Kim Sang Yeol, Michaels Scott D
Department of Biology, Indiana University, Bloomington, IN 47405, USA.
Development. 2006 Dec;133(23):4699-707. doi: 10.1242/dev.02684. Epub 2006 Nov 1.
The floral inhibitor FLOWERING LOCUS C (FLC) is a crucial regulator of flowering time in Arabidopsis, and is positively regulated by the FRIGIDA (FRI) gene in late-flowering winter-annual accessions. In rapid-cycling accessions, FLC expression is suppressed by the autonomous floral-promotion pathway (AP); thus AP mutants contain high levels of FLC and are late flowering. Previous work has shown that the upregulation of FLC in FRI- or AP-mutant backgrounds is correlated to an increase in histone H3 lysine 4 (H3K4) trimethylation at the FLC locus. This increase in trimethylation requires a PAF1-like complex and EARLY FLOWERING IN SHORT DAYS (EFS), a putative histone H3 methyltransferase. We have identified a putative zinc-finger-containing transcription factor, SUF4, that is required for the upregulation of FLC by FRI. suf4 mutations strongly suppress the late-flowering phenotype of FRI, but only weakly suppress AP mutants. As with mutants in efs or the PAF1-like complex, suf4 mutants show reduced H3K4 trimethylation at FLC. An interesting distinction between the phenotypes of suf4 mutants and mutants in efs or the PAF1-like complex is observed in the expression of genes that are adjacent to FLC or FLC-like genes. In efs and PAF1-like-complex mutants, the expression of FLC, FLC-like genes and adjacent genes is suppressed. In suf4 mutants, however, only FLC expression is suppressed. These data are consistent with a model in which SUF4 may act to specifically recruit EFS and the PAF1-like complex to the FLC locus.
开花抑制因子开花位点C（FLOWERING LOCUS C，FLC）是拟南芥开花时间的关键调节因子，在晚花冬性一年生生态型中受FRIGIDA（FRI）基因正向调控。在快速循环生态型中，FLC的表达受自主开花促进途径（AP）抑制；因此，AP突变体中FLC水平较高，开花较晚。先前的研究表明，在FRI或AP突变背景下FLC的上调与FLC基因座处组蛋白H3赖氨酸4（H3K4）三甲基化的增加相关。这种三甲基化的增加需要一个PAF1样复合物和短日照早花（EARLY FLOWERING IN SHORT DAYS，EFS），一种假定的组蛋白H3甲基转移酶。我们鉴定出一种假定的含锌指转录因子SUF4，它是FRI上调FLC所必需的。suf4突变强烈抑制FRI的晚花表型，但仅微弱抑制AP突变体。与efs或PAF1样复合物中的突变体一样，suf4突变体在FLC处的H3K4三甲基化减少。在与FLC或FLC样基因相邻的基因表达中，观察到suf4突变体与efs或PAF1样复合物突变体的表型存在有趣的差异。在efs和PAF1样复合物突变体中，FLC、FLC样基因和相邻基因的表达受到抑制。然而，在suf4突变体中，只有FLC的表达受到抑制。这些数据与一个模型一致，即SUF4可能作用于特异性地将EFS和PAF1样复合物招募到FLC基因座。
