CSIRO Plant Industry, Canberra, Australia; ARC Centre of Excellence in Plant Energy Biology, School of Biochemistry and Molecular Biology, Australian National University, Canberra, Australia.
CSIRO Plant Industry, Canberra, Australia.
Mol Plant. 2009 Jul;2(4):724-737. doi: 10.1093/mp/ssp021. Epub 2009 Apr 20.
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.
低温下 VIN3 的定量诱导对于 PRC2 抑制 FLC 和促进拟南芥开花（春化）是必需的。组蛋白乙酰化是一种与基因转录普遍相关的染色质修饰，在低温下以两个时空不同的阶段在 VIN3 染色质上增加。在短期冷暴露期间，转录起始位点处的组蛋白 H3 乙酰化迅速增加，暗示它是 VIN3 诱导所必需的。在延长的冷暴露期间，VIN3 转录持续进行后，发生了随后的组蛋白 H3 和 H4 乙酰化变化。SAGA 样转录适配器复合物的成员，包括诱导冷适应途径基因表达的组蛋白乙酰转移酶 GCN5，在冷暴露期间不调节 VIN3 诱导，表明冷适应途径和 VIN3 的冷诱导由不同的转录机制调节。其他 11 个组蛋白乙酰转移酶基因的突变不影响 VIN3 的诱导。然而，烟酰胺，一种组蛋白去乙酰化酶抑制剂，诱导 VIN3 并改变 VIN3 基因座处的组蛋白乙酰化。VIN3 的诱导与烟酰胺处理的长度成正比，这与早期开花表型和 FLC 的抑制有关。然而，与春化不同，FLC 的抑制不依赖于 VIN3 活性。烟酰胺处理不会导致自主途径中的任何基因或 PRC2 复合物成员的表达发生变化，PRC2 复合物是 FLC 的特征性抑制剂。我们的数据表明，FLC 通过涉及 SIR2 类组蛋白去乙酰酶的新途径被抑制。
