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ApWD40a是WD40重复蛋白家族的成员之一,对人参链格孢叶枯病菌的真菌发育、毒素合成和致病性至关重要。

ApWD40a, a Member of the WD40-Repeat Protein Family, Is Crucial for Fungal Development, Toxin Synthesis, and Pathogenicity in the Ginseng Alternaria Leaf Blight Fungus .

作者信息

Lan Jinling, Mei Shengjie, Du Yingxue, Chi Meili, Yang Jiayi, Guo Shuliu, Chu Mingliang, He Ronglin, Gao Jie

机构信息

College of Plant Protection, Jilin Agricultural University, Changchun 130118, China.

National Ginseng Products Quality Inspection Testing Center, Yanji 133000, China.

出版信息

J Fungi (Basel). 2025 Jan 14;11(1):59. doi: 10.3390/jof11010059.

DOI:10.3390/jof11010059
PMID:39852478
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11767187/
Abstract

, the primary pathogen that causes ginseng Alternaria leaf blight disease, can lead to a 20-30% reduction in ginseng yield. WD40 repeat-containing proteins are evolutionarily conserved proteins with diverse functions between different organisms. In this study, we characterized the roles of a WD40 repeat-containing protein in . The deletion of impaired the mycelial growth, reduced the sporulation, and significantly decreased the efficiency in utilizing various carbon sources. The Δ mutant showed increased sensitivity to osmotic stress and metal ion stress induced by sorbitol, NaCl, and KCl, but decreased the sensitivity to a cell wall stress factor (SDS) and oxidative stress factors (paraquat and HO). Pathogenicity assays performed on detached ginseng leaves and roots revealed that the disruption of significantly decreased the fungal virulence through attenuating melanin and mycotoxin production by . A comparative transcriptome analysis revealed that was involved in many metabolic and biosynthetic processes, including amino acid metabolism, carbon metabolism, sulfate metabolic pathways, and secondary metabolite pathways. In particular, a significantly upregulated gene that encoded a sulfate permease 2 protein in Δ, named , was deleted in the wild-type strain of . The deletion of resulted in reduced biomass under sulfate-free conditions, demonstrating that the sulfate transport was impaired. Taken together, our findings highlight that played crucial roles in different biological processes and the pathogenicity of through modulating the expressions of genes involved in various primary and secondary metabolic processes.

摘要

引起人参链格孢叶斑病的主要病原菌可导致人参产量降低20%-30%。含WD40重复序列的蛋白质是进化上保守的蛋白质,在不同生物之间具有多种功能。在本研究中,我们表征了一种含WD40重复序列的蛋白质在……中的作用。……的缺失损害了菌丝体生长,减少了孢子形成,并显著降低了利用各种碳源的效率。Δ突变体对由山梨醇、NaCl和KCl诱导的渗透胁迫和金属离子胁迫的敏感性增加,但对细胞壁胁迫因子(SDS)和氧化胁迫因子(百草枯和H₂O₂)的敏感性降低。对离体人参叶片和根进行的致病性测定表明,……的破坏通过减弱……产生黑色素和霉菌毒素而显著降低了真菌毒力。比较转录组分析表明,……参与了许多代谢和生物合成过程,包括氨基酸代谢、碳代谢、硫酸盐代谢途径和次生代谢物途径。特别是,在Δ中一个编码硫酸盐通透酶2蛋白的显著上调基因,命名为……,在……的野生型菌株中被删除。……的缺失导致在无硫酸盐条件下生物量减少,表明硫酸盐运输受损。综上所述,我们的研究结果突出表明,……通过调节参与各种初级和次级代谢过程的基因表达,在不同的生物学过程和……的致病性中发挥了关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9e/11767187/9ca9ba5554ef/jof-11-00059-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9e/11767187/407bda806ee3/jof-11-00059-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9e/11767187/ceb6a4765c1f/jof-11-00059-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9e/11767187/7ce29e97f0d9/jof-11-00059-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9e/11767187/97ecbf4203aa/jof-11-00059-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9e/11767187/7d0315a919a8/jof-11-00059-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9e/11767187/8abe54bb8539/jof-11-00059-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9e/11767187/4890358ec4cb/jof-11-00059-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9e/11767187/9ca9ba5554ef/jof-11-00059-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9e/11767187/407bda806ee3/jof-11-00059-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9e/11767187/ceb6a4765c1f/jof-11-00059-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9e/11767187/7ce29e97f0d9/jof-11-00059-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9e/11767187/97ecbf4203aa/jof-11-00059-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9e/11767187/ba66c60b36f7/jof-11-00059-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9e/11767187/ba1b6715afdb/jof-11-00059-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9e/11767187/7d0315a919a8/jof-11-00059-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9e/11767187/8abe54bb8539/jof-11-00059-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9e/11767187/4890358ec4cb/jof-11-00059-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a9e/11767187/9ca9ba5554ef/jof-11-00059-g010.jpg

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