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Cla4 激酶在构巢曲霉的极性生长过程中触发 Rac1-GEF Cdc24 的降解。

Cla4 kinase triggers destruction of the Rac1-GEF Cdc24 during polarized growth in Ustilago maydis.

机构信息

Department of Biology, University of Marburg, 35032 Marburg, Germany.

出版信息

Mol Biol Cell. 2011 Sep;22(17):3253-62. doi: 10.1091/mbc.E11-04-0314. Epub 2011 Jul 14.

DOI:10.1091/mbc.E11-04-0314
PMID:21757543
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3164470/
Abstract

Dimorphic switching from budding to filamentous growth is a characteristic feature of many pathogenic fungi. In the fungal model organism Ustilago maydis polarized growth is induced by the multiallelic b mating type locus and requires the Rho family GTPase Rac1. Here we show that mating type-induced polarized growth involves negative feedback regulation of the Rac1-specific guanine nucleotide exchange factor (GEF) Cdc24. Although Cdc24 is essential for polarized growth, its concentration is drastically diminished during filament formation. Cdc24 is part of a protein complex that also contains the scaffold protein Bem1 and the PAK kinase Cla4. Activation of Rac1 results in Cla4-dependent degradation of the Rac1-GEF Cdc24, thus creating a regulatory negative feedback loop. We generated mutants of Cdc24 that are resistant to Cla4-dependent destruction. Expression of stable Cdc24 variants interfered with filament formation, indicating that negative feedback regulation of Cdc24 is critical for the establishment of polarized growth.

摘要

从出芽到丝状生长的二态性转换是许多致病性真菌的特征。在真菌模式生物玉米黑粉菌中，极化生长是由多等位基因 b 交配型基因座诱导的，需要 Rho 家族 GTPase Rac1。在这里，我们表明交配型诱导的极化生长涉及 Rac1 特异性鸟嘌呤核苷酸交换因子 (GEF) Cdc24 的负反馈调节。尽管 Cdc24 对于极化生长是必需的，但在丝状形成过程中其浓度会急剧降低。Cdc24 是包含支架蛋白 Bem1 和 PAK 激酶 Cla4 的蛋白质复合物的一部分。Rac1 的激活导致 Cla4 依赖性降解 Rac1-GEF Cdc24，从而形成调节负反馈环。我们生成了对 Cla4 依赖性破坏有抗性的 Cdc24 突变体。稳定 Cdc24 变体的表达干扰了丝状形成，表明 Cdc24 的负反馈调节对于建立极化生长至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2728/3164470/66c9ce2b8e4d/3253fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2728/3164470/76cebd9400d9/3253fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2728/3164470/c3c420eb2d38/3253fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2728/3164470/9f5281c1c80f/3253fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2728/3164470/4e9483251009/3253fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2728/3164470/56f177cfe631/3253fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2728/3164470/66c9ce2b8e4d/3253fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2728/3164470/76cebd9400d9/3253fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2728/3164470/c3c420eb2d38/3253fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2728/3164470/9f5281c1c80f/3253fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2728/3164470/4e9483251009/3253fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2728/3164470/56f177cfe631/3253fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2728/3164470/66c9ce2b8e4d/3253fig6.jpg

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