Ca2+/CaM increases the necrotrophic pathogen resistance through the inhibition of a CaM-regulated dual-specificity protein phosphatase 1 in Arabidopsis
- Authors
- Nhan Thi Nguyen; Kim, Sun Ho; Kim, Kyung Eun; Bahk, Sunghwa; Xuan Canh Nguyen; Kim, Min Gab; Hong, Jong Chan; Chung, Woo Sik
- Issue Date
- Feb-2022
- Publisher
- 한국식물생명공학회
- Keywords
- Calmodulin; Jasmonic acid; Kinase; Pathogen resistance; Phosphatase; Stress
- Citation
- Plant Biotechnology Reports, v.16, no.1, pp 71 - 78
- Pages
- 8
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- Plant Biotechnology Reports
- Volume
- 16
- Number
- 1
- Start Page
- 71
- End Page
- 78
- URI
- https://scholarworks.gnu.ac.kr/handle/sw.gnu/1696
- DOI
- 10.1007/s11816-021-00729-7
- ISSN
- 1863-5466
1863-5474
- Abstract
- Jasmonic acid (JA) is a phytohormone that plays a central role in plant defense against necrotrophic pathogens. JA signaling stimulates the increase of cytosolic calcium ion (Ca2+) and implicates the activity of mitogen-activated protein kinases (MPKs). We previously characterized that Ca2+/calmodulin (CaM) activates MPKs by inhibiting a CaM-regulated dual-specificity protein phosphatase1 (DsPTP1) at the biochemical level. In this study, we reported that Ca2+/CaM-mediated DsPTP1 negatively regulates the resistance to necrotrophic pathogens through the inhibition of JA-responsive MPK6. To elucidate the physiological function of inhibiting DsPTP1 activity by Ca2+/CaM, we constructed transgenic plants overexpressing DsPTP1 wild type (DsPTP1(WT) OX) and CaM deregulated mutant (DsPTP1(K166E) OX). Interestingly, the MPK6 activity was significantly reduced in DsPTP1(K166E) OX plants in response to JA compared to DsPTP1(WT) OX plants. Moreover, transcript levels of JA-responsive gene PDF1.2 and VSP1 were also highly decreased in DsPTP1(K166E) OX plants compared to DsPTP1(WT) OX plants. Furthermore, DsPTP1(K166E) OX plants showed more susceptibility to necrotrophic pathogens than DsPTP1(WT) OX plants. Conclusively, these results suggest that Ca2+/CaM activates the JA-responsive MPKs by inhibiting DsPTP1 for the resistance to the necrotrophic pathogen.
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