BRI1-EMS-suppressor 1 gain-of-function mutant shows higher susceptibility to necrotrophic fungal infection
- Authors
- Shin, Seo Youn; Chung, Hayung; Kim, Sun Young; Nam, Kyoung Hee
- Issue Date
- Feb-2016
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- BRI1-EMS-suppressor 1 (bes1-D); Fungal infection; Alternaria brassicicola; ROS accumulation; PDF1.2 expression
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.470, no.4, pp 864 - 869
- Pages
- 6
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 470
- Number
- 4
- Start Page
- 864
- End Page
- 869
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/9948
- DOI
- 10.1016/j.bbrc.2016.01.128
- ISSN
- 0006-291X
1090-2104
- Abstract
- Brassinosteroids (BRs) are plant-specific steroids that are involved in plant growth and defense responses. However, the exact roles of BR in plant defense are unclear. We used the bes1-D gain-of-function mutant to define the underlying relationship between plant growth and defense through BR signaling and innate immunity. In bes1-D, further downstream component BES1 transcription factor is stabilized, leading to the activation of BR signaling. Previous reports on BES1 target genes showed that approximately 10% are related to biotic stress responses. Therefore, the bes1-D PTI responses were examined. The bes1-D mutant was specifically susceptible to Alternaria brassicicola, a necrotrophic fungus, which successfully produced spore, resulting in considerable cell death. However, it was not affected by a biotrophic pathogen, Pseudomonas syringae pv. tomato (Pst) DC3000. Instead of a ROS burst, a representative initial PTI responses, higher ROS accumulation was sustained in bes1-D than in the wild type plant. PDF1.2 expression was not induced in response to fungal pathogen infection in bes1-D. These results suggest that BES1 is also involved in JA-related defense responses, especially in response to necrotrophic pathogens. (C) 2016 Elsevier Inc. All rights reserved.
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