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裂殖酵母Bgs1葡聚糖合酶参与生长极性和膜运输的调控。

Fission yeast Bgs1 glucan synthase participates in the control of growth polarity and membrane traffic.

作者信息

Ramos Mariona, Martín-García Rebeca, Curto M Ángeles, Gómez-Delgado Laura, Moreno M Belén, Sato Mamiko, Portales Elvira, Osumi Masako, Rincón Sergio A, Pérez Pilar, Ribas Juan C, Cortés Juan C G

机构信息

Instituto de Biología Funcional y Genómica, Consejo Superior de Investigaciones Científicas (CSIC) and Universidad de Salamanca, Salamanca, Spain.

Laboratory of Electron Microscopy and Bio-imaging Center, Japan Women's University, 2-8-1 Mejirodai, Bunkyo-ku, Tokyo, Japan.

出版信息

iScience. 2024 Jul 8;27(8):110477. doi: 10.1016/j.isci.2024.110477. eCollection 2024 Aug 16.

Abstract

Rod-shaped fission yeast grows through cell wall expansion at poles and septum, synthesized by essential glucan synthases. Bgs1 synthesizes the linear β(1,3)glucan of primary septum at cytokinesis. Linear β(1,3)glucan is also present in the wall poles, suggesting additional Bgs1 roles in growth polarity. Our study reveals an essential collaboration between Bgs1 and Tea1-Tea4, but not other polarity factors, in controlling growth polarity. Simultaneous absence of Bgs1 function and Tea1-Tea4 causes complete loss of growth polarity, spread of other glucan synthases, and spherical cell formation, indicating this defect is specifically due to linear β(1,3)glucan absence. Furthermore, linear β(1,3)glucan absence induces actin patches delocalization and sterols spread, which are ultimately responsible for the growth polarity loss without Tea1-Tea4. This suggests strong similarities in Bgs1 functions controlling actin structures during cytokinesis and polarized growth. Collectively, our findings unveil that cell wall β(1,3)glucan regulates polarized growth, like the equivalent extracellular matrix in neuronal cells.

摘要

杆状裂殖酵母通过由必需的葡聚糖合酶合成的细胞壁在两极和隔膜处扩展来生长。Bgs1在胞质分裂时合成初级隔膜的线性β(1,3) - 葡聚糖。线性β(1,3) - 葡聚糖也存在于细胞壁两极,这表明Bgs1在生长极性方面还有其他作用。我们的研究揭示了Bgs1与Tea1 - Tea4之间存在重要协作,但与其他极性因子无关,这种协作在控制生长极性方面发挥作用。同时缺失Bgs1功能和Tea1 - Tea4会导致生长极性完全丧失、其他葡聚糖合酶扩散以及球形细胞形成,这表明此缺陷具体是由于线性β(1,3) - 葡聚糖缺失所致。此外,线性β(1,3) - 葡聚糖缺失会诱导肌动蛋白斑的去定位和甾醇扩散,在没有Tea1 - Tea4的情况下,这些最终导致生长极性丧失。这表明在胞质分裂和极性生长过程中,Bgs1在控制肌动蛋白结构的功能上有很强的相似性。总体而言,我们的研究结果揭示细胞壁β(1,3) - 葡聚糖像神经元细胞中的等效细胞外基质一样调节极性生长。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34ce/11326927/87ce3ed76b60/fx1.jpg

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