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UvATG6 与 BAX 抑制剂 1 蛋白相互作用,并在. 中发挥关键作用,包括生长、分生孢子形成和毒力。

UvATG6 Interacts with BAX Inhibitor 1 Proteins and Plays Critical Roles in Growth, Conidiation, and Virulence in .

机构信息

Hubei Key Laboratory of Plant Pathology, College of Plant Science and Technology, Huazhong Agricultural University, Wuhan, China.

出版信息

Microbiol Spectr. 2023 Jun 15;11(3):e0489822. doi: 10.1128/spectrum.04898-22. Epub 2023 Apr 27.

DOI:10.1128/spectrum.04898-22
PMID:37102873
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10269921/
Abstract

Autophagy and apoptosis are evolutionarily conserved catabolic processes involved in regulating development and cellular homeostasis. Bax inhibitor 1 (BI-1) and autophagy protein 6 (ATG6) perform essential functions in these roles, such as cellular differentiation and virulence in various filamentous fungi. However, the functions of ATG6 and BI-1 proteins in development and virulence in the rice false smut fungus Ustilaginoidea virens are still poorly understood. In this study, UvATG6 was characterized in U. virens. The deletion of almost abolished autophagy in and reduced growth, conidial production and germination, and virulence. Stress tolerance assays showed that mutants were sensitive to hyperosmotic, salt, and cell wall integrity stresses but were insensitive to oxidative stress. Furthermore, we found that UvATG6 interacted with UvBI-1 or UvBI-1b and suppressed Bax-induced cell death. We previously found that UvBI-1 could suppress Bax-induced cell death and was a negative regulator of mycelial growth and conidiation. Unlike UvBI-1, UvBI-1b could not suppress cell death. -deleted mutants exhibited decreased growth and conidiation, while the and double deletion reduced the phenotype, indicating that and antagonistically regulate mycelial growth and conidiation. In addition, the and double mutants exhibited decreased virulence. Our results provide evidence of the cross talk of autophagy and apoptosis in and give clues for studying other phytopathogenic fungi. causes destructive panicle disease in rice, significantly threatening agricultural production. UvATG6 is required for autophagy and contributes to growth, conidiation, and virulence in . Additionally, it interacts with the Bax inhibitor 1 proteins UvBI-1 and UvBI-1b. UvBI-1 suppresses cell death induced by Bax, unlike UvBI-1b. negatively regulates growth and conidiation, while is required for these phenotypes. These results indicate that UvBI-1 and UvBI-1b may antagonistically regulate growth and conidiation. In addition, both of them contribute to virulence. Additionally, our results suggest cross talk between autophagy and apoptosis, contributing to the development, adaptability, and virulence of .

摘要

自噬和细胞凋亡是参与调节发育和细胞内稳态的进化保守的分解代谢过程。Bax 抑制剂 1(BI-1)和自噬蛋白 6(ATG6)在这些角色中发挥着重要的功能,如细胞分化和各种丝状真菌的毒力。然而,ATG6 和 BI-1 蛋白在水稻纹枯病菌 Ustilaginoidea virens 发育和毒力中的功能仍知之甚少。在本研究中,对 U. virens 中的 UvATG6 进行了表征。在 中几乎完全缺失 几乎消除了自噬作用,并降低了生长、分生孢子的产生和萌发以及毒力。应激耐受试验表明, 突变体对高渗、盐和细胞壁完整性应激敏感,但对氧化应激不敏感。此外,我们发现 UvATG6 与 UvBI-1 或 UvBI-1b 相互作用并抑制 Bax 诱导的细胞死亡。我们之前发现 UvBI-1 可以抑制 Bax 诱导的细胞死亡,是菌丝生长和分生孢子形成的负调节剂。与 UvBI-1 不同,UvBI-1b 不能抑制细胞死亡。-缺失突变体表现出生长和分生孢子形成减少,而 和 双缺失减少了表型,表明 和 拮抗调节菌丝生长和分生孢子形成。此外, 和 双突变体的毒力降低。我们的结果提供了自噬和细胞凋亡在 中相互作用的证据,并为研究其他植物病原菌提供了线索。Ustilaginoidea virens 引起水稻破坏性穗部病害,严重威胁农业生产。UvATG6 是自噬所必需的,并有助于 在 中的生长、分生孢子形成和毒力。此外,它与 Bax 抑制剂 1 蛋白 UvBI-1 和 UvBI-1b 相互作用。UvBI-1 抑制 Bax 诱导的细胞死亡,而不像 UvBI-1b。 负调控生长和分生孢子形成,而 是这些表型所必需的。这些结果表明 UvBI-1 和 UvBI-1b 可能拮抗调节生长和分生孢子形成。此外,它们都有助于毒力。此外,我们的结果表明自噬和细胞凋亡之间存在对话,有助于 的发育、适应性和毒力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0899/10269921/366c4b9a75fc/spectrum.04898-22-f009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0899/10269921/7d0a08d9f818/spectrum.04898-22-f001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0899/10269921/27b3d7a6bd94/spectrum.04898-22-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0899/10269921/ac8e17d9c29e/spectrum.04898-22-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0899/10269921/96d39d8aba1b/spectrum.04898-22-f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0899/10269921/d1ad9bc1faec/spectrum.04898-22-f008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0899/10269921/366c4b9a75fc/spectrum.04898-22-f009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0899/10269921/7d0a08d9f818/spectrum.04898-22-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0899/10269921/186f0571b6a2/spectrum.04898-22-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0899/10269921/71763d08e965/spectrum.04898-22-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0899/10269921/e822a43651a8/spectrum.04898-22-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0899/10269921/27b3d7a6bd94/spectrum.04898-22-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0899/10269921/ac8e17d9c29e/spectrum.04898-22-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0899/10269921/96d39d8aba1b/spectrum.04898-22-f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0899/10269921/d1ad9bc1faec/spectrum.04898-22-f008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0899/10269921/366c4b9a75fc/spectrum.04898-22-f009.jpg

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