Calcium Channels, OST1 and Stomatal Defence: Current Status and Beyond

Stomatal immunity is regulated by pathogen-associated molecular patterns (PAMPs)- and abscisic acid (ABA)-triggered signalling in different ways. Cytoplasmic Ca2+ signature in the guard cells plays a vital function in stomatal immunity, but the mechanism of Ca2+ import is unknown. It has been very recently established that the hyperosmolality-gated calcium-permeable channels (OSCAs) and cyclic nucleotide-gated channels (CNGCs) are responsible for the influx of Ca2+ in the cytoplasm, which are activated after BIK1-mediated phosphorylation and ABA interaction during PAMPs- and ABA-triggered stomatal immunity in plants, respectively. Further, ABA-triggered OPEN STOMATA1 (OST1) causes the disassembly of microtubules in the guard cells besides activation of S-type anion channels (SLAC1) for the efflux of cytoplasmic anions that leads to stomata closure.

Automated summary

Stomatal immunity is regulated by PAMPs and ABA-induced signaling, with cytoplasmic Ca2+ playing a crucial role. The influx of Ca2+ is mediated by OSCAs and CNGCs, which are activated by BIK1-mediated phosphorylation and ABA interaction. Additionally, ABA triggers OST1 activation, leading to microtubule disassembly and SLAC1 activation for cytoplasmic anion efflux and stomatal closure.