A putative PKA phosphorylation site S227 in MoSom1 is essential for infection-related morphogenesis and pathogenicity in Magnaporthe oryzae

IF 2.6 2区生物学 Q3 CELL BIOLOGY

Cellular Microbiology Pub Date : 2021-06-05 DOI:10.1111/cmi.13370

Shuzhen Deng, Lin Xu, Zhe Xu, Wuyun Lv, Zhengxian Chen, Nan Yang, Nicholas J. Talbot, Zhengyi Wang

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引用次数: 2

Abstract

In the rice blast fungus Magnaporthe oryzae, the cAMP signalling pathway plays a critical role in regulating leaf surface recognition and the initiation of appressorium development. Direct downstream targets of the cAMP signalling pathway are, however, not well-characterised. The MoSom1 protein functions downstream of the cAMP dependent protein kinase A (cAMP-PKA) and is essential for infection-related morphogenesis and pathogenicity. In this study, we show that mutation of a putative PKA phosphorylation site in MoSom1 is essential for its role in appressorium differentiation and pathogenicity in M. oryzae. Mutation of serine 227 in MoSom1 by deletion or serine (S) substitution to alanine (A), valine (V) or tyrosine (Y), resulted in defects of conidiation, appressorium-like structure formation and fungal pathogenicity. Western blot analysis confirmed that S227 in MoSom1 is a putative PKA phosphorylation site. Furthermore, a ΔMosom1 mutant showed reduced expression of PMK1 and was defective in Pmk1 phosphorylation, indicating that the Pmk1 mitogen-activated protein kinase (MAPK) acts downstream of MoSom1 in M. oryzae. We conclude that the cAMP-PKA pathway may regulate the Pmk1 MAPK pathway through MoSom1 during rice infection by the blast fungus.

Take Aways

S227 is crucial for MoSom1 function in M. oryzae.
S227 in MoSom1 was identified as a putative PKA phosphorylation site in M. oryzae.
S227 is essential for infection-related morphogenesis and pathogenicity in M. oryzae.

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据推测，PKA磷酸化位点S227在水稻大孔霉感染相关的形态发生和致病性中是必不可少的

在稻瘟病菌Magnaporthe oryzae中，cAMP信号通路在调节叶片表面识别和附着胞发育启动中起关键作用。然而，cAMP信号通路的直接下游靶点尚未得到很好的表征。MoSom1蛋白在cAMP依赖性蛋白激酶A (cAMP- pka)下游起作用，对感染相关的形态发生和致病性至关重要。在这项研究中，我们发现MoSom1中一个假定的PKA磷酸化位点的突变对m.o ryzae附着胞分化和致病性的作用至关重要。MoSom1中丝氨酸227的缺失或丝氨酸(S)被丙氨酸(A)、缬氨酸(V)或酪氨酸(Y)取代，导致了孢子萌发、附着胞样结构形成和真菌致病性的缺陷。Western blot分析证实，MoSom1中的S227是推测的PKA磷酸化位点。此外，ΔMosom1突变体显示PMK1表达减少，PMK1磷酸化缺陷，表明m.o ryzae中PMK1丝裂原活化蛋白激酶(MAPK)作用于MoSom1的下游。我们认为cAMP-PKA通路可能在稻瘟病菌侵染水稻过程中通过MoSom1调控Pmk1 - MAPK通路。Take Aways S227对m.o ryzae中MoSom1的功能至关重要。在M. oryzae中，MoSom1中的S227被认为是PKA磷酸化位点。S227是m.o ryzae感染相关形态发生和致病性所必需的。

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来源期刊

Cellular Microbiology 生物-微生物学

CiteScore

9.70

自引率

0.00%

发文量

审稿时长

3 months

期刊介绍： Cellular Microbiology aims to publish outstanding contributions to the understanding of interactions between microbes, prokaryotes and eukaryotes, and their host in the context of pathogenic or mutualistic relationships, including co-infections and microbiota. We welcome studies on single cells, animals and plants, and encourage the use of model hosts and organoid cultures. Submission on cell and molecular biological aspects of microbes, such as their intracellular organization or the establishment and maintenance of their architecture in relation to virulence and pathogenicity are also encouraged. Contributions must provide mechanistic insights supported by quantitative data obtained through imaging, cellular, biochemical, structural or genetic approaches.