Dampened Nuclear Localization of SnRK1 by Brassinosteroid Signaling Inhibits Stomatal Development in Arabidopsis.

Abstract

The balance between stem cell division and differentiation is crucial for flexible organ development. In Arabidopsis leaves, the fate of meristemoids, which exhibit stem cell characteristics, is tightly regulated by multiple intrinsic developmental signals and environmental factors. KIN10, catalytic subunit of Sucrose Non-Fermenting 1 (SNF1) related protein kinase 1 (SnRK1) complex, has been shown to preferentially localize in the nucleus of meristemoids, where it phosphorylates and stabilizes SPEECHLESS transcription factor, thereby promoting stomatal development. However, the regulatory mechanism governing the nuclear localization of KIN10 in meristemoids remains unclear. Here, we demonstrate that brassinosteroid (BR) inhibits KIN10's nuclear localization by modulating KINβ2 through BIN2-mediated phosphorylation. In meristemoids, KIN10 is predominantly nuclear, while KINβ2 is mainly cytosolic. Interfering nuclear localization of KIN10 or enhancing membrane association of KINβ2 impairs stomatal development and leads to excessive epidermal cell proliferation. BR signaling could inhibit KIN10 nuclear localization through enhancing KINβ2 membrane association. BR-INSENSITIVE2 (BIN2) interacts with and phosphorylates KINβ2, which reduces its membrane association and its interaction with KIN10. These findings suggested the precise regulation of subcellular localization of SnRK1 complex, influenced by BR signaling, is critical for meristemoids differentiation and stomatal development.