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CgEde1和CgMca在……的发育和毒力中的作用 。 你提供的原文似乎不完整,“of”后面缺少具体内容。

Roles of CgEde1 and CgMca in Development and Virulence of .

作者信息

Wang Dan, An Bang, Luo Hongli, He Chaozu, Wang Qiannan

机构信息

Sanya Nanfan Research Institute of Hainan University, School of Tropical Agriculture and Forestry, Hainan University, Sanya 572025, China.

Hainan Yazhou Bay Seed Laboratory, Sanya 572025, China.

出版信息

Int J Mol Sci. 2024 Mar 3;25(5):2943. doi: 10.3390/ijms25052943.

DOI:10.3390/ijms25052943
PMID:38474190
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10932086/
Abstract

Anthracnose, induced by , poses a substantial economic threat to rubber tree yields and various other tropical crops. Ede1, an endocytic scaffolding protein, plays a crucial role in endocytic site initiation and maturation in yeast. Metacaspases, sharing structural similarities with caspase family proteases, are essential for maintaining cell fitness. To enhance our understanding of the growth and virulence of , we identified a homologue of Ede1 (CgEde1) in . The knockout of led to impairments in vegetative growth, conidiation, and pathogenicity. Furthermore, we characterized a weakly interacted partner of CgEde1 and CgMca (orthologue of metacaspase). Notably, both the single mutant Δ and the double mutant Δ/Δ exhibited severe defects in conidiation and germination. Polarity establishment and pathogenicity were also disrupted in these mutants. Moreover, a significantly insoluble protein accumulation was observed in Δ and Δ/Δ strains. These findings elucidate the mechanism by which CgEde1 and CgMca regulates the growth and pathogenicity of . Their regulation involves influencing conidiation, polarity establishment, and maintaining cell fitness, providing valuable insights into the intricate interplay between CgEde1 and CgMca in .

摘要

炭疽病由[病原体名称未给出]引起,对橡胶树产量及其他多种热带作物构成重大经济威胁。Ede1是一种内吞支架蛋白,在酵母内吞位点的起始和成熟过程中发挥关键作用。类半胱天冬酶与半胱天冬酶家族蛋白酶在结构上有相似之处,对维持细胞健康至关重要。为加深我们对[病原体名称未给出]生长和毒力的理解,我们在[病原体名称未给出]中鉴定出了Ede1的一个同源物(CgEde1)。[病原体名称未给出]的敲除导致其营养生长、分生孢子形成和致病性受损。此外,我们对CgEde1与CgMca(类半胱天冬酶的直系同源物)的一个弱相互作用伙伴进行了表征。值得注意的是,单突变体Δ和双突变体Δ/Δ在分生孢子形成和萌发方面均表现出严重缺陷。这些突变体的极性建立和致病性也受到破坏。此外,在Δ和Δ/Δ菌株中观察到明显的不溶性蛋白质积累。这些发现阐明了CgEde1和CgMca调节[病原体名称未给出]生长和致病性的机制。它们的调节涉及影响分生孢子形成、极性建立和维持细胞健康,为深入了解[病原体名称未给出]中CgEde1和CgMca之间的复杂相互作用提供了有价值的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/557b/10932086/1dcf3c232ca3/ijms-25-02943-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/557b/10932086/e793740d4fe6/ijms-25-02943-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/557b/10932086/81e318d8b929/ijms-25-02943-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/557b/10932086/897cf6837676/ijms-25-02943-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/557b/10932086/d8546df2cded/ijms-25-02943-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/557b/10932086/83df6c771ac0/ijms-25-02943-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/557b/10932086/0362e7100374/ijms-25-02943-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/557b/10932086/cc5aa356d9ca/ijms-25-02943-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/557b/10932086/9195766f11ed/ijms-25-02943-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/557b/10932086/1dcf3c232ca3/ijms-25-02943-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/557b/10932086/e793740d4fe6/ijms-25-02943-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/557b/10932086/81e318d8b929/ijms-25-02943-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/557b/10932086/897cf6837676/ijms-25-02943-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/557b/10932086/d8546df2cded/ijms-25-02943-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/557b/10932086/83df6c771ac0/ijms-25-02943-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/557b/10932086/0362e7100374/ijms-25-02943-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/557b/10932086/cc5aa356d9ca/ijms-25-02943-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/557b/10932086/9195766f11ed/ijms-25-02943-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/557b/10932086/1dcf3c232ca3/ijms-25-02943-g009.jpg

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