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The Arabidopsis SWI2/SNF2 Chromatin Remodeler BRAHMA Regulates Polycomb Function during Vegetative Development and Directly Activates the Flowering Repressor Gene SVP

机译:拟南芥SWI2 / SNF2染色质重塑剂BRAHMA在营养发育过程中调节多梳功能,并直接激活阻花开花基因SVP

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The chromatin remodeler BRAHMA (BRM) is a Trithorax Group (TrxG) protein that antagonizes the functions of Polycomb Group (PcG) proteins in fly and mammals. Recent studies also implicate such a role for Arabidopsis (Arabidopsis thaliana) BRM but the molecular mechanisms underlying the antagonism are unclear. To understand the interplay between BRM and PcG during plant development, we performed a genome-wide analysis of trimethylated histone H3 lysine 27 (H3K27me3) in brm mutant seedlings by chromatin immunoprecipitation followed by next generation sequencing (ChIP-seq). Increased H3K27me3 deposition at several hundred genes was observed in brm mutants and this increase was partially supressed by removal of the H3K27 methyltransferase CURLY LEAF (CLF) or SWINGER (SWN). ChIP experiments demonstrated that BRM directly binds to a subset of the genes and prevents the inappropriate association and/or activity of PcG proteins at these loci. Together, these results indicate a crucial role of BRM in restricting the inappropriate activity of PcG during plant development. The key flowering repressor gene SHORT VEGETATIVE PHASE (SVP) is such a BRM target. In brm mutants, elevated PcG occupancy at SVP accompanies a dramatic increase in H3K27me3 levels at this locus and a concomitant reduction of SVP expression. Further, our gain- and loss-of-function genetic evidence establishes that BRM controls flowering time by directly activating SVP expression. This work reveals a genome-wide functional interplay between BRM and PcG and provides new insights into the impacts of these proteins in plant growth and development.
机译:染色质重塑剂BRAHMA(BRM)是Trithorax Group(TrxG)蛋白,在飞行和哺乳动物中拮抗Polycomb Group(PcG)蛋白的功能。最近的研究也暗示拟南芥(Arabidopsis thaliana)BRM具有这种作用,但拮抗作用的分子机制尚不清楚。为了了解植物发育过程中BRM和PcG之间的相互作用,我们通过染色质免疫沉淀,然后进行下一代测序(ChIP-seq),对brm突变苗中的三甲基化组蛋白H3赖氨酸27(H3K27me3)进行了全基因组分析。在brm突变体中观察到数百个基因的H3K27me3沉积增加,并且通过去除H3K27甲基转移酶CURLY LEAF(CLF)或SWINGER(SWN)可以部分抑制这种增加。 ChIP实验证明BRM直接与基因的一个子集结合,并防止了PcG蛋白在这些基因座上的不适当结合和/或活性。总之,这些结果表明BRM在限制植物发育过程中PcG的不适当活性方面起着至关重要的作用。关键的开花抑制基因短植物期(SVP)就是这样的BRM靶标。在brm突变体中,SVP的PcG占用率升高伴随着该基因座H3K27me3水平的急剧增加,并伴随着SVP表达的降低。此外,我们的功能获得和丧失功能的遗传证据表明,BRM通过直接激活SVP表达来控制开花时间。这项工作揭示了BRM和PcG之间的全基因组功能相互作用,并为这些蛋白质对植物生长和发育的影响提供了新的见解。

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