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Wiley, The Plant Journal, 3(59), p. 488-498, 2009

DOI: 10.1111/j.1365-313x.2009.03883.x

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Mechanisms of gene repression by vernalization in Arabidopsis

This paper was not found in any repository, but could be made available legally by the author.
This paper was not found in any repository, but could be made available legally by the author.

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Abstract

FLOWERING LOCUS C (FLC) is a major regulator of flowering time in Arabidopsis. Repression of FLC occurs in response to prolonged cold exposure (vernalization) and is associated with an enrichment of the repressive histone modification trimethylated H3 lysine 27 (H3K27me3) and a depletion of the active histone modification H3K4me3 at FLC chromatin. In two cases genes adjacent to FLC are also repressed by vernalization. NEOMYCIN PHOSPHOTRANSFERASE II (NPTII) adjacent to an FLC transgene is repressed by vernalization, and this is associated with an increase in H3K27me3, demonstrating that the epigenetic repression of FLC can confer a repressed epigenetic state to an adjacent transcription unit. The second case involves the two genes adjacent to the endogenous FLC gene, UPSTREAM OF FLC (UFC) and DOWNSTREAM OF FLC (DFC). Both genes are repressed by vernalization (Finnegan et al., 2004), but they require neither cis-acting nor trans-acting factors derived from the FLC gene nor the VERNALIZATION2 (VRN2) complex which trimethylates H3K27. This demonstrates that there are two different mechanisms of gene repression by vernalization. We further show that repression and H3K27 trimethylation of FLC still occurs in mutants of the VRN2 complex. In contrast, the VRN2 complex is essential for repression and H3K27 trimethylation of the FLC-related MADS AFFECTING FLOWERING (MAF) genes by vernalization. This suggest that other proteins are able to repress FLC, but not MAF, gene expression.