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DNA Repair and Mutagenesis
Nucleotide excision repair in mammalian cells: genes and proteins Mismatch repair The SOS response and recombinational repair in prokaryotes Mutagenesis in proKaryote Mutagenisation in eukaryotes Other DNA damage tolerance responses in eUKaryotes.
The SAD1/RAD53 protein kinase controls multiple checkpoints and DNA damage-induced transcription in yeast.
The observation that SAD1 controls three distinct checkpoints suggests a common mechanism for cell cycle arrest at these points, and implicate protein phosphorylation in the cellular response to DNA damage and replication blocks.
Characterization of a mutant strain of Saccharomyces cerevisiae with a deletion of the RAD27 gene, a structural homolog of the RAD2 nucleotide excision repair gene
Levels of the RAD27 gene transcript are cell cycle regulated in a manner similar to those for several other genes whose products are known to be involved in DNA replication, and the possible role of Rad27 protein in DNA repair and replication is discussed.
RAD9-dependent G1 arrest defines a second checkpoint for damaged DNA in the cell cycle of Saccharomyces cerevisiae.
- W. Siede, A. Friedberg, E. Friedberg
- BiologyProceedings of the National Academy of Sciences…
- 1 September 1993
It is suggested that the RAD9 gene product may interact with cellular components common to the G1/S and G2/M transition points in the cell cycle of this yeast and facilitate the repair of lesions that are otherwise processed to lethal and/or mutagenic damage during DNA replication.
The Saccharomyces cerevisiae Ku autoantigen homologue affects radiosensitivity only in the absence of homologous recombination.
The results give further support to the notion that, in contrast to higher eukaryotic cells, homologous recombination is the favored pathway of double-strand break repair in yeast whereas other competing mechanisms such as the suggested pathway of DNA-PK-dependent direct break rejoining are only of minor importance.
Characterization of G1 checkpoint control in the yeast Saccharomyces cerevisiae following exposure to DNA-damaging agents.
It is suggested that an intermediate of nucleotide excision repair, such as DNA strand breaks or single-stranded DNA tracts, is required to activate RAD9-dependent G1 and G1/S checkpoint controls.
The Saccharomyces cerevisiae MEC1 gene, which encodes a homolog of the human ATM gene product, is required for G1 arrest following radiation treatment
An additional defect in G1 arrest following treatment with UV light or gamma rays is shown and a defective arrest stage at or upstream of START in the yeast cell cycle is mapped.
The conserved Mec1/Rad53 nuclear checkpoint pathway regulates mitochondrial DNA copy number in Saccharomyces cerevisiae.
Results indicate that signaling through the Mec1/Rad53 pathway increases mtDNA copy number by altering deoxyribonucleoside triphosphate pools through the activity of ribonucleotide reductase, and suggests that homologous pathways in humans may likewise regulate mtDNA content under physiological conditions.
Regulation of the RAD2 gene of Saccharomyces cervisiae
- W. Siede, G. Robinson, D. Kalainov, T. Malley, E. Friedberg
- BiologyMolecular microbiology
- 1 December 1989
It is concluded that induction of RAD2 by DNA‐damaging agents is positively regulated and enhanced transcription is not dependent on the presence of upstream sequences required for regulation of induction by DNA damage.
Cloning and characterization of RAD17, a gene controlling cell cycle responses to DNA damage in Saccharomyces cerevisiae.
- W. Siede, G. Nusspaumer, V. Portillo, R. Rodriguez, E. Friedberg
- BiologyNucleic acids research
- 1 May 1996
The RAD17 gene is cloned by complementation of the UV sensitivity of a rad17-1 mutant and an ORF is identified encoding a predicted gene product with homology to the Schizosaccharomyces pombe rad1+ gene product and to Ustilago maydis Rec1, a known 3'->5'exonuclease.