Get help with access Institutional accessĪccess to restricted content on Oxford Academic is often provided through institutional subscriptions and purchases. Our results demonstrate that PcG proteins promote FM determinacy at multiple levels of the floral gene regulatory network, silencing initially floral regulators such as AGL24 that promotes FM indeterminacy and, subsequently, meristematic pluripotency genes such as WUS and STM during FM arrest.
Nonetheless, WUS remained essential for the FM activity. Loss of STM can rescue supernumerary floral organs and FM indeterminacy in H3K27me3-deficient flowers, indicating that the hyperactivity of the FMs is at least partially a result of ectopic STM expression. Strong depletion of H3K27me3 levels results in misexpression of the FM identity gene AGL24, which partially causes floral reversion leading to ap1-like flowers and indeterminate FMs ectopically expressing WUS and SHOOT MERISTEMLESS ( STM). To this end, we report the genome-wide dynamics of H3K27me3 levels during FM arrest and the consequences of strongly depleted PcG activity on early flower morphogenesis including enlarged and indeterminate FMs. However, the role of H3K27me3 in silencing of other meristematic regulator and pluripotency genes during FM determinacy has not yet been studied. Epigenetic silencing of the stem cell factor gene WUSCHEL ( WUS) in floral meristems (FMs) depends on H3K27me3 deposition by PcG proteins. Polycomb group (PcG) protein-mediated histone methylation (H3K27me3) controls the correct spatiotemporal expression of numerous developmental regulators in Arabidopsis.
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