Covo Shay, Chiou Eric, Gordenin Dmitry A, Resnick Michael A
Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, United States of America.
PLoS One. 2014 Dec 31;9(12):e113435. doi: 10.1371/journal.pone.0113435. eCollection 2014.
Sister chromatid cohesion (SCC), which is established during DNA replication, ensures genome stability. Establishment of SCC is inhibited in G2. However, this inhibition is relived and SCC is established as a response to DNA damage, a process known as Damage Induced Cohesion (DIC). In yeast, Chk1, which is a kinase that functions in DNA damage signal transduction, is considered an activator of SCC through DIC. Nonetheless, here we show that, unlike SCC mutations, loss of CHK1 did not increase spontaneous or damage-induced allelic recombination or aneuploidy. We suggest that Chk1 has a redundant role in the control of DIC or that DIC is redundant for maintaining genome stability.
姐妹染色单体黏连（SCC）在DNA复制过程中建立，可确保基因组稳定性。SCC的建立在G2期受到抑制。然而，这种抑制会被解除，并且SCC会作为对DNA损伤的反应而建立，这一过程称为损伤诱导黏连（DIC）。在酵母中，Chk1是一种在DNA损伤信号转导中起作用的激酶，被认为是通过DIC激活SCC的因子。尽管如此，我们在此表明，与SCC突变不同，CHK1缺失并不会增加自发或损伤诱导的等位基因重组或非整倍体。我们认为，Chk1在DIC控制中具有冗余作用，或者DIC对于维持基因组稳定性是冗余的。
