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一种RACK1家族蛋白通过作为丝裂原活化蛋白激酶(MAPK)信号模块的支架来调节致病性。

A RACK1 family protein regulates pathogenicity of by acting as a scaffold for MAPK signal modules.

作者信息

Kong Guanghui, Li Rui, Huang Weixiong, Yang Yaowen, Guan Tianfang, Liu Jinghan, Li Wen, Hsiang Tom, Xi Pinggen, Li Minhui, Jiang Zide

机构信息

Guangdong Province Key Laboratory of Microbial Signals and Disease Control/National Key Laboratory of Green Pesticide, South China Agricultural University, Guangzhou, China.

State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources, College of Agriculture, Guangxi University, Nanning, China.

出版信息

Virulence. 2025 Dec;16(1):2503429. doi: 10.1080/21505594.2025.2503429. Epub 2025 May 13.

DOI:10.1080/21505594.2025.2503429
PMID:40356437
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12077431/
Abstract

Litchi downy blight caused by is the most destructive disease of litchi (). RACK1 (Receptor for activated C kinase 1) is a group of scaffold proteins, mainly involved in the regulation of various signaling pathways by interacting with signal transduction proteins and affecting the activity of these proteins. In this study, a RACK1 homologue identified in , and named PlRACK1. The protein was found to interact with the mitogen-activated protein kinases, PlMAPK1 and PlMAPK2. CRISPR/Cas9-mediated genome editing technology was used to knock out , and we found that it was involved in mycelial growth, cell wall integrity, ROS metabolism, laccase activity, and pathogenicity of . PlMAPK1 interacted with RACK1, and they jointly regulated sporangiophore branching of . . Transcriptome analysis showed that . MAPK Phosphatase 1 (PlMKP1) and beta-glucoside (PlBglX) were regulated by PlRACK1, both of which were also required for the pathogenicity of . . As well, PlMKP1 also interacted with PlMAPK1 and PlMAPK2. These results provide insights into the direct interactions between RACK1, MAPKs, and MKP, and their functions in growth, development, and pathogenesis in a plant pathogenic oomycete.

摘要

由[病原体名称未给出]引起的荔枝霜霉病是荔枝([荔枝学名未给出])最具毁灭性的病害。RACK1(活化C激酶1受体)是一组支架蛋白,主要通过与信号转导蛋白相互作用并影响这些蛋白的活性来参与各种信号通路的调控。在本研究中,在[物种名称未给出]中鉴定出一个RACK1同源物,并将其命名为PlRACK1。发现该蛋白与丝裂原活化蛋白激酶PlMAPK1和PlMAPK2相互作用。利用CRISPR/Cas9介导的基因组编辑技术敲除[基因名称未给出],我们发现它参与了[病原体名称未给出]的菌丝生长、细胞壁完整性、活性氧代谢、漆酶活性和致病性。PlMAPK1与RACK1相互作用,它们共同调节[病原体名称未给出]的孢子囊梗分支。转录组分析表明,[具体转录组分析结果未给出]。MAPK磷酸酶1(PlMKP1)和β-葡萄糖苷酶(PlBglX)受PlRACK1调控,它们也是[病原体名称未给出]致病性所必需的。此外,PlMKP1也与PlMAPK1和PlMAPK2相互作用。这些结果为RACK1、MAPKs和MKP之间的直接相互作用及其在植物病原卵菌的生长、发育和致病过程中的功能提供了见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6568/12077431/7888d6c4246e/KVIR_A_2503429_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6568/12077431/e6b2bf028a78/KVIR_A_2503429_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6568/12077431/c4cf2cab1a94/KVIR_A_2503429_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6568/12077431/56e840530888/KVIR_A_2503429_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6568/12077431/a75f2cbeb96d/KVIR_A_2503429_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6568/12077431/ed8eca892cc0/KVIR_A_2503429_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6568/12077431/ef1bdb154db7/KVIR_A_2503429_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6568/12077431/008e211d4b28/KVIR_A_2503429_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6568/12077431/7888d6c4246e/KVIR_A_2503429_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6568/12077431/e6b2bf028a78/KVIR_A_2503429_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6568/12077431/c4cf2cab1a94/KVIR_A_2503429_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6568/12077431/56e840530888/KVIR_A_2503429_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6568/12077431/a75f2cbeb96d/KVIR_A_2503429_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6568/12077431/ed8eca892cc0/KVIR_A_2503429_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6568/12077431/ef1bdb154db7/KVIR_A_2503429_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6568/12077431/008e211d4b28/KVIR_A_2503429_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6568/12077431/7888d6c4246e/KVIR_A_2503429_F0008_OC.jpg

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