Histone Acetylation, VERNALIZATION INSENSITIVE 3 , FLOWERING LOCUS C , and the Vernalization Response

Oct 15, 2009Molecular plant

How chemical changes in DNA packaging and specific genes relate to the plant's response to cold needed for flowering

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Abstract

Low temperatures induce VIN3 in Arabidopsis, which is essential for the repression of FLC and promoting flowering.

Histone acetylation at the VIN3 gene increases during cold exposure, occurring in two phases.
Short-term cold exposure leads to rapid acetylation of histone H3 at the VIN3 transcription start site.
Prolonged cold exposure results in additional acetylation changes in histones H3 and H4.
VIN3 induction during cold exposure is regulated by mechanisms distinct from those of the cold acclimation pathway.
Nicotinamide treatment, a histone deacetylase inhibitor, induces VIN3 and alters its histone acetylation.
FLC repression following nicotinamide treatment occurs independently of VIN3 activity.

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The quantitative induction of VIN3 by low temperatures is required for PRC2 repression of FLC and promotion of flowering (vernalization) in Arabidopsis. Histone acetylation, a chromatin modification commonly associated with gene transcription, increased on VIN3 chromatin in two spatially and temporally distinct phases in response to low temperatures. During short-term cold exposure, histone H3 acetylation at the transcription start site rapidly increased, implying that it is required for VIN3 induction. Subsequent changes in histone H3 and H4 acetylation occurred following continued VIN3 transcription during prolonged cold exposure. Members of the SAGA-like transcriptional adaptor complex, including the histone acetyltransferase GCN5, which induces expression of the cold acclimation pathway genes, do not regulate VIN3 induction during cold exposure, indicating that the cold acclimation pathway and the cold-induction of VIN3 are regulated by different transcriptional mechanisms. Mutations in the other 11 histone acetyltransferase genes did not affect VIN3 induction. However, nicotinamide, a histone deacetylase inhibitor, induced VIN3 and altered histone acetylation at the VIN3 locus. VIN3 induction was proportional to the length of nicotinamide treatment, which was associated with an early-flowering phenotype and repression of FLC. However, unlike vernalization, the repression of FLC was independent of VIN3 activity. Nicotinamide treatment did not cause a change in the expression of any genes in the autonomous pathway or members of the PRC2 complex, the well characterized repressors of FLC. Our data suggest that FLC is repressed via a novel pathway involving the SIR2 class of histone deacetylases.

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Histone Acetylation, VERNALIZATION INSENSITIVE 3 , FLOWERING LOCUS C , and the Vernalization Response

Abstract

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