E69K mutation in β-tubulin 2 blocks cell wall integrity signaling during plant cell elongation.

IF 6.2 1区生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

EMBO Reports Pub Date : 2025-09-30 DOI:10.1038/s44319-025-00507-4

Huanhuan Yang, Jie Wang, Guangda Wang, Chaofeng Wang, Xiaxia Zhang, Juan Tian, Yanjun Yu, Zhaosheng Kong

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引用次数: 0

Abstract

The intact cell wall is the prerequisite for plant cell morphogenesis. Loss of function in FRA1/KINESIN-4A, which encodes a microtubule-based kinesin motor, causes dwarfed growth phenotypes with reduced cell wall mechanics. However, the underlying mechanisms remain elusive. Here, using genetic screening, we identify a suppressor of fra1 (sofa1) mutation that specifically suppresses the dwarf phenotype of the fra1 mutant. The sofa1 carries an E69K mutation in β-Tubulin 2 (TUB2), and the dominant suppressive effect of E69K mutation is conserved among β-tubulins. We further reveal that incorporation of TUB2^E69K affects microtubule stability, yet fails to rescue the cell wall defects or lateral displacement of microtubules in fra1. Combining with transcriptomic analysis, we propose that the E69K mutation of TUB2 potentially restores the cell elongation by blocking the cell wall integrity (CWI) signaling. Our study sheds new light on the complex mechanism underlying the dwarfism of the fra1 mutant, and further proposes a potential model by which microtubules control plant cell elongation.

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β-微管蛋白2 E69K突变阻断植物细胞伸长过程中细胞壁完整性信号传导。

完整的细胞壁是植物细胞形态发生的前提。编码微管驱动蛋白马达的FRA1/ kinesin - 4a的功能丧失，导致细胞壁力学降低的生长表型矮化。然而，潜在的机制仍然难以捉摸。在这里，通过遗传筛选，我们确定了一个fra1 （sofa1）突变的抑制因子，它特异性地抑制了fra1突变体的矮化表型。sofa1在β-微管蛋白2 （TUB2）中携带E69K突变，E69K突变的显性抑制作用在β-微管蛋白中保守。我们进一步发现，TUB2E69K的掺入会影响微管的稳定性，但不能挽救fra1的细胞壁缺陷或微管的侧向位移。结合转录组学分析，我们提出TUB2的E69K突变可能通过阻断细胞壁完整性（CWI）信号通路来恢复细胞伸长。我们的研究揭示了fra1突变体矮化的复杂机制，并进一步提出了微管控制植物细胞伸长的潜在模型。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

EMBO Reports 生物-生化与分子生物学

CiteScore

11.20

自引率

1.30%

发文量

267

审稿时长

1 months

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