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MSI4/FVE interacts with CUL4–DDB1 and a PRC2-like complex to control epigenetic regulation of flowering time in Arabidopsis

机译:MSI4 / FVE与CUL4–DDB1和类似PRC2的复合体相互作用,以控制拟南芥开花时间的表观遗传调控。

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摘要

Flowering at the right time is crucial to ensure successful plant reproduction and seed yield and is dependent on both environmental and endogenous parameters. Among the different pathways that impinge on flowering, the autonomous pathway promotes floral transition independently of day length through the repression of the central flowering repressor FLOWERING LOCUS C (FLC). FLC blocks floral transition by repressing flowering time integrators such as FLOWERING LOCUS T (FT). MSI4/FVE is a key regulator of the autonomous pathway that reduces FLC expression. Here we report that the MSI4 protein is a DDB1 and CUL4-associated factor that represses FLC expression through its association with a CLF-Polycomb Repressive Complex 2 (PRC2) in Arabidopsis. Thus, the lack of MSI4 or decreased CUL4 activity reduces H3K27 trimethylation on FLC, but also on its downstream target FT, resulting in increased expression of both genes. Moreover, CUL4 interacts with FLC chromatin in an MSI4-dependant manner, and the interaction between MSI4 and CUL4–DDB1 is necessary for the epigenetic repression of FLC. Overall our work provides evidence for a unique functional interaction between the cullin-RING ubiquitin ligase (CUL4–DDB1MSI4) and a CLF–PRC2 complex in the regulation of flowering timing in Arabidopsis.
机译:在正确的时间开花对于确保植物成功繁殖和种子产量至关重要,并且取决于环境和内源性参数。在影响开花的不同途径中,自主途径通过抑制中央开花阻遏物FLOWERING LOCUS C(FLC)来促进花期独立于日长。 FLC通过抑制开花时间积分器(例如FLOWERING LOCUS T(FT))来阻止花期过渡。 MSI4 / FVE是减少FLC表达的自主途径的关键调节因子。在这里,我们报道MSI4蛋白是DDB1和CUL4相关因子,通过与拟南芥属CLF-Polycomb Repressive Complex 2(PRC2)的结合来抑制FLC表达。因此,缺少MSI4或降低CUL4活性会降低FLC上的H3K27三甲基化,但也会降低其下游目标FT上的H3K27三甲基化,从而导致两个基因的表达均增加。此外,CUL4以MSI4依赖的方式与FLC染色质相互作用,而MSI4与CUL4-DDB1之间的相互作用对于FLC的表观遗传抑制是必需的。总体而言,我们的工作提供了在拟南芥开花时间调控中cullin-ring泛素连接酶(CUL4-DDB1MSI4)和CLF-PRC2复合物之间独特的功能相互作用的证据。

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