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绒毡蛋白 ClVelB 参与弯孢叶斑病菌营养分化、氧化应激响应、次生代谢和致病过程的调控。

Involvement of a velvet protein ClVelB in the regulation of vegetative differentiation, oxidative stress response, secondary metabolism, and virulence in Curvularia lunata.

机构信息

School of Agriculture and Biology, Shanghai Jiaotong University, 800 Dongchuan Road, Shanghai 200240, P. R. China.

State Key Laboratory of Microbial Metabolism, Shanghai Jiaotong University, 800 Dongchuan Road, Shanghai 200240, P. R. China.

出版信息

Sci Rep. 2017 Apr 10;7:46054. doi: 10.1038/srep46054.

DOI:10.1038/srep46054
PMID:28393907
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5385503/
Abstract

The ortholog of Aspergillus nidulans VelB, which is known as ClVelB, was studied to gain a broader insight into the functions of a velvet protein in Curvularia lunata. With the expected common and specific functions of ClVelB, the deletion of clvelB results in similar though not identical phenotypes. The pathogenicity assays revealed that ΔClVelB was impaired in colonizing the host tissue, which corresponds to the finding that ClVelB controls the production of conidia and the methyl 5-(hydroxymethyl) furan-2-carboxylate toxin in C. lunata. However, the deletion of clvelB led to the increase in aerial hyphae and melanin formation. In addition, ΔClVelB showed a decreased sensitivity to iprodione and fludioxonil fungicides and a decreased resistance to cell wall-damaging agents and osmotic stress and tolerance to HO. The ultrastructural analysis indicated that the cell wall of ΔClVelB became thinner, which agrees with the finding that the accumulated level of glycerol in ΔClVelB is lower than the wild-type. Furthermore, the interaction of ClVelB with ClVeA and ClVosA was identified in the present research through the yeast two-hybrid and bimolecular fluorescence complementation assays. Results indicate that ClVelB plays a vital role in the regulation of various cellular processes in C. lunata.

摘要

青霉 nidulans VelB 的同源物,即 ClVelB,被研究以更深入地了解弯孢霉中 velvet 蛋白的功能。ClVelB 具有预期的共同和特定功能,clvelB 的缺失导致类似但不完全相同的表型。致病性测定表明,ΔClVelB 在定植宿主组织方面受损,这与 ClVelB 控制弯孢霉产孢和甲基 5-(羟甲基)糠酸 2-羧酸毒素的发现一致。然而,clvelB 的缺失导致气生菌丝和黑色素形成增加。此外,ΔClVelB 对异菌脲和氟啶胺杀菌剂的敏感性降低,对细胞壁损伤剂和渗透压胁迫的抗性降低,对 HO 的耐受性增加。超微结构分析表明,ΔClVelB 的细胞壁变薄,这与甘油在 ΔClVelB 中的积累水平低于野生型的发现一致。此外,本研究通过酵母双杂交和双分子荧光互补测定鉴定了 ClVelB 与 ClVeA 和 ClVosA 的相互作用。结果表明,ClVelB 在弯孢霉的各种细胞过程的调节中起着至关重要的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dff/5385503/db09daedc599/srep46054-f13.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dff/5385503/bb59cc62be71/srep46054-f5.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dff/5385503/966131531ec1/srep46054-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dff/5385503/bee5d2d206f5/srep46054-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dff/5385503/5329e830b563/srep46054-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dff/5385503/9e7e3d44dfb7/srep46054-f10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dff/5385503/0560bc2d727f/srep46054-f11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dff/5385503/385609f50b6a/srep46054-f12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dff/5385503/db09daedc599/srep46054-f13.jpg

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