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Cited 7 time in webofscience Cited 8 time in scopus
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Ca2+/CaM increases the necrotrophic pathogen resistance through the inhibition of a CaM-regulated dual-specificity protein phosphatase 1 in Arabidopsis

Authors
Nhan Thi NguyenKim, Sun HoKim, Kyung EunBahk, SunghwaXuan Canh NguyenKim, Min GabHong, Jong ChanChung, 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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