The velvet proteins CsVosA and CsVelB coordinate growth, cell wall integrity, sporulation, conidial viability and pathogenicity in the rubber anthracnose fungus Colletotrichum siamense

The velvet proteins CsVosA and CsVelB coordinate growth, cell wall integrity, sporulation, conidial viability and pathogenicity in the rubber anthracnose fungus Colletotrichum siamense
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绒状蛋白 CsVosA 和 CsVelB 协调橡胶炭疽真菌(Colletotrichum siamense)的生长、细胞壁完整性、孢子形成、分生孢子活力和致病性

DOI:
10.1016/j.micres.2022.127290
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发表时间:
2023
影响因子:
6.7
通讯作者:
Zhiqiang Liu
Zhiqiang Liu
中科院分区:
生物学2区
文献类型:
--
作者:
Jing Gao;Shuangzhen Zhou;Wen Tang;Jinhong Wang;Huanqing Liu;Ying Zhang;Liya Wang;Xiaoyu Li;Zhiqiang Liu

文献摘要

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炭疽病(Colletotrichumsiamense)是炭疽菌属复合种的一员,是引起橡胶炭疽病的主要病原菌,给天然橡胶生产造成巨大的经济损失。天鹅绒家族蛋白是真菌特有的蛋白质,在调节发育和次生代谢方面发挥着重要作用。在本研究中,我们鉴定了两种天鹅绒蛋白CsVosA和CsVelB Inc.研究了Nidulans曲霉中VOSA和VelB的同源基因。CsVosA定位于胞核,CsVelB定位于胞核和胞浆。CsvosAorCsvelB基因缺失会导致菌丝生长缓慢,CsvelB基因敲除突变体的菌丝密度也较低。CsVosA和CsVelB参与调节几丁质的代谢和分布,导致FC细胞壁完整性的变化。西门斯。此外,CsvosAor CsvelB的破坏会降低分生孢子的产量和活力,ΔCsvosA和ΔCsvelB突变体也失去了产生子实体的能力。致病力分析表明,缺失CsvosA或CsvelB可以降低毒力,这两个天鹅绒基因是Fc完全毒力所必需的。西门斯。酵母双杂交和双分子荧光互补分析表明,CsVosA能与CsVelB相互作用,在分生孢子OFC中形成CsVosA-CsVelB复合体。Siamense,它可能在维持细胞壁完整性和分生孢子活力方面发挥重要作用。此外,CsVelB还参与调节Fc黑色素的产生。西门斯。综上所述,CsVosA和CsVelB调控营养生长、细胞壁完整性、无性/有性产孢量、分生孢子活力和致病力。西门斯。
Colletotrichumsiamense, a member ofColletotrichum gloeosporioidescomplex species, is the primary pathogen causing rubber anthracnose, which leads to significant economic loss in natural rubber production. Velvet family proteins are fungal-specific proteins and play an essential role in regulating development and secondary metabolism. In this study, we characterized two velvet proteins CsVosA and CsVelB inC. siamenseas the orthologs of VosA and VelB inAspergillus nidulans. CsVosA is located in the nucleus, and CsVelB displays a localization in both the nucleus and the cytoplasm. DeletingCsvosAorCsvelBresults in a slow growth rate, and the CsvelB-knockout mutants also exhibit low mycelial density. CsVosA and CsVelB are involved in regulating chitin metabolism and distribution, leading to the variation in the cell wall integrity ofC. siamense. Furthermore, disruption ofCsvosAorCsvelBcan decrease conidial production and viability, and the ΔCsvosAand ΔCsvelBmutants also lose the ability to produce fruiting bodies. Pathogenicity assays show that deleting CsvosA or CsvelB can lower the virulence, and the two velvet genes are essential for the full virulence ofC. siamense. Based on the results of the yeast two-hybrid analysis and bimolecular fluorescence complementation assays, CsVosA can interact with CsVelB and form the complex CsVosA-CsVelB in the conidia ofC. siamense, which may play essential roles in maintaining the cell wall integrity and conidial viability. In addition, CsVelB is also involved in regulating melanin production ofC. siamense. In conclusion, CsVosA and CsVelB regulate vegetative growth, cell wall integrity, asexual/sexual sporulation, conidial viability and virulence inC. siamense.