ATHK1is Involved In The Signal Transduction Of ABA-induced Stomatal Closure

Stomatal pores are formed by pairs of specialized epidermal guard cells andserve as major gateways for both exchange of CO₂to O₂and transpiration. Plants alsoneed to control humidity beyond water loss while photosynthesis is carried out. Whenplants face with stress, ABA was produced and activates a series of responses tocontrol stomatal aperture, and at last even close it to avoid more water lost.The stress hormone ABA activates complex signaling pathways in guard cellsthat are mediated by hydrogen peroxide, calcium variation and potassium channelregulation. Recent research in guard cells has led to a new hypothesis that ATHK1involves into the signal pathway of ABA-induced stomatal closure.Epidermal bioanalysis data shown that ABA, concentration from0to100μmol/L, were added respectively to show different responses between WT and athk1plants. Moreover, H₂O₂, a second messenger in ABA signaling, was used as anotherstimulus to stomatal closure, but its effect was inhibited seriously in athk1mutants.Patch clamp data showed that, contrary to wildtype plants, mutants did not displaytypical-responded inwardly decreasing of potassium current. Otherwise, DPI, theinhibitor of NADPHase could affect of H₂O₂on potassium channel in wildtype plantbut showed little effect on mutants. It seemed that ATHK1may downstream ofhydrogen peroxide in ABA-induced stomatal closure.Water loss assay also displayed that mutants lost more water faster than that ofwildtype plants did, and these differences may not affect by stomata numbers of bothplants because an examination showed that there was no distinct difference onstomata density between them.ABA induced H₂O₂production in both wildtype plants and mutants, but ABAcould neither regulate Ca²⁺channel on guard cell membrane nor enhance calciumconcentration in guard cells in athk1mutants. Furthermore, Ca²⁺oscillation inwildtype plant guard cells did not occurred in athk1mutants. Genetic analysis uncovered the fact that ATHK1expressed more RNAs inwildtype plants than that of athk1mutants. It seemed that the insensitive to ABA orH₂O₂in mutants was originated from less expression of ATHK1.There are clear evidences that ATHK1participated in the process ofABA-induced stomatal closure and ATHK1functions downstream of H₂O₂. ATHK1regulates calcium channel and adjustes Ca²⁺concentration in guard cells. Byregulating the activity of inward potassium channel, ATHK1adjusts the turgor inguard cells, and finally, reduceing the tugor to induce stomatal closure.