{"title":"ClBeclin1 Positively Regulates Citrus Defence Against Citrus Yellow Vein Clearing Virus Through Mediating Autophagy-Dependent Degradation of ClAPX1.","authors":"Jiajun Wang, Ling Yu, Jinfa Zhao, Shimin Fu, Yalin Mei, Binghai Lou, Yan Zhou","doi":"10.1111/mpp.70041","DOIUrl":null,"url":null,"abstract":"<p><p>Autophagy, one of the most widespread and highly conserved protein degradation systems in eukaryotic cells, plays an important role in plant growth, development and stress response. Beclin 1 is a core component of the phosphatidylinositol 3-kinase (PI3K) autophagy complex and positively regulates plant immunity against viruses. The upregulation of Eureka lemon ClBeclin1 was observed in response to citrus yellow vein clearing virus (CYVCV) infection. However, the function of ClBeclin1 and the underlying mechanism during CYVCV colonisation remain unclear. Here, the resistance evaluation of the overexpression and silencing of ClBeclin1 in Eureka lemon hairy roots revealed it as a positive regulator of citrus immunity against CYVCV. Transcriptomic profiling and metabolic analyses along with genetic evidence implied that the overexpression of ClBeclin1 positively triggered reactive oxygen species (ROS)- and jasmonic acid (JA)-mediated immunity in citrus. The accumulation of ROS and JA contents was attributed to the autophagic degradation of the ROS scavenger ClAPX1 via ClBeclin1 overexpression. Exogenous application of either H<sub>2</sub>O<sub>2</sub> or JA significantly reduced CYVCV colonisation and vein-clearing symptoms on the host. Collectively, our findings indicate that ClBeclin1 activation contributes to citrus immunity against CYVCV through triggering ROS- and JA-mediated defence responses, and the accumulation of ROS and JA resulted from the autophagic degradation of ClAPX1 by ClBeclin1.</p>","PeriodicalId":18763,"journal":{"name":"Molecular plant pathology","volume":"25 12","pages":"e70041"},"PeriodicalIF":4.8000,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11631719/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular plant pathology","FirstCategoryId":"97","ListUrlMain":"https://doi.org/10.1111/mpp.70041","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
Autophagy, one of the most widespread and highly conserved protein degradation systems in eukaryotic cells, plays an important role in plant growth, development and stress response. Beclin 1 is a core component of the phosphatidylinositol 3-kinase (PI3K) autophagy complex and positively regulates plant immunity against viruses. The upregulation of Eureka lemon ClBeclin1 was observed in response to citrus yellow vein clearing virus (CYVCV) infection. However, the function of ClBeclin1 and the underlying mechanism during CYVCV colonisation remain unclear. Here, the resistance evaluation of the overexpression and silencing of ClBeclin1 in Eureka lemon hairy roots revealed it as a positive regulator of citrus immunity against CYVCV. Transcriptomic profiling and metabolic analyses along with genetic evidence implied that the overexpression of ClBeclin1 positively triggered reactive oxygen species (ROS)- and jasmonic acid (JA)-mediated immunity in citrus. The accumulation of ROS and JA contents was attributed to the autophagic degradation of the ROS scavenger ClAPX1 via ClBeclin1 overexpression. Exogenous application of either H2O2 or JA significantly reduced CYVCV colonisation and vein-clearing symptoms on the host. Collectively, our findings indicate that ClBeclin1 activation contributes to citrus immunity against CYVCV through triggering ROS- and JA-mediated defence responses, and the accumulation of ROS and JA resulted from the autophagic degradation of ClAPX1 by ClBeclin1.
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.