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Mechanism of light signal transduction in guard cells of green leaves

绿叶保卫细胞光信号转导机制

基本信息

批准号：
03640570
负责人：
SHIMAZAKI Kenichiro
金额：
$ 1.15万
依托单位：
KYUSHU UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1991
资助国家：
日本
起止时间：
1991 至 1992
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-03640570/
关键词：
Stomata Blue light effect Calmodulin Vicia faba L Guard cells Proton pump Protein phosphorylation ミオシン軽鎖光情報伝達

项目摘要

1 Signal transduction processes in the blue light-dependent proton extrusion by guard cell protoplasts from Vicia faba was investigated using pharmacological tools. Blue light-dependent proton extrusion was inhibited by calmodulin (CaM) antagonists and myosin light chain kinase (MLCK) inhibitors. Other protein kinase inhibitors do not suppress the proton extrusion. The light-dependent stomatal opening in the epidermis of Commelina benghalensis ssp. was suppressed by CaM antagonists and MLCK inhibitors. Furthermore, fusicoccin, a fungal phytotoxin, resumed the proton extrusion and stomatal opening in the presence of these inhibitors. These results suggest that CaM-antagonists and MLCK inhibitors inhibit the signal transduction pathway of blue light response of stomata.2 Protein phosphorylation and dephosphorylation of guard cell protoplasts in response to light and dark was studied. Several proteins with molecular masses of 42, 40, 34, 32, 26 and 19 kD were phosphorylated. Illumination of the dark-adapted protoplasts with red light caused the dephosphorylation of the 26 kD protein. Several lines of evidence indicates that the 26 KD protein is the light-harvesting chlorophyll a/b protein complex of photosystem II. The light-induced dephosphorylation was inhibited by okadaic acid, an inhibitor of serine/threonie protein phosphatase, suggesting that the dephosphorylation is mediated by type-2A protein phosphatase under the light absorbed by photosystem I.

利用药理学手段研究了蚕豆保护细胞原生质体蓝光依赖性质子挤压的信号转导过程。钙调素（CaM）拮抗剂和肌球蛋白轻链激酶（MLCK）抑制剂可抑制蓝光依赖性质子挤出。其他蛋白激酶抑制剂不抑制质子挤压。白头草表皮气孔开度的光依赖性。被CaM拮抗剂和MLCK抑制剂抑制。此外，真菌植物毒素fusicoccin在这些抑制剂的存在下恢复了质子挤压和气孔打开。这些结果表明，cam -拮抗剂和MLCK抑制剂抑制了气孔蓝光反应的信号转导途径研究了保护细胞原生质体在光照和黑暗条件下蛋白磷酸化和去磷酸化的变化。分子质量为42、40、34、32、26和19 kD的蛋白被磷酸化。红光照射暗适应原生质体导致26 kD蛋白的去磷酸化。多项证据表明，26 KD蛋白是光系统II的捕光叶绿素a/b蛋白复合体。丝氨酸/苏氨酸蛋白磷酸酶抑制剂冈田酸可抑制光诱导的去磷酸化，提示在光系统I吸收的光下，去磷酸化是由2a型蛋白磷酸酶介导的。