Yu Lu, Yang Yuchen, Xiong Dianguang, Tian Chengming
The Key Laboratory for Silviculture and Conservation of Ministry of Education, College of Forestry, Beijing Forestry Universitygrid.66741.32, Beijing, China.
Beijing Key Laboratory for Forest Pest Control, Beijing Forestry Universitygrid.66741.32, Beijing, China.
Microbiol Spectr. 2022 Aug 31;10(4):e0017622. doi: 10.1128/spectrum.00176-22. Epub 2022 Jun 23.
Pmk1, a highly conserved pathogenicity-related mitogen-activated protein kinase (MAPK) in pathogenic fungi, is phosphorylated and activated by MAP2K and acts as a global regulator of fungal infection and invasive growth by modulating downstream targets. However, the hierarchical CcPmk1 regulatory network in , the main causal agent of canker disease in many woody plant species, is still unclear. In this study, we analyzed and compared the phosphoproteomes and metabolomes of Δ and wild-type strains and identified pathogenicity-related downstream targets of CcPmk1. We found that CcPmk1 could interact with the downstream homeobox transcription factor CcSte12 and affect its phosphorylation. In addition, the Δ displayed defective phenotypes that were similar to yet not identical to that of the Δ and included significantly reduced fungal growth, conidiation, and virulence. Remarkably, CcPmk1 could phosphorylate proteins translated from a putative secondary metabolism-related gene cluster, which is specific to , and the phosphorylation of several peptides was completely abolished in the Δ. Functional analysis of the core gene () in this gene cluster revealed its essential roles in fungal growth and virulence. Metabolomic analysis showed that amino acid metabolism and biosynthesis of secondary metabolites, lipids, and lipid-like molecules significantly differed between wild type and Δ. Importantly, most of the annotated lipids and lipid-like molecules were significantly downregulated in the Δ compared to the wild type. Collectively, these findings suggest that CcPmk1 may regulate a small number of downstream master regulators to control fungal growth, conidiation, and virulence in . Understanding the pathogenic mechanisms of plant pathogens is a prerequisite to developing effective disease-control methods. The Pmk1 MAPK is highly conserved among phytopathogenic fungi and acts as a global regulator of fungal pathogenicity by modulating downstream transcription factors or other components. However, the regulatory network of CcPmk1 from remains enigmatic. The present data provide evidence that the core pathogenicity regulator CcPmk1 modulates a few downstream master regulators to control fungal virulence in through transcription or phosphorylation and that CcPmk1 may be a potential target for disease control.
Pmk1是致病真菌中一种高度保守的与致病性相关的丝裂原活化蛋白激酶（MAPK），它被MAP2K磷酸化并激活，通过调节下游靶点，作为真菌感染和侵袭性生长的全局调节因子。然而，在许多木本植物溃疡病的主要病原菌中，分层的CcPmk1调控网络仍不清楚。在本研究中，我们分析并比较了Δ菌株和野生型菌株的磷酸化蛋白质组和代谢组，并鉴定了CcPmk1与致病性相关的下游靶点。我们发现CcPmk1可以与下游同源盒转录因子CcSte12相互作用并影响其磷酸化。此外，Δ菌株表现出与Δ菌株相似但不完全相同的缺陷表型，包括真菌生长、产孢和毒力显著降低。值得注意的是，CcPmk1可以磷酸化从一个特定于该病原菌的假定次生代谢相关基因簇翻译而来的蛋白质，并且在Δ菌株中几种肽段的磷酸化完全消失。对该基因簇中的核心基因（）进行功能分析，揭示了其在真菌生长和毒力中的重要作用。代谢组学分析表明，野生型和Δ菌株之间氨基酸代谢以及次生代谢产物、脂质和类脂分子的生物合成存在显著差异。重要的是，与野生型相比，Δ菌株中大多数注释的脂质和类脂分子显著下调。总的来说，这些发现表明CcPmk1可能通过调节少数下游主调控因子来控制该病原菌的真菌生长、产孢和毒力。了解植物病原菌的致病机制是开发有效病害控制方法的前提。Pmk1 MAPK在植物病原真菌中高度保守，通过调节下游转录因子或其他成分作为真菌致病性的全局调节因子。然而，来自该病原菌的CcPmk1调控网络仍然神秘。目前的数据提供了证据，表明核心致病性调节因子CcPmk1通过转录或磷酸化调节少数下游主调控因子来控制该病原菌的真菌毒力，并且CcPmk1可能是病害控制的潜在靶点。
