| Sugars,as signalling molecules,play a central role in regularization of plants metabolism,development,and physiology.The stomata,which are formed by pairs of guard cells,control gas exchange and transpiration.Stomatal movement is regulated by multiple external signals,such as light and carbon dioxide,and phytohormones,including ethylene and ABA.Approximately 100 years ago,some researchers have proposed that sugar could affect stomatal movement.Several researchs have suggested that the accumulation of sucrose,which is a glucose-fructose disaccharide,regulates the osmotic state of guard cells,thereby promoting stomatal opening.In contrast,the accumulation of sucrose in guard cell apoplast was shown to close stomata owing to an extracellular osmotic effect.D-glucose also acts as a signalling molecule to cause stomatal closure.In this process,hexokinase(HXK),which is a cytoplasmic enzyme involved in hexose phosphorylation,functions as a D-glucose sensor.Moreover,it has been reported that H2O2,a form of reactive oxygen species(ROS),Ca2+,and water channels are involved in D-glucose-induced stomatal closure.However,up to date,the role and the potential mechanism of sugar in the regulation of stomatal movement have not been fully elucidated.Here,we select Arabidopsis(Arabidopsis thaliana)wild-type(WT)(Col-0)and relevant mutant as plant material,through stomatal bioassay combined with fluorescent microscope method,to study the roles of ethylene,ABA,H2O2 and NO,and the relationship between them in D-glucose-induced stomatal closure.The main results are as follows:1.D-glucose closed stomata of WT,but did not close stomata of WT treated with ethylene sythesis inhibitor aminooxyacetic acid(AOA)and ethylene receptor inhibitor AgNO3,and ethylene sythesis mutants acv5-1,acs6-1 and ccs5-1/6-1,and ethylene receptor mutants etr1-1,etr1-3,ein4,ran1-1 and ran1-2.The results show that ethylene is involved in D-glucose-induced stomatal closure.2.D-glucose closed stomata of WT,the effect was abolished in WT treated with ABA sythesis inhibitor fluridone(FLU),and ABA sythesis mutants nced3,nced5,nced3nced5,ubu2-4 and and ABA receptor mutantpyrlpyllpyl2pyl4,indicating that ABA mediates D-glucose-induced stomatal closure.3.D-glucose induced H2O2 and NO production in the guard cells of WT,but did not in those of ethylene sythesis mutants acs5-1,acs6-1 and acs5-1/6-1,ethylene receptor mutants etr1-1,etr1-3,ein4,ran1-1 and ran1-2.H2O2 and NO donor SNP rescued the defects of ethylene sythesis mutants acs5-/,acs6-1 and acs5-1/6-1,ethylene receptor mutants etr1-3,ein4,ran1-1 and ran1-2 in D-glucose-incuced stomatal closure.The data indicate that ethylene mediates D-glucose-induced stomatal closure via inducing H2O2 and NO production.4.D-glucose induced H2O2 and NO production in the guard cells of WT,but it did not in those of ABA sythesis mutants nced3,nced5,nced3nced5,aba2-4 and aha3-1,and ABA receptor mutants pyrlpyllpyl2pyl4.H2O2 and SNP rescued the failures of ABA sythesis mutants nced3,nced5,nced3nced5,aba2-4 and aba3-1,and ABA receptor mutants pyrlpyllpyl2pyl4 in D-glucose-incuced stomatal closure.These results show that ABA is involved in D-glucose-incuced stomatal closure through stimulating H2O2 and NO sythesis.5.ABA closed the stomata of ethylene sythesis and ethylene receptor mutants acs5-1,acs6-1,acs5-1/6-1,etr1-1,etr1-3,ein4,ran1-1 and ran1-2,but ethylene precursor 1-amino-cyclopropane-1-carboxylic acid(ACC)did not close these of ABA sythesis mutants nced3,nced5,nced3nced5,aba2-4 and aba3-1,and ABA receptor mutants pyr1pyl 1 pyl2pyl4.These data suggests that ethylene mediates D-glucose-incuced stomatal closure via promoting ABA sythesis.In summary,our results provid evidences that D-glucose-led ethylene productions timulates synthesis of ABA,thereafter inducing H2O2 and NO producing and stomatal closure. |
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