LC2,OsVIL3

| Categories genes  | Tags leaf development  brassinosteroid  vernalization  phytohormone  flower  floral  auxin  leaf  cell division  heading date  lamina 
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  • Key message
    • LC2 is mainly expressed in the lamina joint during leaf development, and particularly, is induced by the phytohormones abscisic acid, gibberellic acid, auxin, and brassinosteroids
    • The LC2 gene was isolated through positional cloning, and encodes a vernalization insensitive 3-like protein
    • Here we demonstrated that rice LC2 (OsVIL3) and OsVIL2 (two OsVILs, possible components of PRC2 complex) promote rice flowering
    • Interestingly, LC2 binds to the promoter region of a floral repressor OsLF and represses the OsLF expression via H3K27 tri-methylation modification
    • These results first demonstrated that the putative PRC2 in rice is involved in photoperiod flowering regulation, which is different from that of Arabidopsis, and revealed that LC2 binds the promoter region of target gene, presenting a possible mechanism of the recruitment process of PRC2 complex to its target genes
    • LC2 and OsVIL2 promote rice flowering by photoperoid-induced epigenetic silencing of OsLF
    • To understand the molecular mechanism controlling rice leaf angles, one rice leaf inclination2 (lc2, three alleles) mutant was identified and functionally characterized
    • Compared to wild-type plants, lc2 mutants have enlarged leaf angles due to increased cell division in the adaxial epidermis of lamina joint
    • Complementary expression of LC2 reversed the enlarged leaf angles of lc2 plants, confirming its role in controlling leaf inclination
    • LC2 is localized in the nucleus and defects of LC2 result in altered expression of cell division and hormone-responsive genes, indicating an important role of LC2 in regulating leaf inclination and mediating hormone effects
    • Our results showed that expressions of LC2 and OsVIL2 are induced by SD (short-day) conditions and both lc2 mutant and OsVIL2-RNAi lines display delayed heading date, consistent with the reduced expression levels of Hd1 and Hd3a
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