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首页> 外文期刊>Molecular Plant >Histone acetylation, VERNALIZATION INSENSITIVE 3, FLOWERING LOCUS C, and the vernalization response. (Special Issue: Molecular Plant on epigenetics and plant development.)
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Histone acetylation, VERNALIZATION INSENSITIVE 3, FLOWERING LOCUS C, and the vernalization response. (Special Issue: Molecular Plant on epigenetics and plant development.)

机译：组蛋白乙酰化，常态化敏感性3 ，花丛C 和春化反应。 （特刊：关于表观遗传学和植物发育的分子植物。）

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摘要

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.
机译：低温定量诱导 VIN3 是PRC2抑制 FLC 并促进拟南芥开花（春化）所必需的。组蛋白乙酰化是一种通常与基因转录相关的染色质修饰，响应低温，在 VIN3 染色质上在两个时空不同的阶段增加。在短期冷暴露期间，转录起始位点的组蛋白H3乙酰化迅速增加，这暗示 VIN3 诱导是必需的。在长时间的冷暴露期间，持续不断的 VIN3 转录后，组蛋白H3和H4乙酰化发生了随后的变化。 SAGA样转录衔接子复合物的成员，包括诱导冷驯化途径基因表达的组蛋白乙酰基转移酶GCN5，不调节冷暴露过程中的 VIN3 诱导，表明冷驯化途径和VIN3 的冷诱导受到不同转录机制的调控。其他11个组蛋白乙酰转移酶基因的突变不会影响 VIN3 的诱导。但是，组蛋白脱乙酰基酶抑制剂烟酰胺诱导 VIN3 并改变了 VIN3 位点的组蛋白乙酰化。 VIN3 诱导与烟酰胺处理时间长短成正比，这与早期开花表型和 FLC 的抑制有关。但是，与春化不同， FLC 的抑制与VIN3活性无关。烟酰胺处理不会导致自主途径或PRC2复合物（即FLC 的阻遏物）中任何基因的表达发生变化。我们的数据表明 FLC 通过一种涉及SIR2类组蛋白脱乙酰基酶的新型途径被抑制。

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