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AGC/AKT蛋白激酶SCH9对[病原体名称未给出]的致病发育和越冬存活至关重要。

AGC/AKT Protein Kinase SCH9 Is Critical to Pathogenic Development and Overwintering Survival in .

作者信息

Batool Wajjiha, Liu Chang, Fan Xiaoning, Zhang Penghui, Hu Yan, Wei Yi, Zhang Shi-Hong

机构信息

The Key Laboratory for Extreme-Environmental Microbiology, College of Plant Protection, Shenyang Agricultural University, Shenyang 110866, China.

出版信息

J Fungi (Basel). 2022 Jul 31;8(8):810. doi: 10.3390/jof8080810.

DOI:10.3390/jof8080810
PMID:36012798
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9410157/
Abstract

Primary inoculum that survives overwintering is one of the key factors that determine the outbreak of plant disease. Pathogenic resting structures, such as chlamydospores, are an ideal inoculum for plant disease. Puzzlingly, , a devastating fungal pathogen responsible for blast disease in rice, hardly form any morphologically changed resting structures, and we hypothesize that mainly relies on its physiological alteration to survive overwintering or other harsh environments. However, little progress on research into regulatory genes that facilitate the overwintering of rice blast pathogens has been made so far. Serine threonine protein kinase AGC/AKT, MoSch9, plays an important role in the spore-mediated pathogenesis of . Building on this finding, we discovered that in genetic and biological terms, MoSch9 plays a critical role in conidiophore stalk formation, hyphal-mediated pathogenesis, cold stress tolerance, and overwintering survival of . We discovered that the formation of conidiophore stalks and disease propagation using spores was severely compromised in the mutant strains, whereas hyphal-mediated pathogenesis and the root infection capability of were completely eradicated due to MoSch9 deleted mutants' inability to form an appressorium-like structure. Most importantly, the functional and transcriptomic study of wild-type and MoSch9 mutant strains showed that MoSch9 plays a regulatory role in cold stress tolerance of through the transcription regulation of secondary metabolite synthesis, ATP hydrolyzing, and cell wall integrity proteins during osmotic stress and cold temperatures. From these results, we conclude that MoSch9 is essential for fungal infection-related morphogenesis and overwintering of .

摘要

存活过越冬期的初始接种体是决定植物病害爆发的关键因素之一。诸如厚垣孢子等致病休眠结构是植物病害的理想接种体。令人费解的是,导致水稻稻瘟病的毁灭性真菌病原体几乎不形成任何形态发生变化的休眠结构,我们推测它主要依靠其生理变化来度过越冬期或其他恶劣环境。然而,迄今为止,在促进稻瘟病菌越冬的调控基因研究方面进展甚微。丝氨酸苏氨酸蛋白激酶AGC/AKT,即MoSch9,在稻瘟病菌的孢子介导致病过程中发挥重要作用。基于这一发现,我们发现,从遗传学和生物学角度来看,MoSch9在分生孢子梗形成、菌丝介导致病、耐冷胁迫和稻瘟病菌越冬存活方面发挥关键作用。我们发现,在突变菌株中,分生孢子梗的形成以及利用孢子进行的病害传播严重受损,而由于MoSch9缺失突变体无法形成附着胞样结构,稻瘟病菌的菌丝介导致病和根部感染能力被完全消除。最重要的是,对野生型和MoSch9突变菌株的功能和转录组学研究表明,在渗透胁迫和低温期间,MoSch9通过对次生代谢物合成、ATP水解和细胞壁完整性蛋白的转录调控,在稻瘟病菌的耐冷胁迫中发挥调节作用。从这些结果来看,我们得出结论,MoSch9对稻瘟病菌的真菌感染相关形态发生和越冬至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afd6/9410157/0c9d2734368d/jof-08-00810-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afd6/9410157/2e28dd2eacc3/jof-08-00810-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afd6/9410157/4ebd1dacef52/jof-08-00810-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afd6/9410157/63c85b10760f/jof-08-00810-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afd6/9410157/3b33b53e2be2/jof-08-00810-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afd6/9410157/30b441dc6376/jof-08-00810-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afd6/9410157/dd65bac40075/jof-08-00810-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afd6/9410157/0c9d2734368d/jof-08-00810-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afd6/9410157/2e28dd2eacc3/jof-08-00810-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afd6/9410157/4ebd1dacef52/jof-08-00810-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afd6/9410157/63c85b10760f/jof-08-00810-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afd6/9410157/3b33b53e2be2/jof-08-00810-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afd6/9410157/30b441dc6376/jof-08-00810-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afd6/9410157/dd65bac40075/jof-08-00810-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afd6/9410157/0c9d2734368d/jof-08-00810-g007.jpg

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