促分裂原活化蛋白激酶MPK9和MPK12调节壳聚糖诱导的气孔关闭。
MAP kinases, MPK9 and MPK12, regulate chitosan-induced stomatal closure.
作者信息
Salam Mohammad Abdus, Jammes Fabien, Hossain Mohammad Anowar, Ye Wenxiu, Nakamura Yoshimasa, Mori Izumi C, Kwak June M, Murata Yoshiyuki
机构信息
Graduate School of Natural Science and Technology, Okayama University, 1-1-1 Tsushima-naka, Okayama 700-8530, Japan.
出版信息
Biosci Biotechnol Biochem. 2012;76(9):1785-7. doi: 10.1271/bbb.120228. Epub 2012 Sep 7.
Chitosan (CHT)-induced stomatal closure was inhibited by an MAPKK inhibitor, PD98059, and was impaired in mpk9 mpk12 but not in mpk9 or mpk12. CHT induced the production of reactive oxygen species, cytosolic alkalization, and cytosolic Ca(2+) oscillation in mpk9 mpk12. These results suggest that MPK9 and MPK12 are involved in CHT-induced stomatal closure.
壳聚糖（CHT）诱导的气孔关闭被丝裂原活化蛋白激酶激酶（MAPKK）抑制剂PD98059抑制，并且在mpk9 mpk12双突变体中受损，但在mpk9或mpk12单突变体中未受损。CHT诱导mpk9 mpk12双突变体中活性氧的产生、细胞质碱化和细胞质Ca(2+)振荡。这些结果表明，MPK9和MPK12参与了CHT诱导的气孔关闭。
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