient microorganisms for the deconstruction of cellulosic biomass. To achieve this high level of cellulolytic activity, <i>C. thermocellum</i> uses large multienzyme complexes known as cellulosomes to break down complex polysaccharides, notably cellulose, found in plant cell walls. The attachment of bacterial cells to the nearby substrate via the cellulosome has been hypothesized to be the reason for this high efficiency. The region lying between the cell and the substrate has shown great variation and dynamics that are affected by the growth stage of cells and the substrate used for growth. Here, we used both super-resolution imaging and machine-learning approaches to study the distribution of <i>C. thermocellum</i> cellulosomes at different stages of growth. We show that <i>C. thermocellum</i> initially retains its cellulosomes primarily on the cell surface but then relocates large cellulosome clusters to the interface with biomass, therefore depleting its cell surface of cellulosomes. These results indicate dynamic redistribution of cellulosomes during growth, with a functional shift toward substrate-associated degradation later during growth on biomass.</p>","PeriodicalId":18081,"journal":{"name":"Life Science Alliance","volume":"9 3","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12811415/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145989823","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}
引用次数: 0
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