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Cell cycle progression in the presence of irreparable DNA damage is controlled by a Mec1‐ and Rad53‐dependent checkpoint in budding yeast
Progression through S phase of UV‐treated NER‐deficient mec1 and rad53 mutants correlates with late origin firing, suggesting that unregulated DNA replication in the presence of irreparable UV‐induced lesions might result from a failure to prevent initiation at late origins.
The 70 kDa subunit of replication protein A is required for the G1/S and intra-S DNA damage checkpoints in budding yeast.
The hypersensitivity to UV and MMS treatments observed in the rfa1-M4 mutant might only be due to impairment of RPA function in DNA repair, while the rFA1- M2 mutation seems to affect both the DNA repair and checkpoint functions of Rpa70.
Mutations in the gene encoding the 34 kDa subunit of yeast replication protein A cause defective S phase progression.
It is shown that unbalanced stoichiometry of the RPA subunits does not affect cell growth and cell cycle progression until the level of Rpa34 becomes rate-limiting, at which point cells arrest with a late S/G2 DNA content.
Checkpoint proteins influence telomeric silencing and length maintenance in budding yeast.
The finding that telomere shortening, but not increased telomeric repression of gene expression in rad53 mutants, can be suppressed by increasing dNTP synthetic capacity in these strains suggests that transcriptional silencing and telomeres integrity involve separable functions of Rad53.
The set1Delta mutation unveils a novel signaling pathway relayed by the Rad53-dependent hyperphosphorylation of replication protein A that leads to transcriptional activation of repair genes.
The deletion of the amino-terminal region of Rfa2p suppresses the sensitivity to ultraviolet radiation of a mec3Delta checkpoint mutant, abolishes the URS-mediated repression, and increases the expression of repair genes.