Department of Biochemistry, University of Wisconsin, Madison, WI 53706-1544, USA.
Plant Cell Physiol. 2012 May;53(5):834-46. doi: 10.1093/pcp/pcs021. Epub 2012 Feb 28.
The winter-annual habit of Arabidopsis thaliana requires active alleles of flowering locus C (FLC), which encodes a potent flowering repressor, and FRIGIDA (FRI), an activator of FLC. FLC activation by FRI is accompanied by an increase in specific histone modifications, such as tri-methylation of histone H3 at lysine 4 (H3K4me3), and requires three H3K4 methyltransferases, the Drosophila Trithorax-class Arabidopsis trithorax1 (ATX1) and ATX2, and yeast Set1-class ATX-related7/set domain group25 (ATXR7/SDG25). However, lesions in all of these genes failed to suppress the enhanced FLC expression caused by FRI completely, suggesting that another H3K4 methyltransferase may participate in the FLC activation. Here, we show that ATXR3/SDG2, which is a member of a novel class of H3K4 methyltransferases, also contributes to FLC activation. An ATXR3 lesion suppressed the enhanced FLC expression and delayed flowering caused by an active allele of FRI in non-vernalized plants. The decrease in FLC expression in atxr3 mutants was accompanied by reduced H3K4me3 levels at FLC chromatin. We also found that the rapid flowering of atxr3 was epistatic to that of atxr7, suggesting that ATXR3 functions in FLC activation in sequence with ATXR7. Our results indicate that the novel-class H3K4 methyltransferase, ATXR3, is a transcriptional activator that plays a role in the FLC activation and establishing the winter-annual habit. In addition, ATXR3 also contributes to the activation of other FLC clade members, such as flowering locus M/MADS affecting flowering1 (FLM/MAF1) and MAF5, at least partially explaining the ATXR3 function in delayed flowering caused by non-inductive photoperiods.
拟南芥的冬性习性需要开花位点 C (FLC) 的活性等位基因，该基因编码一种有效的开花抑制剂，以及 FRIGIDA (FRI)，它是 FLC 的激活剂。FRI 对 FLC 的激活伴随着特定组蛋白修饰的增加，例如组蛋白 H3 赖氨酸 4 三甲基化 (H3K4me3)，并且需要三种 H3K4 甲基转移酶，果蝇类转录激活因子复合物 1 （ATX1）和 ATX2，以及酵母 SET1 类 ATX 相关 7/SET 结构域组 25 (ATXR7/SDG25)。然而，这些基因的突变都不能完全抑制 FRI 引起的 FLC 表达增强，这表明另一种 H3K4 甲基转移酶可能参与 FLC 的激活。在这里，我们表明 ATXR3/SDG2，作为一种新型 H3K4 甲基转移酶的成员，也有助于 FLC 的激活。在未春化的植物中，ATXR3 突变体抑制了 FRI 活性等位基因引起的 FLC 表达增强和开花延迟。在 atxr3 突变体中，FLC 染色质上的 H3K4me3 水平降低，导致 FLC 表达减少。我们还发现，atxr3 的快速开花与 atxr7 的快速开花是上位的，这表明 ATXR3 在 FLC 激活中与 ATXR7 序列相关。我们的结果表明，新型 H3K4 甲基转移酶 ATXR3 是一种转录激活因子，在 FLC 激活和建立冬性习性中发挥作用。此外，ATXR3 还有助于其他 FLC 家族成员的激活，如开花位点 M/MADS 影响开花 1 (FLM/MAF1) 和 MAF5，至少部分解释了 ATXR3 在非诱导光周期引起的开花延迟中的作用。
