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编码泛酸盐转运蛋白对于真菌的生长、菌丝体穿透和致病性是必需的。

encoding a pantothenate transporter protein is required for fungal growth, mycelial penetration and pathogenicity of .

作者信息

Kamau Stephen Mwangi, Li Yongtai, Sun Tiange, Liu Feng, Zhu Qian-Hao, Zhang Xinyu, Sun Jie, Li Yanjun

机构信息

The Key Laboratory of Oasis Eco-Agriculture, Agriculture College, Shihezi University, Shihezi, Xinjiang, China.

CSIRO Agriculture and Food, Canberra, ACT, Australia.

出版信息

Front Microbiol. 2025 Jan 17;15:1508765. doi: 10.3389/fmicb.2024.1508765. eCollection 2024.

DOI:10.3389/fmicb.2024.1508765
PMID:39895932
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11783681/
Abstract

INTRODUCTION

The soil-borne vascular fungus is a phytopathogenic fungus known to attack cotton crop causing Verticillium wilt. In previous study, we identified a pantothenate transporter gene () in which can be induced by root exudates from a susceptible cotton variety.

METHODS

In this study, we generated deletion mutants and complementary strain via homologous recombination by a PEG-mediated transformation method and used for the gene functional characterization.

RESULTS AND DISCUSSION

The deletion mutants displayed reduced colony growth, melanin production, spore yield and germination rate, showed abnormal mycelial branching and decreased ability of mycelial penetration and utilization of nutrients (carbon, amino acids and vitamin), leading to a lower pathogenicity. Comparative transcriptome analysis of wild-type and mutant strain cultivated on sterilized carboxymethyl cellophane membranes found that the amino sugar and nucleotide sugar metabolism pathway, which was related to chitin synthesis and degradation as well as UDP-glucose synthesis, was the most significantly down-regulated pathway in deletion mutant. Chitin and β-1,3-glucan content determination found that the chitin content in deletion mutants was significantly lower, while β-1,3-glucan content was higher than that of wild-type and complementary strains. The ratio change of chitin and β-1,3-glucan content in deletion mutants might lead to abnormal branching of mycelium, resulting in the reduced penetration ability of . The decreased chitin content in mutants impaired the fungal cell wall integrity, leading to their increased sensitivity to external stresses.

CONCLUSION

Together, the results demonstrated that is required for growth, development, resistance to external stresses, mycelial penetration and pathogenicity of .

摘要

引言

土壤传播的维管束真菌是一种植物病原真菌,已知会侵袭棉花作物,导致棉花黄萎病。在先前的研究中,我们在[具体真菌名称]中鉴定出一个泛酸盐转运蛋白基因([基因名称]),该基因可被感病棉花品种的根系分泌物诱导。

方法

在本研究中,我们通过聚乙二醇(PEG)介导的转化方法,利用同源重组产生了[基因名称]缺失突变体和互补菌株,并用于该基因的功能表征。

结果与讨论

[基因名称]缺失突变体的菌落生长、黑色素产生、孢子产量和萌发率均降低,菌丝分支异常,菌丝穿透和营养物质(碳、氨基酸和维生素)利用能力下降,导致致病性降低。对在无菌羧甲基纤维素膜上培养的野生型和突变菌株进行比较转录组分析发现,与几丁质合成与降解以及尿苷二磷酸葡萄糖合成相关的氨基糖和核苷酸糖代谢途径是[基因名称]缺失突变体中下调最显著的途径。几丁质和β-1,3-葡聚糖含量测定发现,[基因名称]缺失突变体中的几丁质含量显著降低,而β-1,3-葡聚糖含量高于野生型和互补菌株。[基因名称]缺失突变体中几丁质和β-1,3-葡聚糖含量的比例变化可能导致菌丝分支异常,从而导致[具体真菌名称]的穿透能力降低。[基因名称]突变体中几丁质含量的降低损害了真菌细胞壁的完整性,导致它们对外界压力的敏感性增加。

结论

总之,结果表明[基因名称]是[具体真菌名称]生长、发育、对外界压力的抗性、菌丝穿透和致病性所必需的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/e66567296a05/fmicb-15-1508765-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/e9e592f41061/fmicb-15-1508765-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/bc50c6f1b303/fmicb-15-1508765-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/02f728004bf2/fmicb-15-1508765-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/4b9a5a7254c7/fmicb-15-1508765-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/121fccf21988/fmicb-15-1508765-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/246a119d0069/fmicb-15-1508765-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/c7939896b866/fmicb-15-1508765-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/46e838ab333b/fmicb-15-1508765-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/03ec7f04af79/fmicb-15-1508765-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/e66567296a05/fmicb-15-1508765-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/e9e592f41061/fmicb-15-1508765-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/bc50c6f1b303/fmicb-15-1508765-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/02f728004bf2/fmicb-15-1508765-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/4b9a5a7254c7/fmicb-15-1508765-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/121fccf21988/fmicb-15-1508765-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/246a119d0069/fmicb-15-1508765-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/c7939896b866/fmicb-15-1508765-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/46e838ab333b/fmicb-15-1508765-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/03ec7f04af79/fmicb-15-1508765-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a52/11783681/e66567296a05/fmicb-15-1508765-g010.jpg

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