4.7 Article

The tomato Arp2/3 complex is required for resistance to the powdery mildew fungus Oidium neolycopersici

期刊

PLANT CELL AND ENVIRONMENT
卷 42, 期 9, 页码 2664-2680

出版社

WILEY
DOI: 10.1111/pce.13569

关键词

actin cytoskeleton; Arp2; 3 complex; ARPC3; powdery mildew; resistance; Solanum habrochaites

资金

  1. 111 Project from the Ministry of Education of China [B07049]
  2. Key Industrial Chain Projects of Shaanxi [2019ZDLNY03-07]
  3. National Natural Science Foundation of China [31571960]
  4. Northwest AAMP
  5. F University extension Project [2018-10]
  6. U.S. National Science Foundation [IOS-1557437]
  7. National Institutes of General Medical Sciences [1R01GM125743]

向作者/读者索取更多资源

The actin-related protein 2/3 complex (Arp2/3 complex), a key regulator of actin cytoskeletal dynamics, has been linked to multiple cellular processes, including those associated with response to stress. Herein, the Solanum habrochaites ARPC3 gene, encoding a subunit protein of the Arp2/3 complex, was identified and characterized. ShARPC3 encodes a 174-amino acid protein possessing a conserved P21-Arc domain. Silencing of ShARPC3 resulted in enhanced susceptibility to the powdery mildew pathogen Oidium neolycopersici (On-Lz), demonstrating a role for ShARPC3 in defence signalling. Interestingly, a loss of ShARPC3 coincided with enhanced susceptibility to On-Lz, a process that we hypothesize is the result of a block in the activity of SA-mediated defence signalling. Conversely, overexpression of ShARPC3 in Arabidopsis thaliana, followed by inoculation with On-Lz, showed enhanced resistance, including the rapid induction of hypersensitive cell death and the generation of reactive oxygen. Heterologous expression of ShARPC3 in the arc18 mutant of Saccharomyces cerevisiae (i.e., increment arc18) resulted in complementation of stress-induced phenotypes, including high-temperature tolerance. Taken together, these data support a role for ShARPC3 in tomato through positive regulation of plant immunity in response to O. neolycopersici pathogenesis.

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