Abstract：
Chitosan (CHT) is a deacylated derivative of chitin and improves growth and yield performance, activates defensive genes, and also induces stomatal closure in plants. Glutathione (GSH) has significant functions in the growth, development, defense systems, signaling, and gene expression. GSH negatively regulates abscisic acid-, methyl jasmonate-, and salicylic acid-induced stomatal closure. However, the negative regulation by GSH of CHT-induced stomatal closure is still unknown. Regulation of CHT-induced stomatal closure by GSH in guard cells was investigated using two GSH-deficient mutants, cad2-1 and chlorina 1-1 (ch1-1), and a GSH-decreasing chemical, 1-chloro-2,4-dinitrobenzene (CDNB). The cad2-1 and ch1-1 mutations and CDNB treatment enhanced CHT-induced stomatal closure. Treatment with glutathione monoethyl ester restored the GSH level in the guard cells of cad2-1 and ch1-1 and complemented the stomatal phenotype of the mutants. These results indicate that GSH negatively regulates CHT-induced stomatal closure in Arabidopsis thaliana.
摘要：
壳聚糖(CHT)是几丁质的脱酰化衍生物,可提高生长性能和产量,激活防御基因,并诱导植物气孔关闭。谷胱甘肽(GSH)具有显著的生长功能,发展,防御系统,信令,和基因表达。谷胱甘肽负调节脱落酸（ABA）-，茉莉酸甲酯（MeJA）-，和水杨酸（SA）诱导的气孔关闭。然而,GSH对CHT诱导的气孔关闭的负调控尚不清楚。使用两个GSH缺陷型突变体研究了GSH在保卫细胞中对CHT诱导的气孔关闭的调节，cad2-1和ch1-1，以及一种减少GSH的化学物质，1-氯-2,4-二硝基苯(CDNB)。cad2-1和ch1-1突变和CDNB处理增强了CHT诱导的气孔关闭。用谷胱甘肽单乙酯（GSHmee）处理恢复了cad2-1和ch1-1的保卫细胞中的GSH水平，并补充了突变体的气孔表型。这些结果表明，GSH负调节CHT诱导的拟南芥气孔关闭。
