Regulation of heterochromatic DNA replication by histone H3 lysine 27 methyltransferases.
Regulation of heterochromatic DNA replication by histone H3 lysine 27 methyltransferases.
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多种途径可防止 DNA 在每个细胞周期中多次复制。这些途径通过严格控制复制前复合物的活性来阻止再复制，这些复合物在基因组中称为起源的特定位点组装。在这里，我们发现同源组蛋白 3 赖氨酸 27 (H3K27) 单甲基转移酶、拟南芥三胸相关蛋白 5 (ATXR5) 和 ATXR6 的突变会导致特定基因组位置的重新复制。这些位置的绝大多数对应于拟南芥基因组的转座子和其他重复和沉默元件。这些位点也对应于高水平的 H3K27 单甲基化，并且催化 SET 结构域的突变足以导致再复制缺陷。 ATXR5和ATXR6的突变也会导致转座子表达上调，并对植物发育产生多效性影响。这些结果揭示了一种防止拟南芥中异染色质过度复制的新途径。
Multiple pathways prevent DNA replication from occurring more than once per cell cycle. These pathways block re-replication by strictly controlling the activity of pre-replication complexes, which assemble at specific sites in the genome called origins. Here we show that mutations in the homologous histone 3 lysine 27 (H3K27) monomethyltransferases, ARABIDOPSIS TRITHORAX-RELATED PROTEIN5 (ATXR5) and ATXR6, lead to re-replication of specific genomic locations. The vast majority of these locations correspond to transposons and other repetitive and silent elements of the Arabidopsis genome. These sites also correspond to high levels of H3K27 monomethylation, and mutation of the catalytic SET domain is sufficient to cause the re-replication defect. Mutation of ATXR5 and ATXR6 also causes upregulation of transposon expression and has pleiotropic effects on plant development. These results uncover a novel pathway that prevents over-replication of heterochromatin in Arabidopsis.
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