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膜黏蛋白Msb2调节黄曲霉中黄曲霉毒素的生物合成和致病性。

The membrane mucin Msb2 regulates aflatoxin biosynthesis and pathogenicity in fungus Aspergillus flavus.

作者信息

Qin Ling, Li Ding, Zhao Jiaru, Yang Guang, Wang Yinchun, Yang Kunlong, Tumukunde Elisabeth, Wang Shihua, Yuan Jun

机构信息

Key Laboratory of Pathogenic Fungi and Mycotoxins of Fujian Province, Key Laboratory of Biopesticide and Chemical Biology of Education Ministry, School of Life Sciences, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.

出版信息

Microb Biotechnol. 2021 Mar;14(2):628-642. doi: 10.1111/1751-7915.13701. Epub 2020 Nov 7.

DOI:10.1111/1751-7915.13701
PMID:33159717
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7936294/
Abstract

As a pathogenic fungus, Aspergillus flavus can produce carcinogenic aflatoxins (AFs), which poses a great threat to crops and animals. Msb2, the signalling mucin protein, is a part of mitogen-activated protein kinase (MAPK) pathway which contributes to a range of physiological processes. In this study, the roles of membrane mucin Msb2 were explored in A. flavus by the application of gene disruption. The deletion of msb2 gene (Δmsb2) caused defects in vegetative growth, sporulation and sclerotia formation when compared to WT and complement strain (Δmsb2 ) in A. flavus. Using thin-layer chromatography (TLC) and high-performance liquid chromatography (HPLC) analysis, it was found that deletion of msb2 down-regulated aflatoxin B (AFB ) synthesis and decreased the infection capacity of A. flavus. Consistently, Msb2 responds to cell wall stress and osmotic stress by positively regulating the phosphorylation of MAP kinase. Notably, Δmsb2 mutant exhibited cell wall defect, and it was more sensitive to inhibitor caspofungin when compared to WT and Δmsb2 . Taking together, these results revealed that Msb2 plays key roles in morphological development process, stresses adaptation, secondary metabolism and pathogenicity in fungus A. flavus.

摘要

作为一种致病真菌，黄曲霉能够产生致癌的黄曲霉毒素（AFs），这对农作物和动物构成了巨大威胁。信号黏蛋白Msb2是丝裂原活化蛋白激酶（MAPK）途径的一部分，该途径参与一系列生理过程。在本研究中，通过基因敲除技术探究了膜黏蛋白Msb2在黄曲霉中的作用。与黄曲霉的野生型（WT）和互补菌株（Δmsb2 +）相比，msb2基因缺失（Δmsb2）导致其营养生长、产孢和菌核形成出现缺陷。通过薄层色谱（TLC）和高效液相色谱（HPLC）分析发现，msb2基因的缺失下调了黄曲霉毒素B（AFB）的合成，并降低了黄曲霉的侵染能力。同样，Msb2通过正向调节MAP激酶的磷酸化来响应细胞壁应激和渗透应激。值得注意的是，Δmsb2突变体表现出细胞壁缺陷，与WT和Δmsb2 +相比，它对卡泊芬净抑制剂更为敏感。综上所述，这些结果表明Msb2在黄曲霉的形态发育过程、应激适应、次级代谢和致病性中发挥着关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/7936294/29953fcbf12f/MBT2-14-628-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/7936294/9104fa7d6ec5/MBT2-14-628-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/7936294/99cbfc04b034/MBT2-14-628-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/7936294/65d1391739cb/MBT2-14-628-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/7936294/46e1b01b079e/MBT2-14-628-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/7936294/eb12162ea672/MBT2-14-628-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/7936294/52b036a5b2d7/MBT2-14-628-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/7936294/849cdf1e4604/MBT2-14-628-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/7936294/9e23b41ce3f2/MBT2-14-628-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/7936294/29953fcbf12f/MBT2-14-628-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/7936294/9104fa7d6ec5/MBT2-14-628-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/7936294/99cbfc04b034/MBT2-14-628-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/7936294/65d1391739cb/MBT2-14-628-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/7936294/46e1b01b079e/MBT2-14-628-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/7936294/eb12162ea672/MBT2-14-628-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/7936294/52b036a5b2d7/MBT2-14-628-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/7936294/849cdf1e4604/MBT2-14-628-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/7936294/9e23b41ce3f2/MBT2-14-628-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/7936294/29953fcbf12f/MBT2-14-628-g009.jpg

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