The trxG family histone methyltransferase SET DOMAIN GROUP 26 promotes flowering via a distinctive genetic pathway
The trxG family histone methyltransferase SET DOMAIN GROUP 26 promotes flowering via a distinctive genetic pathway
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DOI：
10.1111/tpj.12729
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发表时间：
2015-01-01
期刊：
影响因子：
7.2
通讯作者：
Shen, Wen-Hui
中科院分区：
文献类型：
--
作者：
Berr, Alexandre;Shafiq, Sarfraz;Shen, Wen-Hui
组蛋白甲基化是许多过程的主要组成部分，例如开花时间的确定，它通过整合内源和环境信号的多种遗传途径进行微调。先前的研究发现 SET DOMAIN GROUP26 (SDG26) 是一种参与开花激活的组蛋白甲基转移酶，因为 SDG26 功能丧失会导致拟南芥出现晚花表型。然而，SDG26 的功能和潜在的分子机制仍然很大程度上未知。在本研究中，我们通过将sdg26突变体与其他组蛋白甲基化酶突变体结合进行遗传分析，包括甲基转移酶突变体拟南芥trithorax1（atx1）、sdg25和curly leaf（clf），以及去甲基化酶双突变体lsd1-like1 lsd1-like2（ldl1ldl2）。我们发现早花突变体 sdg25、atx1 和 clf 与晚花突变体 sdg26 拮抗相互作用，而晚花突变体 ldl1 ldl2 与 sdg26 协同相互作用。基于微阵列分析，我们观察到 sdg26 和其他突变体之间差异表达的基因存在弱重叠。我们对开花基因染色质的分析表明，SDG26 蛋白与关键的开花整合子 SUPPRESSOR OF OVEREXPRESSION OF CONSTANS1/AGAMOUS-LIKE 20 (SOC1/AGL20) 结合，并且是组蛋白 H3 赖氨酸 4 三甲基化 (H3K4me3) 和组蛋白 H3 赖氨酸 36 三甲基化 (H3K36me3) 所必需的。轨迹。总之，我们的结果表明，SDG26 通过独特的遗传途径促进开花时间，并且 SDG26 功能的丧失导致其靶基因 SOC1 处的 H3K4me3 和 H3K36me3 减少，从而导致该基因和晚花表型的抑制。 (ii) 它提供了对SDG26在开花时间控制方面的调控机制的充分理解； (iii)由于SOC1和SDG26在高等植物中进化上保守，因此所揭示的机制可以扩展到其他植物物种。
Histone methylation is a major component in numerous processes such as determination of flowering time, which is fine-tuned by multiple genetic pathways that integrate both endogenous and environmental signals. Previous studies identified SET DOMAIN GROUP26 (SDG26) as a histone methyltransferase involved in the activation of flowering, as loss of function of SDG26 caused a late-flowering phenotype in Arabidopsis thaliana. However, the SDG26 function and the underlying molecular mechanism remain largely unknown. In this study, we undertook a genetic analysis by combining the sdg26 mutant with mutants of other histone methylation enzymes, including the methyltransferase mutants Arabidopsis trithorax1 (atx1), sdg25 and curly leaf (clf), as well as the demethylase double mutant lsd1-like1 lsd1-like2 (ldl1ldl2). We found that the early-flowering mutants sdg25, atx1 and clf interact antagonistically with the late-flowering mutant sdg26, whereas the late-flowering mutant ldl1 ldl2 interacts synergistically with sdg26. Based on microarray analysis, we observed weak overlaps in the genes that were differentially expressed between sdg26 and the other mutants. Our analyses of the chromatin of flowering genes revealed that the SDG26 protein binds at the key flowering integrator SUPPRESSOR OF OVEREXPRESSION OF CONSTANS1/AGAMOUS-LIKE 20 (SOC1/AGL20), and is required for histone H3 lysine4 trimethylation (H3K4me3) and histone H3 lysine36 trimethylation (H3K36me3) at this locus. Together, our results indicate that SDG26 promotes flowering time through a distinctive genetic pathway, and that loss of function of SDG26 causes a decrease in H3K4me3 and H3K36me3 at its target gene SOC1, leading to repression of this gene and the late-flowering phenotype.Significance Statement Our finding is of high interest because: (i) previous studies primarily report on FLC and FT, very little is known about chromatin regulation at SOC1; (ii) it provides ample understanding of regulatory mechanism of SDG26 in flowering time control; (iii) the uncovered mechanism may be extended to other plant species since SOC1 as well as SDG26 are evolutionarily conserved in higher plants.