The epidermis-specific cyclin CYCP3;1 is involved in the excess brassinosteroid signaling-inhibited root meristem cell division.

Abstract

Cell division is precisely regulated and highly tissue-specific; studies have suggested that diverse signals in the epidermis, especially the epidermal brassinosteroids (BRs), can regulate root growth. However, the underlying molecular mechanisms that integrate hormonal cues such as BR signaling with other endogenous, tissue-specific developmental programs to regulate epidermal cell proliferation remain unclear. In this study, we used molecular and biochemical approaches, microscopic imaging and genetic analysis to investigate the function and mechanisms of a P-type cyclin in root growth regulation. We found that CYCP3;1, specifically expressed in the root meristem epidermis and lateral root cap, can regulate meristem cell division. Mitotic analyses and biochemical studies demonstrated that CYCP3;1 promotes cell division at the G2-M duration by associating and activating cyclin-dependent kinase B2-1 (CDKB2;1). Furthermore, we found that CYCP3;1 expression was inhibited by BR signaling through BRI1-EMS-SUPPRESSOR1 (BES1), a positive downstream transcription factor in the BR signaling pathway. These findings not only provide a mechanism of how root epidermal-specific regulators modulate root growth, but also reveal why the excess of BRs or enhanced BR signaling inhibits cell division in the meristem to negatively regulate root growth.