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乙烯通过GPCR和MAPK依赖的方式促进附着胞和致病性相关基因的表达。

Ethylene Promotes Expression of the Appressorium- and Pathogenicity-Related Genes via GPCR- and MAPK-Dependent Manners in .

作者信息

Ren Dandan, Wang Tan, Zhou Ganghan, Ren Weiheng, Duan Xiaomin, Gao Lin, Chen Jiaxu, Xu Ling, Zhu Pinkuan

机构信息

School of Life Sciences, East China Normal University, Shanghai 200241, China.

出版信息

J Fungi (Basel). 2022 May 26;8(6):570. doi: 10.3390/jof8060570.

Abstract

Ethylene (ET) represents a signal that can be sensed by plant pathogenic fungi to accelerate their spore germination and subsequent infection. However, the molecular mechanisms of responses to ET in fungi remain largely unclear. In this study, was investigated via transcriptomic analysis to reveal the genes that account for the ET-regulated fungal development and virulence. The results showed that ET promoted genes encoding for fungal melanin biosynthesis enzymes, extracellular hydrolases, and appressorium-associated structure proteins at 4 h after treatment. When the germination lasted until 24 h, ET induced multiple appressoria from every single spore, but downregulated most of the genes. Loss of selected ET responsive genes encoding for scytalone dehydratase () and cerato-platanin virulence protein () were unable to alter ET sensitivity of in vitro but attenuated the influence of ET on pathogenicity. Knockout of the G-protein-coupled receptors CgGPCR3-1/2 and the MAPK signaling pathway components CgMK1 and CgSte11 resulted in reduced ET sensitivity. Taken together, this study in reports that ET can cause transcription changes in a large set of genes, which are mainly responsible for appressorium development and virulence expression, and these processes are dependent on the GPCR and MAPK pathways.

摘要

乙烯(ET)是一种可被植物病原真菌感知的信号,能加速其孢子萌发及后续感染。然而,真菌中对ET响应的分子机制仍 largely 不清楚。在本研究中,通过转录组分析进行了调查,以揭示解释ET调节真菌发育和毒力的基因。结果表明,处理后4小时,ET促进了编码真菌黑色素生物合成酶、细胞外水解酶和附着胞相关结构蛋白的基因。当萌发持续到24小时时,ET从每个单个孢子诱导多个附着胞,但下调了大多数基因。编码鬼臼毒素脱水酶()和角斑漆斑菌毒力蛋白()的选定ET响应基因的缺失在体外无法改变的ET敏感性,但减弱了ET对致病性的影响。G蛋白偶联受体CgGPCR3 - 1/2以及MAPK信号通路组分CgMK1和CgSte11的敲除导致ET敏感性降低。综上所述,本研究报道ET可导致大量基因的转录变化,这些基因主要负责附着胞发育和毒力表达,且这些过程依赖于GPCR和MAPK途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9811/9224669/9e80da38ed50/jof-08-00570-g001.jpg

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