Abstract |
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.
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Authors | Shay Covo, Eric Chiou, Dmitry A Gordenin, Michael A Resnick |
Journal | PloS one
(PLoS One)
Vol. 9
Issue 12
Pg. e113435
( 2014)
ISSN: 1932-6203 [Electronic] United States |
PMID | 25551702
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, N.I.H., Intramural)
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Chemical References |
- Cell Cycle Proteins
- Chromosomal Proteins, Non-Histone
- cohesins
- Protein Kinases
- Checkpoint Kinase 1
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Topics |
- Alleles
- Aneuploidy
- Cell Cycle Proteins
(metabolism)
- Checkpoint Kinase 1
- Chromatids
(genetics)
- Chromosomal Proteins, Non-Histone
(metabolism)
- Chromosomes, Fungal
(genetics)
- DNA Damage
(genetics)
- DNA Replication
(genetics)
- Genomic Instability
- Protein Kinases
(metabolism)
- Recombination, Genetic
- Saccharomyces cerevisiae
(enzymology, genetics, metabolism)
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