Wang Shaowei, Li Guihua, Wei Yi, Wang Gang, Dang Yuejia, Zhang Penghui, Zhang Shi-Hong
College of Plant Sciences, Jilin University, Changchun, China.
Key Laboratory of Zoonosis Research, Ministry of Education, Jilin University, Changchun, China.
Front Microbiol. 2021 Jan 14;11:605738. doi: 10.3389/fmicb.2020.605738. eCollection 2020.
The phosphorylation status of proteins, which is determined by protein tyrosine kinases (PTKs) and protein tyrosine phosphatases (PTPs), governs many cellular actions. In fungal pathogens, phosphorylation-mediated signal transduction has been considered to be one of the most important mechanisms in pathogenicity. is an economically important corn pathogen. However, whether phosphorylation is involved in its pathogenicity is unknown. A mitochondrial protein tyrosine phosphatase gene, designated , was deduced in through the use of bioinformatics and confirmed by enzyme activity assays and observation of its subcellular localization. We then created a deletion mutant (Δ) to analyze its biological function. The results indicated that the loss of dramatically affected the formation of conidia and the development and differentiation into appressoria. However, the colony growth and conidial morphology of the Δ strains were unaffected. Importantly, the Δ mutant strains exhibited an obvious reduction of virulence, and the delayed infected hyphae failed to expand in the host cells. In comparison with the wild-type, Δ accumulated a larger amount of HO and was sensitive to exogenous HO. Interestingly, the host cells infected by the mutant also exhibited an increased accumulation of HO around the infection sites. Since the expression of the , , , and genes was upregulated with the HO treatment, our results suggest that the mitochondrial protein tyrosine phosphatase PTPM1 plays an essential role in promoting the pathogenicity of by regulating the excessive and production of HO.
蛋白质的磷酸化状态由蛋白质酪氨酸激酶（PTKs）和蛋白质酪氨酸磷酸酶（PTPs）决定，它控制着许多细胞活动。在真菌病原体中，磷酸化介导的信号转导被认为是致病性中最重要的机制之一。[病原体名称]是一种具有经济重要性的玉米病原体。然而，磷酸化是否参与其致病性尚不清楚。通过生物信息学方法在[病原体名称]中推导得到一个线粒体蛋白质酪氨酸磷酸酶基因，命名为[基因名称]，并通过酶活性测定和亚细胞定位观察进行了确认。然后我们构建了一个[基因名称]缺失突变体（Δ[基因名称]）来分析其生物学功能。结果表明，[基因名称]的缺失显著影响分生孢子的形成以及附着胞的发育和分化。然而，Δ[基因名称]菌株的菌落生长和分生孢子形态未受影响。重要的是，Δ[基因名称]突变体菌株的毒力明显降低，感染菌丝在宿主细胞中延迟生长且无法扩展。与野生型相比，Δ[基因名称]积累了大量的H₂O₂并且对外源H₂O₂敏感。有趣的是，被突变体感染的宿主细胞在感染部位周围也表现出H₂O₂积累增加。由于[相关基因名称]、[相关基因名称]、[相关基因名称]、[相关基因名称]和[相关基因名称]基因的表达在H₂O₂处理后上调，我们的结果表明线粒体蛋白质酪氨酸磷酸酶PTPM1通过调节过量的H₂O₂产生在促进[病原体名称]的致病性中起重要作用。
