Recovery, Repair, and Mutagenesis in Schizosaccharomyces pombe

Phipps, J.; Nasim, A.; Miller, Darla R.

doi:10.1016/s0065-2660(08)60511-8

Cited by 119 publications

(75 citation statements)

References 233 publications

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“…The Smc5-Smc6 complex was first discovered through the analysis of a radiation sensitive mutant in Schizosaccharomyces pombe named rad18-X, [12][13][14] which carries a mutation in the SMC6 gene. Epistasis analysis of rad18-X showed that the function of Smc6p was in postreplicative repair through the Rad51p pathway for homologous recombination.…”

Section: Introductionmentioning

confidence: 99%

Smc5-Smc6 Complex Preserves Nucleolar Integrity in S. cerevisiae

Torres-Rosell¹,

Machín²,

Aragón³

2005

Cell Cycle

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Section: Introductionmentioning

confidence: 99%

Smc5-Smc6 Complex Preserves Nucleolar Integrity in S. cerevisiae

Torres-Rosell¹,

Machín²,

Aragón³

2005

Cell Cycle

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“…Studies in fission and budding yeasts have demonstrated that genes that promote survival in UV light encode both DNA repair factors (2,3) and checkpoint proteins that regulate the cell cycle in response to DNA damage (4,5). These genes are conserved among eukaryotes, so diverse model systems may be used to address questions of molecular mechanism (6).…”

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confidence: 99%

UV irradiation induces a postreplication DNA damage checkpoint

Callegari

Kelly

2006

Proc. Natl. Acad. Sci. U.S.A.

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Eukaryotic cells irradiated with high doses of UV exhibit cell-cycle responses referred to as G 1͞S, intraS, and G2͞M checkpoints. After a moderate UV dose that approximates sunlight exposure and is lethal to fission yeast checkpoint mutants, we found unexpectedly that these cell-cycle responses do not occur. Instead, cells at all stages of the cell cycle carry lesions into S phase and delay cell-cycle progression for hours after the completion of bulk DNA synthesis. Both DNA replication and the checkpoint kinase, Chk1, are required to generate this cell-cycle response. UV-irradiation of ⌬chk1 cells causes chromosome damage and loss of viability only after cells have replicated irradiated DNA and entered mitosis. These data suggest that an important physiological role of the cell-cycle response to UV is to provide time for postreplication repair.cell cycle ͉ chk1 ͉ nucleotide excision repair ͉ yeast U V radiation from sunlight exposure induces DNA damage that is potentially lethal to cells and is carcinogenic to animals (1). Studies in fission and budding yeasts have demonstrated that genes that promote survival in UV light encode both DNA repair factors (2, 3) and checkpoint proteins that regulate the cell cycle in response to DNA damage (4, 5). These genes are conserved among eukaryotes, so diverse model systems may be used to address questions of molecular mechanism (6).The pyrimidine dimer is the most abundant form of DNA damage known to be induced by UV (7). This lesion is removed from duplex DNA by nucleotide excision repair (NER). When present during S phase, pyrimidine dimers cause gaps in the daughter DNA strand (8-12). The repair of these gaps is referred to as postreplication repair and involves bypass polymerases, homologous recombination, and other processes (13).Several eukaryotic cell-cycle responses have been observed after high-dose UV irradiation. Fission yeast UV-irradiated in G 2 delay the onset of mitosis, a response conserved in human cells that has been termed a G 2 ͞M DNA damage checkpoint (5, 14-16). It is posited that the UV sensitivity of fission yeast G 2 ͞M checkpoint mutants results from a failure to make time for the repair of UV-induced DNA lesions before mitosis (5). Budding yeast exhibit a G 1 ͞S checkpoint response that delays S phase entry after UV irradiation in G 1 (17). Because activation of the G 1 ͞S checkpoint requires NER genes, it has been suggested that the checkpoint monitors the presence of NER intermediates (12,(18)(19)(20). Mammalian cells exhibit a p53-dependent G 1 ͞S DNA damage checkpoint response that can eliminate damaged cells through apoptosis, delay entry into S phase, and facilitate NER (21). Like the G 1 ͞S checkpoint of yeast, the induction of p53 in G 1 requires NER and is independent of DNA replication (22). A NER-independent checkpoint is activated when UV lesions are present during S phase in Xenopus egg extracts and budding yeast NER mutants (18,23). In both model systems, UV lesions cause an arrest in S phase; however, this arrest appears to be ch...

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“…The other five linkage groups define apparently new genes, which we are designating husl-hus5. Mutations in the three rad genes were initially isolated on the basis of their sensitivity to ionizing and UV radiation (Phipps et al 1985). Recently, these genes have been shown to be required for radiation-induced cell cycle arrest in G2, as is the budding yeast RAD9 gene (A1- Khodairy and Carr 1992;Rowley et al 1992a).…”

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Fission yeast genes involved in coupling mitosis to completion of DNA replication.

Enoch

Carr²,

Nurse³

1992

Genes Dev.

352

341

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We have isolated fission yeast mutants that enter mitosis when DNA replication is blocked with hydroxyurea. The mutants define eight linkage groups, three of which consist of alleles of the radl, rad3, and radl 7 genes. Recently, these fission yeast genes have been shown to be required for radiation-induced cell cycle arrest, as is the budding yeast RAD9 gene. The other five genes are called bus (hydroxy_urea sensitive) 1-5. We propose that these genes participate in an intraceUular signal transduction pathway that monitors the completion of DNA replication and transmits information to the mitotic control protein cdc2. Mutations that bypass the requirement for cdc25 (an activator of the mitotic regulator cdc2) also uncouple mitosis from DNA replication. However, mitosis is blocked by inhibitors of DNA replication in strains in which the cdc25 gene has been deleted, indicating that although cdc25 influences the coupling of mitosis to the completion of DNA replication, it is not essential for this control.[Key Words: Cell cycle; checkpoint; radiation; cdc25; S. pombe] Received May 4, 1992; revised version accepted August 27, 1992.A normal cell cycle consists of a temporally ordered series of events. This order is maintained partly by mechanisms that can monitor completion of earlier events, called "checkpoint" (Hartwell and Weinert 1989) or "feedback" (Murray and Kirschner 1989)controls. Elimination of such controls by mutation or chemical treatment disrupts the dependencies characteristic of ordered progression through the cell cycle (for review, see Hartwell and Weinert 1989). Although mutations that abolish several different cell cycle checkpoints have been identified (Weinert and Hartwell 1988;Hoyt et al. 1991;Li and Murray 1991), it is not clear how these controls work. Early steps must "signal" late steps, but little is known about what these signals are or how they are monitored.We are investigating this problem by studying the coupling of mitosis to the completion of DNA replication in the fission yeast Schizosaccharomyces pombe. This sys-

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Recovery, Repair, and Mutagenesis in Schizosaccharomyces pombe

Cited by 119 publications

References 233 publications

Smc5-Smc6 Complex Preserves Nucleolar Integrity in S. cerevisiae

Smc5-Smc6 Complex Preserves Nucleolar Integrity in S. cerevisiae

UV irradiation induces a postreplication DNA damage checkpoint

Fission yeast genes involved in coupling mitosis to completion of DNA replication.

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