Checkpoint proteins control morphogenetic events during DNA replication stress in Saccharomyces cerevisiae.
Checkpoint proteins control morphogenetic events during DNA replication stress in Saccharomyces cerevisiae.
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DOI：
10.1083/jcb.200605080
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发表时间：
2006-12-04
期刊：
影响因子：
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通讯作者：
Kolodner RD
中科院分区：
文献类型：
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作者：
Enserink JM;Smolka MB;Zhou H;Kolodner RD
在酿酒酵母的DNA复制应激反应中，DNA复制检查点维持复制叉的稳定性，防止染色体过早分离，并导致细胞停滞为大芽细胞。检查点激酶Mec1和Rad53在这个检查点起作用。用复制抑制剂处理mec1或rad53Δ突变体会导致复制叉崩溃和部分复制染色体的不适当分配，从而导致细胞死亡。我们描述了包括Rad53在内的各种复制应激检查点蛋白在控制细胞形态方面以前未被认识到的功能。检查点突变体具有异常的细胞形态和细胞壁，并表现出缺陷的芽位点选择。Rad53与septin环通路组分存在遗传相互作用，并与其他检查点蛋白一起控制复制胁迫下Swe1的及时降解，从而促进芽的正常生长。因此，在复制应激过程中，检查点蛋白在协调DNA复制的形态发生事件中起着重要作用。
In response to DNA replication stress in Saccharomyces cerevisiae, the DNA replication checkpoint maintains replication fork stability, prevents precocious chromosome segregation, and causes cells to arrest as large-budded cells. The checkpoint kinases Mec1 and Rad53 act in this checkpoint. Treatment of mec1 or rad53Δ mutants with replication inhibitors results in replication fork collapse and inappropriate partitioning of partially replicated chromosomes, leading to cell death. We describe a previously unappreciated function of various replication stress checkpoint proteins, including Rad53, in the control of cell morphology. Checkpoint mutants have aberrant cell morphology and cell walls, and show defective bud site selection. Rad53 shows genetic interactions with septin ring pathway components, and, along with other checkpoint proteins, controls the timely degradation of Swe1 during replication stress, thereby facilitating proper bud growth. Thus, checkpoint proteins play an important role in coordinating morphogenetic events with DNA replication during replication stress.