摘要
Extracellular calmodulin (CaM) plays significant roles in many physiological proc-esses,but little is known about its mechanism of regulating stomatal movements. In this paper, whether CaM exists in the guard cell walls of Arabidopsis and whether depolymerization of actin cytoskeleton is involved in extracellular CaM-induced stomatal closing are investigated. It is found that CaM exists in guard cell walls of Arabidopsis, and its molecular weight is about 17 kD. Bioassay using CaM antagonists W7-agarose and anti-CaM serum shows that the endogenous extracellular CaM promotes stomatal closure and delays stomatal opening. The long radial actin filaments in guard cells undergo disruption in a time-dependent manner during exogenous CaM-induced stomatal closing. Pharmacological experiments show that depolymerization of ac-tin cytoskeleton enhances the effect of exogenous CaMinduced stomatal closing and polym-erization reduces the effect. We also find that exogenous CaM triggers an increase in [Ca2+]cyt of guard cells. If [Ca2+]cyt increase is blocked with EGTA, exogenous CaM-induced stomatal closure is inhibited. These results indicate that extracellular CaM causes elevation of [Ca2+]cyt in guard cells, subsequently resulting in disruption of actin filaments and finally leading to guard cells closure.
Extracellular calmodulin (CaM) plays significant roles in many physiological proc-esses,but little is known about its mechanism of regulating stomatal movements. In this paper, whether CaM exists in the guard cell walls of Arabidopsis and whether depolymerization of actin cytoskeleton is involved in extracellular CaM-induced stomatal closing are investigated. It is found that CaM exists in guard cell walls of Arabidopsis, and its molecular weight is about 17 kD. Bioassay using CaM antagonists W7-agarose and anti-CaM serum shows that the endogenous extracellular CaM promotes stomatal closure and delays stomatal opening. The long radial actin filaments in guard cells undergo disruption in a time-dependent manner during exogenous CaM-induced stomatal closing. Pharmacological experiments show that depolymerization of ac-tin cytoskeleton enhances the effect of exogenous CaMinduced stomatal closing and polym-erization reduces the effect. We also find that exogenous CaM triggers an increase in [Ca2+]cyt of guard cells. If [Ca2+]cyt increase is blocked with EGTA, exogenous CaM-induced stomatal closure is inhibited. These results indicate that extracellular CaM causes elevation of [Ca2+]cyt in guard cells, subsequently resulting in disruption of actin filaments and finally leading to guard cells closure.
作者
XIAO Yumei1, CHEN Yuling1,2, HUANG Rongfeng3, CHEN Jia1 & WANG Xue-chen1 1. The National Key Laboratory of Plant Physiology and Biochemistry, College of Biological Sciences, China Agricultural University, Bei-jing 100094, China
2. College of Life Sciences, Hebei Normal University, Shijiazhuang 050016, China
3. Biotechnology Research Institute, Chinese Academy of Agricultural Sciences, Beijing 100081, China
作者简介
Correspondence should be addressed to Wang Xue-chen( email:xcwang@cau.edu.cn)
