The Functions Of Heterotrimeric G-protein In ABA-and NO-mediated Stomatal Movement

Abscisic Acid (ABA), a phytohormone that has comprehensive biological function, regulates stomatal movement in Arabidopsis thaliana. ABA can inhibit the stomatal opening, additionally induce stomata closure. Nitric oxide (NO) is a key signaling molecular in plants involved in various biological pathways. NO has been reported as a new member of signal transduction pathway in guard cell recently. Plant heterotrimeric G-protein signal is one of the conservative signals in plants cell. Recently, there are a large number of reports about mechanism of ABA-induced stomatal closure, moreover it has established that NO and some components of heterotrimeric G-protein signaling mediate in the ABA regulated stomatal movement. But there is little information available about the functions of other components of heterotrimeric G-protein signaling in ABA signal transduction pathway, furthermore there is no report concerning the function of G-protein in guard cell NO signal.In this study, by using Arabidopsis null mutants of gpa1-4,agb1-2,αβ36,rgs1-2,gcr1-5 and Atrack1 absent of the AtGPA1,AtAGB1,AtGPA1/AtAGB1,AtRGS1,AtGCR1,AtRACK1 respectively and their wild type, together with epidermal strip bioassay and fluorescence microscopy, we discussed the function of the components of heterotrimeric G-protein signaling medited in ABA and NO signaling in guard cell. The major results are showed as followings:1) Enogenous ABA induces stomatal closure in Arabidopsis wild type, and this process is mediated by AtGPA1. AtRGS1 and AtGCR1 may act as a negative regulator in GPA1-mediated stomatal closure process promoted by ABA. AGB1 and AtRACK1 are dispensable components in this process and maybe have negative function in ABA synthesis. 2) In Arabidopsis wild type, enogenous ABA can inhibite stomatal opening, and this process is mediated by AtGPA1 and AtAGB1, forthmore they maybe involved in two parallel pathways in ABA signal.AtRGS1 and AtGCR1 may act as a negative regulator of GPA1-mediated stomatal opening process inhibited by ABA. AtRACK1 is a dispensable component in this process and maybe have negative function in ABA synthesis.3) Enogenous NO induces Arabidopsis wild type stomatal closure, and this process is mediated by AtRGS1 and AtGCR1 maybe interact with AtGPA1 and exert positive function. AtGPA1 is dispensable and may act upstream of NO in this process. AGB1 and AtRACK1 are dispensable components in this process and maybe have a negative function.4) We identify that enogenous NO inhibites stomatal opening in Arabidopsis wild type. Components of heterotrimeric G-protein signaling do not involved in this process, or maybe exert negative function.5) Both the ABA and the NO effects on stomatal closure and opening are genetically independently, they may be controlled by different mechanism and procedure.6) In Arabidopsis guard cells, GAP1 mediates ABA induction on NO synthesis, and AGB1 is partly involved in this process. RGS1 may exert positive function and GCR1,RACK1 may have negative function in the course.