The pepperRING-typeE3ligase,CaATIR1, positively regulates abscisic acid signalling and drought response by modulating the stability ofCaATBZ1
- Authors
- Joo, Hyunhee; Lim, Chae Woo; Lee, Sung Chul
- Issue Date
- Aug-2020
- Publisher
- WILEY
- Keywords
- bZIP transcription factor; protein degradation; ubiquitination
- Citation
- PLANT CELL AND ENVIRONMENT, v.43, no.8, pp 1911 - 1924
- Pages
- 14
- Journal Title
- PLANT CELL AND ENVIRONMENT
- Volume
- 43
- Number
- 8
- Start Page
- 1911
- End Page
- 1924
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/42007
- DOI
- 10.1111/pce.13789
- ISSN
- 0140-7791
1365-3040
- Abstract
- Protein degradation by the ubiquitin/26S proteasome system is a critical process that modulates many eukaryotic cellular processes. E3 ligase usually modulates stress response by adjusting the stability of transcription factors. Previous studies have shown that a RING-type E3 ligase, CaASRF1, positively modulates abscisic acid (ABA) signalling and ABA-mediated drought response by modulating the stability of CaAIBZ1 and CaATBZ1. In this study, we conducted yeast two-hybrid (Y2H) screening with CaATBZ1 to isolate an additional modulator, identified as CaATIR1 (CapsicumannuumATBZ1InteractingRING finger protein1). CaATIR1 has E3 ligase activity and promoted CaATBZ1 degradation using the 26S proteasome system. We investigated the loss-of and gain-of functions of this E3 ligase by using silencing pepper and overexpressing (OX) Arabidopsis plants, respectively. In response to ABA and drought treatments,CaATIR1-silenced pepper plants showed ABA insensitive and drought-sensitive phenotypes, whileCaATIR1-OX plants showed the opposite phenotypes. Additionally,CaATBZ1-silencing rescued the ABA insensitive and drought-sensitive phenotypes ofCaATIR1-silencing pepper plants. Taken together, these data demonstrate that the stability of CaATBZ1 mediated by CaATIR1 has a crucial role in drought stress signalling in pepper plants.
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Collections - College of Natural Sciences > Department of Life Science > 1. Journal Articles
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