AI Article Synopsis
- CAF-I and RCAF are complexes that assist in chromatin assembly during DNA replication and repair, contributing to genome stability.
- Research showed that asf1 mutants require replication checkpoint proteins for normal S-phase progression, while cac1 mutants only have a weak dependence on these proteins.
- High Ddc2.GFP foci levels in asf1 mutants indicate a stronger reliance on checkpoint proteins, while cac1 mutants exhibit lower levels, suggesting that defects in these complexes lead to different types of DNA damage and instability at replication forks.
Article Abstract
The chromatin-assembly factor I (CAF-I) and the replication-coupling assembly factor (RCAF) complexes function in chromatin assembly during DNA replication and repair and play a role in the maintenance of genome stability. Here, we have investigated their role in checkpoints and S-phase progression. FACS analysis of mutants lacking Asf1 or Cac1 as well as various checkpoint proteins indicated that normal rates of S-phase progression in asf1 mutants have a strong requirement for replication checkpoint proteins, whereas normal S-phase progression in cac1 mutants has only a weak requirement for either replication or DNA-damage checkpoint proteins. Furthermore, asf1 mutants had high levels of Ddc2.GFP foci that were further increased in asf1 dun1 double mutants consistent with a requirement for checkpoint proteins in S-phase progression in asf1 mutants, whereas cac1 mutants had much lower levels of Ddc2.GFP foci that were not increased by a dun1 mutation. Our data suggest that RCAF defects lead to unstable replication forks that are then stabilized by replication checkpoint proteins, whereas CAF-I defects likely cause different types of DNA damage.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1533778 | PMC |
| http://dx.doi.org/10.1073/pnas.0511102103 | DOI Listing |
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