The Mechanism Investigation Of Arabidopsis Secreted Peptide PIP1 Regulated Stomatal Movements

Pathogen infection is one of the most harmful biotic stresses of plant which restrains plant growth as well as crop yields dramatically, so the investigation of plant immunity signaling is not only meaningful for better understanding of plant-pathogen interaction, but also helpful for further development of stress-tolerant, high-yield agriculture. Accumulating data show that, besides of pathogen-associated molecular patterns (PAMPs) and endogenous damage-associated molecular patterns (DAMPs), the plant secreted peptides also mediate plant immunity in response to pathogen infection.Stomata are tiny pores surrounded by pairs of guard cells in leaf epidermis of higher plants and mainly regulate CO2 uptake for photosynthesis and water loss for transpiration. Recently, evidence shows that stomata also serve as the first gate in the plant immune responses. Plants could actively close stomata upon perception of pathogen bacterial or flg22, a peptide corresponding to the flagellin epitope recognized by cell membrane-localized receptor FLAGELLIN SENSING2 (FLS2). However, little is known about the effect of the secreted peptides on stomatal movements. Our previous data showed that the PAMP-Induced Peptide 1 (PIP1) in Arabidopsis could trigger immune responses resemble with flg22. In this study, we found that PIP1 could also regulate stomatal movements and share common signal components with abscisic acid (ABA) in guard cell signaling.Here we demonstrated that exogenous application of PIP 1 could trigger stomatal closure with its plasma-localized receptor RLK7. Patch clamp data show that PIP1 could activate S-type anion channels to facilitate solute efflux to close stomata. Further data showed that BAK1 instead of BIK1 functions in PIP 1-induced stomatal closure and the MAP kinases MPK3 and MPK6 are involved in PIP 1-triggered stomatal closure. OST1 was reported to be essential for triggering stomatal closure in response to both abiotic and biotic stresses but our data suggested OST1 is not required for PIP 1-mediated stomatal response. Besides, at the cellular level, our data demonstrated both Ca2+ and ROS are important second messengers involved in PIP1-induced stomatal closure.In conclusion, our results demonstrated that PIP1-induced stomatal closure relies on RLK7. PIP1-RLK7 works cooperatively with flg22-FLS2 signaling for the induction of stomatal closure to improve the ability of plant resistance to pathogen infection and shares common downstream signaling components with ABA signaling pathways.