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FERONIA 通过调节 CC1 的磷酸化来控制微管阵列行为以响应盐胁迫。

FERONIA adjusts CC1 phosphorylation to control microtubule array behavior in response to salt stress.

机构信息

Key Laboratory of Plant Design, National Key Laboratory of Plant Molecular Genetics, Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences, Shanghai 200032, China.

Department of Plant and Environmental Sciences, Copenhagen Plant Science Center, University of Copenhagen, 1871 Frederiksberg C, Denmark.

出版信息

Sci Adv. 2024 Nov 29;10(48):eadq8717. doi: 10.1126/sciadv.adq8717.

DOI:10.1126/sciadv.adq8717
PMID:39612333
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11606495/
Abstract

Cell wall remodeling is important for plants to adapt to environmental stress. Under salt stress, cortical microtubules undergo a depolymerization-reassembly process to promote the biosynthesis of stress-adaptive cellulose, but the regulatory mechanisms underlying this process are still largely unknown. In this study, we reveal that FERONIA (FER), a potential cell wall sensor, interacts with COMPANION OF CELLULOSE SYNTHASE1 (CC1) and its closest homolog, CC2, two proteins that are required for cortical microtubule reassembly under salt stress. Biochemical data indicate that FER phosphorylates CC1 on multiple residues in its second and third hydrophobic microtubule-binding regions and that these phosphorylations modulate CC1 trafficking and affect the ability of CC1 to engage with microtubules. Furthermore, CC1 phosphorylation level is altered upon exposure to salt stress, which coincides with the changes of microtubule organization. Together, our study outlines an important intracellular mechanism that maintains microtubule arrays during salt exposure in plant cells.

摘要

细胞壁重塑对于植物适应环境胁迫非常重要。在盐胁迫下,皮质微管经历解聚-组装过程,以促进应激适应性纤维素的生物合成,但该过程的调节机制在很大程度上仍不清楚。在这项研究中,我们揭示了 FERONIA(FER),一种潜在的细胞壁传感器,与 COMPANION OF CELLULOSE SYNTHASE1(CC1)及其最接近的同源物 CC2 相互作用,这两种蛋白在盐胁迫下皮质微管的重新组装中是必需的。生化数据表明,FER 在其第二和第三个疏水性微管结合区域的多个残基上对 CC1 进行磷酸化,这些磷酸化修饰调节 CC1 的运输,并影响 CC1 与微管结合的能力。此外,暴露于盐胁迫会改变 CC1 的磷酸化水平,这与微管组织的变化一致。总之,我们的研究概述了一个重要的细胞内机制,该机制在植物细胞暴露于盐时维持微管阵列。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d38/11606495/db5bd73c24e6/sciadv.adq8717-f7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d38/11606495/fb44186efd42/sciadv.adq8717-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d38/11606495/db5bd73c24e6/sciadv.adq8717-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d38/11606495/4efe2f43c3f4/sciadv.adq8717-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d38/11606495/55e35acca4df/sciadv.adq8717-f2.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d38/11606495/db5bd73c24e6/sciadv.adq8717-f7.jpg

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