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Improved oxidative tolerance in suspension‐cultured cells of C 4 ‐pepc transgenic rice by H 2 O 2 and Ca 2+ under PEG‐6000
Author(s) -
Qian Baoyun,
Li Xia,
Liu Xiaolong,
Wang Man
Publication year - 2015
Publication title -
journal of integrative plant biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.734
H-Index - 83
eISSN - 1744-7909
pISSN - 1672-9072
DOI - 10.1111/jipb.12283
Subject(s) - egta , phosphoenolpyruvate carboxylase , ruthenium red , calcium , chemistry , biochemistry , channel blocker , oxidative stress , enzyme , organic chemistry
To understand the molecular responses of PC (Overexpressing the maize C 4 ‐ pepc gene, which encodes phosphoenolpyruvate carboxylase (PEPC)), to drought stress at cell level, we analyzed changes in the levels of signaling molecules (hydrogen peroxide (H 2 O 2 ), calcium ion (Ca 2+ ), and nitric oxide (NO)) in suspension‐cultured PC and wild‐type (WT) rice ( Oryza sativa L.) cell under drought stress induced by 20% polyethylene glycol 6000 (PEG‐6000). Results demonstrated that PC improved drought tolerance by enhancing antioxidant defense, retaining higher relative water content, survival percentages, and dry weight of cells. In addition, PEPC activity in PC under PEG treatment was strengthened by addition of H 2 O 2 inhibitor, dimethylthiourea (DMTU) and NO synthesis inhibitor, 2‐(4‐carboxyphenyl)‐4,4,5,5‐tetramethylimidazoline‐1‐oxyl‐3‐oxide (cPTIO), respectively, while that in PC was weakened by addition of free calcium chelator, ethylene glycol‐bis(b‐aminoethylether)‐ N , N , N ′, N ′‐tetraacetic acid (EGTA) + calcium channel outflow inhibitor, ruthenium red (RR) + plasma membrane channel blocker La(NO 3 ) 3 , but EGTA + RR did not. Results also showed that NO and Ca 2+ was lying downstream of H 2 O 2 in drought‐induced signaling. Calcium ion was also involved in the expression of C 4 ‐pepc in PC. These results suggested that PC could improve oxidative tolerance in suspension‐cultured cells and the acquisition of this tolerance required downregulation of H 2 O 2 and the entry of extracellular Ca 2+ into cells across the plasma membrane for regulation of PEPC activity and C 4 ‐pepc expression.