Regulation of Flowering Time by Histone Acetylation in <i>Arabidopsis</i>

TLDR

The autonomous floral‑promotion pathway in Arabidopsis promotes flowering independently of photoperiod and vernalization by repressing the MADS‑box transcription factor FLOWERING LOCUS C, which blocks the transition from vegetative to reproductive development. FLD, a component of this pathway, encodes a plant homolog of a histone deacetylase complex protein; loss of FLD causes hyperacetylation of FLC chromatin, increased FLC expression, and markedly delayed flowering, demonstrating that the autonomous pathway partly represses FLC via histone deacetylation while other mechanisms also contribute.

Abstract

The Arabidopsis autonomous floral-promotion pathway promotes flowering independently of the photoperiod and vernalization pathways by repressing FLOWERING LOCUS C ( FLC ), a MADS-boxtranscription factor that blocks the transition from vegetative to reproductive development. Here, we report that FLOWERING LOCUS D ( FLD ), one of sixgenes in the autonomous pathway, encodes a plant homolog of a protein found in histone deacetylase complexes in mammals. Lesions in FLD result in hyperacetylation of histones in FLC chromatin, up-regulation of FLC expression, and extremely delayed flowering. Thus, the autonomous pathway regulates flowering in part by histone deacetylation. However, not all autonomous-pathway mutants exhibit FLC hyperacetylation, indicating that multiple means exist by which this pathway represses FLC expression.