Asf1 links Rad53 to control of chromatin assembly
Asf1 links Rad53 to control of chromatin assembly
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DOI：
10.1101/gad.873201
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发表时间：
2001-05-01
影响因子：
10.5
通讯作者：
Elledge, SJ
中科院分区：
文献类型：
--
作者：
Hu, FH;Alcasabas, AA;Elledge, SJ
检查点激酶 Rad53 有缺陷的酵母无法从短暂的 DNA 复制阻断中恢复并合成完整的染色体。与此恢复过程相关的 Rad53 效应器尚不清楚。在这里，我们报道染色质组装因子Asf1的过量产生可以抑制mrc1rad53双突变体的Ts表型和rad53突变体的HU敏感性。消除沉默也可以抑制这种致死性，进一步表明染色质结构与检查点功能有关。我们发现 Asf1 和 Rad53 存在于一个动态复合体中，该复合体响应复制阻断和 DNA 损伤而解离。因此，检查点通路直接调节染色质组装，以促进 DNA 损伤和复制阻断时的存活。
Yeast defective in the checkpoint kinase Rad53 fail to recover from transient DNA replication blocks and synthesize intact chromosomes. The effecters of Rad53 relevant to this recovery process are unknown. Here we report that overproduction of the chromatin assembly factor Asf1 can suppress the Ts phenotype of mrc1rad53 double mutants and the HU sensitivity of rad53 mutants. Eliminating silencing also suppresses this lethality, further implicating chromatin structure in checkpoint function. We find that Asf1 and Rad53 exist in a dynamic complex that dissociates in response to replication blocks and DNA damage. Thus, checkpoint pathways directly regulate chromatin assembly to promote survival in response to DNA damage and replication blocks.