毒力
效应器
生物
分泌物
质外体
细胞生物学
病菌
微生物学
尖孢镰刀菌
乙酰化
信号肽
生物化学
肽序列
遗传学
细胞壁
基因
作者
Jingtao Li,Xiaoying Ma,Chenyang Wang,Sihui Liu,Gang Yu,Mingming Gao,Hengwei Qian,Mengjie Liu,B.F. Luisi,Dean W. Gabriel,Wenxing Liang
出处
期刊:eLife
[eLife Sciences Publications, Ltd.]
日期:2022-11-14
卷期号:11
被引量:6
摘要
Pathogens utilize a panoply of effectors to manipulate plant defense. However, despite their importance, relatively little is actually known about regulation of these virulence factors. Here, we show that the effector Fol-Secreted Virulence-related Protein1 (FolSvp1), secreted from fungal pathogen Fusarium oxysporum f. sp. lycopersici (Fol), directly binds and translocates the tomato pathogenesis-related protein1, SlPR1, from the apoplast outside the plasma membrane to the host nucleus via its nuclear localization signal. Relocation of SlPR1 abolishes generation of the defense signaling peptide, CAPE1, from its C-terminus, and as a consequence, facilitates pathogen invasion of plants. The action of FolSvp1 requires covalent modification by acetylation for full virulence in host tomato tissues. The modification is catalyzed by the Fol FolArd1 lysine acetyltransferase prior to secretion. Addition of an acetyl group to one residue, K167, prevents ubiquitination-dependent degradation of FolSvp1 in both Fol and plant cells with different mechanisms, allowing it to function normally in fungal invasion. Either inactivation of FolSvp1 or removal of the acetyl group on K167 leads to impaired pathogenicity of Fol. These findings indicate that acetylation can regulate the stability of effectors of fungal plant pathogens with impact on virulence.
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