TY - JOUR
T1 - Early signalling pathways in rice roots under vanadate stress
AU - Lin, Chung Wen
AU - Lin, Chung Yi
AU - Chang, Ching Chun
AU - Lee, Ruey Hua
AU - Tsai, Tsung Mu
AU - Chen, Po Yu
AU - Chi, Wen Chang
AU - Huang, Hao Jen
N1 - Funding Information:
This work was supported by research grants from National Science Council (NSC 96-2311-B-006-001) and the Ministry of Education of the Republic of China (“Landmark Project Grant” for NCKU's “Top-University Project”).
PY - 2009/5
Y1 - 2009/5
N2 - Vanadate is beneficial to plant growth at low concentration. However, plant exposure to high concentrations of vanadate has been shown to arrest cell growth and lead to cell death. We are interested in understanding the signalling pathways of rice roots in response to vanadate stress. In this study, we demonstrated that vanadate induced rice root cell death and suppressed root growth. In addition, we found that vanadate induced ROS accumulation, increased lipid peroxidation and elicited a remarkable increase of MAPKs and CDPKs activities in rice roots. In contrast, pre-treatment of rice roots with ROS scavenger (sodium benzoate), serine/threonine protein phosphatase inhibitor (endothall), and CDPK antagonist (W7), reduced the vanadate-induced MAPKs activation. Furthermore, the expression of a MAPK gene (OsMPK3) and four tyrosine phosphatase genes (OsDSP3, OsDSP5, OsDSP6, and OsDSP10) were regulated by vanadate in rice roots. Collectively, these results strongly suggest that ROS, protein phosphatase, and CDPK may function in the vanadate-triggered MAPK signalling pathway cause cell death and retarded growth in rice roots.
AB - Vanadate is beneficial to plant growth at low concentration. However, plant exposure to high concentrations of vanadate has been shown to arrest cell growth and lead to cell death. We are interested in understanding the signalling pathways of rice roots in response to vanadate stress. In this study, we demonstrated that vanadate induced rice root cell death and suppressed root growth. In addition, we found that vanadate induced ROS accumulation, increased lipid peroxidation and elicited a remarkable increase of MAPKs and CDPKs activities in rice roots. In contrast, pre-treatment of rice roots with ROS scavenger (sodium benzoate), serine/threonine protein phosphatase inhibitor (endothall), and CDPK antagonist (W7), reduced the vanadate-induced MAPKs activation. Furthermore, the expression of a MAPK gene (OsMPK3) and four tyrosine phosphatase genes (OsDSP3, OsDSP5, OsDSP6, and OsDSP10) were regulated by vanadate in rice roots. Collectively, these results strongly suggest that ROS, protein phosphatase, and CDPK may function in the vanadate-triggered MAPK signalling pathway cause cell death and retarded growth in rice roots.
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U2 - 10.1016/j.plaphy.2009.01.005
DO - 10.1016/j.plaphy.2009.01.005
M3 - Article
C2 - 19250836
AN - SCOPUS:63449134915
SN - 0981-9428
VL - 47
SP - 369
EP - 376
JO - Plant Physiology and Biochemistry
JF - Plant Physiology and Biochemistry
IS - 5
ER -