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内体分选转运复合体III(ESCRT-III)的一个亚基MoIst1参与了[真菌名称未给出]的真菌发育、致病性和自噬过程。

A Subunit of ESCRT-III, MoIst1, Is Involved in Fungal Development, Pathogenicity, and Autophagy in .

作者信息

Sun Lixiao, Qian Hui, Wu Minghua, Zhao Wenhui, Liu Mengyu, Wei Yunyun, Zhu Xueming, Li Lin, Lu Jianping, Lin Fucheng, Liu Xiaohong

机构信息

State Key Laboratory for Managing Biotic and Chemical Treats to the Quality and Safety of Agro-Products, Institute of Biotechnology, Zhejiang University, Hangzhou, China.

State Key Laboratory for Managing Biotic and Chemical Treats to the Quality and Safety of Agro-Products, Institute of Plant Protection and Microbiology, Zhejiang Academy of Agricultural Sciences, Hangzhou, China.

出版信息

Front Plant Sci. 2022 Apr 7;13:845139. doi: 10.3389/fpls.2022.845139. eCollection 2022.

DOI:10.3389/fpls.2022.845139
PMID:35463448
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9021896/
Abstract

The culprit of rice blast, , is a filamentous fungus that seriously affects the yield and quality of rice worldwide. MoIst1, a subunit of ESCRT-III, is involved in identified ubiquitinated proteins and transports them into the intraluminal vesicles of multivesicular bodies (MVBs) for degradation in lysosomes. Here, we identify and characterize MoIst1 in . Disruption of MoIst1 leads to a significant decrease in sporulation and formation of appressoria, defects in response to oxidative stress, cell wall stress, hyperosmotic stress, and reduced pathogenicity. Deletion of MoIst1 also caused the decreased Pmk1 phosphorylation levels, appressorium formation, the delayed translocation and degradation of lipid droplets and glycogen, resulting in a decreased appressorium turgor. In addition, deletion of MoIst1 leads to an abnormal autophagy. In summary, our results indicate that MoIst1 is involved in sporulation, appressorium development, plant penetration, pathogenicity, and autophagy in .

摘要

稻瘟病菌是一种丝状真菌,严重影响全球水稻的产量和品质。MoIst1是内体分选转运复合体III(ESCRT-III)的一个亚基,参与识别泛素化蛋白并将其转运至多泡体(MVB)的腔内小泡中,以便在溶酶体中降解。在此,我们对稻瘟病菌中的MoIst1进行了鉴定和表征。MoIst1的缺失导致孢子形成和附着胞形成显著减少,对氧化应激、细胞壁应激、高渗应激的反应存在缺陷,并且致病性降低。MoIst1的缺失还导致Pmk1磷酸化水平降低、附着胞形成减少、脂滴和糖原的转运及降解延迟,从而导致附着胞膨压降低。此外,MoIst1的缺失导致自噬异常。总之,我们的结果表明,MoIst1参与了稻瘟病菌的孢子形成、附着胞发育、侵染植物、致病性和自噬过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/9021896/4c7109f3e9a9/fpls-13-845139-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/9021896/8f1a573d351d/fpls-13-845139-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/9021896/139a07396711/fpls-13-845139-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/9021896/73f0e9ec2afb/fpls-13-845139-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/9021896/6057c7e6caec/fpls-13-845139-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/9021896/83cee582d671/fpls-13-845139-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/9021896/2adedc7ba573/fpls-13-845139-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/9021896/4c7109f3e9a9/fpls-13-845139-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/9021896/8f1a573d351d/fpls-13-845139-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/9021896/139a07396711/fpls-13-845139-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/9021896/73f0e9ec2afb/fpls-13-845139-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/9021896/6057c7e6caec/fpls-13-845139-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/9021896/83cee582d671/fpls-13-845139-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/9021896/2adedc7ba573/fpls-13-845139-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d98/9021896/4c7109f3e9a9/fpls-13-845139-g007.jpg

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