Cells, Vol. 12, Pages 127: Calcium Channels, OST1 and Stomatal Defence: Current Status and Beyond

Figure 1. Calcium channels-mediated regulation of stomatal defence. Tan et al. [5] and Thor et al. [6] reveal the identification of Ca2+-permeable channels, belonging to cyclic nucleotide-gated channels (CNGCs) and hyperosmolality-gated calcium-permeable channels (OSCAs) associated with stomatal immunity. Abscisic acid (ABA) activates the CNGCs localized in the plasma membrane of guard cells for the influx of Ca2+ in the cytoplasm that leads to Ca2+-dependent stomatal closure by activating the S-type anion channel (SLAC1) [5]. However, the mechanism of ABA-CNGC interaction is still not known. In addition, ABA also releases OPEN STOMATA1 (OST1) from TYPE-2C protein-phosphatases (PP2C) after forming the ‘ABA-ABA receptor-PP2C complex’. The OST1 undergoes either autophosphorylation or transphosphorylation by BAK1 and directly activates SLAC1 that leads to the Ca2+-independent stomatal closure [3,9,15,17]. Further, Wang et al. [7] recently described OST1-mediated phosphorylation and dissociation of MAP SPIRAL1 (SPR1) from microtubules, thereby causing the disassembly of microtubules that leads to stomata closure during ABA-mediated stomatal immunity. Thor et al. [6] describe the role of OSCA channels (OSCA1.3 and OSCA1.7) in stomatal defence. The recognition of flagellin protein (flg22) by the leucine-rich repeat (LRR) domain of FLAGELLIN SENSITIVE2 (FLS2) and BRI1-associated kinase 1 (BAK1) receptors leads to the phosphorylation of BOTRYTIS-INDUCED KINASE1 (BIK1), which further phosphorylates the plasma membrane-localized OSCA channels in the guard cells, thereby activating them for the influx of Ca2+ from the apoplast to the cytoplasm [11]. This Ca2+ signature is possibly recognized by specific calcium-binding proteins/kinases that lead to the activation of SLAC1 by phosphorylation. SLAC1 facilitate the efflux of anions from the cytoplasm which ultimately leads to water loss and stomata closure. In addition, NADPH oxidase (RBOH) activation occurs by coordinated regulation through Ca2+ binding and phosphorylation by BIK1, CDPK, and OST1 that perhaps lead to H2O2-mediated signalling for stomatal defence, but the exact mechanism is not known.

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