SsPtc3 Modulating SsSmk1-MAPK and Autophagy to Facilitate Growth and Pathogenicity in Sclerotinia sclerotiorum.

IF 4.8 1区 农林科学 Q1 PLANT SCIENCES Molecular plant pathology Pub Date : 2024-12-01 DOI:10.1111/mpp.70037
Wenli Jiao, Dongmeng Ma, Qi Zuo, Yalan Li, Jun Hu, Dongmei Jia, Yanhua Zhang, Jinliang Liu, Xianghui Zhang, Hongyu Pan
{"title":"SsPtc3 Modulating SsSmk1-MAPK and Autophagy to Facilitate Growth and Pathogenicity in Sclerotinia sclerotiorum.","authors":"Wenli Jiao, Dongmeng Ma, Qi Zuo, Yalan Li, Jun Hu, Dongmei Jia, Yanhua Zhang, Jinliang Liu, Xianghui Zhang, Hongyu Pan","doi":"10.1111/mpp.70037","DOIUrl":null,"url":null,"abstract":"<p><p>The compound appressoria of Sclerotinia sclerotiorum can produce cell wall-degrading enzymes, effectors and toxins, which promote penetration and the death of host cells. Subsequently, invasive hyphae (IH) branch rapidly as necrotrophic growth and disease symptoms are observed. S. sclerotiorum can respond to complex stresses and regulate its metabolism to adapt to the external environment. Here we demonstrated that type 2C Ser/Thr phosphatase (PP2C) SsPtc3 responds to nutritional, osmotic, cell wall and oxidative stresses. Loss of function ΔSsptc3 mutants displayed defects in mycelial growth, sclerotia formation and reduced virulence. Phosphoproteomic analyses revealed that SsPtc3 is involved in autophagy and MAPK signalling pathways. We obtained evidence that SsPtc3 negatively modulates the phosphorylation of SsSmk1. SsSmk1 is essential for mycelial growth, compound appressorium formation and pathogenicity, SsPtc3 modulated phosphorylation homeostasis of SsSmk1 to maintain hyphal growth. SsPtc3 interacted with SsAtg1 to influence autophagic flux under starvation. Taken together, these results reveal that SsPtc3 responds to various stresses that modulate autophagy and phosphorylation of SsSmk1-MAPK, which facilitates the growth and virulence of S. sclerotiorum.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"25 12","pages":"e70037"},"PeriodicalIF":4.8000,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11609052/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular plant pathology","FirstCategoryId":"97","ListUrlMain":"https://doi.org/10.1111/mpp.70037","RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"PLANT SCIENCES","Score":null,"Total":0}
引用次数: 0

Abstract

The compound appressoria of Sclerotinia sclerotiorum can produce cell wall-degrading enzymes, effectors and toxins, which promote penetration and the death of host cells. Subsequently, invasive hyphae (IH) branch rapidly as necrotrophic growth and disease symptoms are observed. S. sclerotiorum can respond to complex stresses and regulate its metabolism to adapt to the external environment. Here we demonstrated that type 2C Ser/Thr phosphatase (PP2C) SsPtc3 responds to nutritional, osmotic, cell wall and oxidative stresses. Loss of function ΔSsptc3 mutants displayed defects in mycelial growth, sclerotia formation and reduced virulence. Phosphoproteomic analyses revealed that SsPtc3 is involved in autophagy and MAPK signalling pathways. We obtained evidence that SsPtc3 negatively modulates the phosphorylation of SsSmk1. SsSmk1 is essential for mycelial growth, compound appressorium formation and pathogenicity, SsPtc3 modulated phosphorylation homeostasis of SsSmk1 to maintain hyphal growth. SsPtc3 interacted with SsAtg1 to influence autophagic flux under starvation. Taken together, these results reveal that SsPtc3 responds to various stresses that modulate autophagy and phosphorylation of SsSmk1-MAPK, which facilitates the growth and virulence of S. sclerotiorum.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
SsPtc3调控SsSmk1-MAPK和自噬促进菌核菌生长和致病性
菌核菌复合附着胞可以产生细胞壁降解酶、效应物和毒素,促进宿主细胞的渗透和死亡。随后,随着坏死生长和疾病症状的出现,侵入性菌丝(IH)迅速分支。菌丝体能够对复杂的应激作出反应,调节自身代谢以适应外界环境。在这里,我们证明了2C型丝氨酸/苏氨酸磷酸酶(PP2C) SsPtc3响应营养、渗透、细胞壁和氧化应激。功能丧失ΔSsptc3突变体在菌丝生长、菌核形成和毒力降低方面表现出缺陷。磷酸化蛋白质组学分析显示SsPtc3参与自噬和MAPK信号通路。我们获得了SsPtc3负向调节SsSmk1磷酸化的证据。SsSmk1对菌丝生长、复合附着胞形成和致病性至关重要,SsPtc3调节SsSmk1磷酸化的稳态以维持菌丝生长。饥饿状态下,SsPtc3与SsAtg1相互作用影响自噬通量。综上所述,这些结果表明SsPtc3响应各种胁迫,调节自噬和SsSmk1-MAPK的磷酸化,从而促进菌核葡萄球菌的生长和毒力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Molecular plant pathology
Molecular plant pathology 生物-植物科学
CiteScore
9.40
自引率
4.10%
发文量
120
审稿时长
6-12 weeks
期刊介绍: Molecular Plant Pathology is now an open access journal. Authors pay an article processing charge to publish in the journal and all articles will be freely available to anyone. BSPP members will be granted a 20% discount on article charges. The Editorial focus and policy of the journal has not be changed and the editorial team will continue to apply the same rigorous standards of peer review and acceptance criteria.
期刊最新文献
N Protein of Tomato Spotted Wilt Virus Proven to Be Antagonistic Against Tomato Yellow Leaf Curl Virus in Nicotiana benthamiana. Papain-Like Cysteine Proteases Contribute to Functional Cleavage of Begomoviral V2 Effector Required for Relevant Virulences. Apple Bitter Rot: Biology, Ecology, Omics, Virulence Factors, and Management of Causal Colletotrichum Species. Characterisation of a Betasatellite Associated With Tomato Yellow Leaf Curl Guangdong Virus and Discovery of an Unusual Modulation of Virus Infection Associated With C4 Protein. Two TAL Effectors of Xanthomonas citri pv. malvacearum Induce Water Soaking by Activating GhSWEET14 Genes in Cotton.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1