一种用于 DNA 复制的表观遗传控制机制。
A mechanism for epigenetic control of DNA replication.
机构信息
Oklahoma Medical Research Foundation, Cell Cycle and Cancer Biology Research Program, Oklahoma City, Oklahoma 73104, USA.
University of Oklahoma Health Sciences Center, Department of Cell Biology, Oklahoma City, Oklahoma 73104, USA.
出版信息
Genes Dev. 2018 Feb 1;32(3-4):224-229. doi: 10.1101/gad.306464.117. Epub 2018 Feb 26.
DNA replication origins in hyperacetylated euchromatin fire preferentially during early S phase. However, how acetylation controls DNA replication timing is unknown. TICRR/TRESLIN is an essential protein required for the initiation of DNA replication. Here, we report that TICRR physically interacts with the acetyl-histone binding bromodomain (BRD) and extraterminal (BET) proteins BRD2 and BRD4. Abrogation of this interaction impairs TICRR binding to acetylated chromatin and disrupts normal S-phase progression. Our data reveal a novel function for BET proteins and establish the TICRR-BET interaction as a potential mechanism for epigenetic control of DNA replication.
DNA 复制起点在 hyperacetylated euchromatin 中优先在早期 S 期引发。然而，乙酰化如何控制 DNA 复制时间尚不清楚。TICRR/TRESLIN 是 DNA 复制起始所必需的一种必需蛋白。在这里，我们报告 TICRR 与乙酰化组蛋白结合溴结构域（BRD）和端外（BET）蛋白 BRD2 和 BRD4 发生物理相互作用。这种相互作用的中断会损害 TICRR 与乙酰化染色质的结合，并破坏正常的 S 期进展。我们的数据揭示了 BET 蛋白的新功能，并确立了 TICRR-BET 相互作用作为表观遗传控制 DNA 复制的潜在机制。
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