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KMT2-Cre1-Hyd4 调控途径协调调控感染相关形态发生以促进真菌感染。

Coordinated regulation of infection-related morphogenesis by the KMT2-Cre1-Hyd4 regulatory pathway to facilitate fungal infection.

机构信息

CAS Key Laboratory of Insect Developmental and Evolutionary Biology, CAS Center for Excellence in Molecular Plant Sciences, Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200032, China.

CAS Center for Excellence in Biotic Interactions, University of Chinese Academy of Sciences, Beijing 100049, China.

出版信息

Sci Adv. 2020 Mar 25;6(13):eaaz1659. doi: 10.1126/sciadv.aaz1659. eCollection 2020 Mar.

DOI:10.1126/sciadv.aaz1659
PMID:32232158
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7096160/
Abstract

Entomopathogenic fungi can overcome insecticide resistance and represent promising tools for the control of mosquitoes. Better understanding of fungus-mosquito interactions is critical for improvement of fungal efficacy. Upon insect cuticle induction, pathogenic fungi undergo marked infection-related morphological differentiation. However, regulatory mechanisms of fungal infection-related morphogenesis are poorly understood. Here, we show that a histone lysine methyltransferase KMT2 in (MrKMT2) is up-regulated upon cuticle induction. MrKMT2 plays crucial roles in regulating infection-related morphogenesis and pathogenicity by up-regulating the transcription factor gene via H3K4 trimethylation during mosquito cuticle infection. MrCre1 further regulates the cuticle-induced gene to modulate infection structure (appressorium) formation and virulence. Overall, the MrKMT2-MrCre1-MrHyd4 regulatory pathway regulates infection-related morphogenesis and pathogenicity in . These findings reveal that the epigenetic regulatory mechanism plays a pivotal role in regulating fungal pathogenesis in insects, and provide new insights into molecular interactions between pathogenic fungi and insect hosts.

摘要

昆虫病原真菌可以克服杀虫剂抗性,是控制蚊子的有前途的工具。更好地了解真菌与蚊子的相互作用对于提高真菌的功效至关重要。在昆虫表皮诱导后,病原真菌经历明显的与感染相关的形态分化。然而,真菌感染相关形态发生的调控机制还知之甚少。在这里,我们表明在 (MrKMT2)中组蛋白赖氨酸甲基转移酶 KMT2 (MrKMT2)在表皮诱导时上调。MrKMT2 通过在蚊子表皮感染过程中通过 H3K4 三甲基化上调转录因子基因 ,在调节与感染相关的形态发生和致病性方面发挥关键作用。MrCre1 进一步调节表皮诱导基因 来调节感染结构(附着胞)的形成和毒力。总的来说,MrKMT2-MrCre1-MrHyd4 调控途径调节 在与感染相关的形态发生和致病性。这些发现表明,表观遗传调控机制在调节昆虫中的真菌发病机制方面起着关键作用,并为病原真菌与昆虫宿主之间的分子相互作用提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bd4/7096160/7fc9ed9ebdda/aaz1659-F6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bd4/7096160/1da64e115f5c/aaz1659-F1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bd4/7096160/345cc3cea3ae/aaz1659-F2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bd4/7096160/370a71f80470/aaz1659-F3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bd4/7096160/36c0a38fa3a6/aaz1659-F4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bd4/7096160/376a732cb8ae/aaz1659-F5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bd4/7096160/7fc9ed9ebdda/aaz1659-F6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bd4/7096160/1da64e115f5c/aaz1659-F1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bd4/7096160/345cc3cea3ae/aaz1659-F2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bd4/7096160/370a71f80470/aaz1659-F3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bd4/7096160/36c0a38fa3a6/aaz1659-F4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bd4/7096160/376a732cb8ae/aaz1659-F5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bd4/7096160/7fc9ed9ebdda/aaz1659-F6.jpg

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