Mechanism of light signal transduction in guard cells of green leaves

1利用药理学手段研究了蚕豆保卫细胞原生质体蓝光依赖质子排出过程中的信号转导过程。钙调素(CaM)拮抗剂和肌球蛋白轻链激酶(MLCK)抑制剂可抑制依赖蓝光的质子排出。其他蛋白激酶抑制剂不能抑制质子挤出。孟加拉鸭茅(Commelina benghalica SSP.)表皮的光敏气孔开放被钙调素拮抗剂和MLCK抑制剂抑制。此外，真菌植物毒素褐变素在这些抑制剂的存在下，恢复了质子排出和气孔开放。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。2.研究了保卫细胞原生质体对光和暗反应中蛋白质的磷酸化和去磷酸化。几种分子质量分别为42、40、34、32、26和19kD的蛋白质被磷酸化。用红光照射暗适应的原生质体可引起26kD蛋白的去磷酸化。一些证据表明，26kD蛋白是光系统II的捕光叶绿素a/b蛋白复合体。光诱导的去磷酸化被丝氨酸/苏氨酸蛋白磷酸酶抑制剂冈田酸抑制，提示光系统I吸收的光下，这种去磷酸化是由2A型蛋白磷酸酶介导的。

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.