Genetic Control of the DNA Polymerase α-Primase complex in the Yeast Saccharomyces cerevisiae

Plevani, Paolo; Foiani, Marco; Francesconi, Stefania; Pizzagalli, Antonella; Santocanale, Corrado; Muzi, M. Falconi; Piatti, Simonetta; Piseri, Anna; Derossi, Daniele; Longhese, Maria Pia; Locati, F.; Tazzi, Remo; Lucchini, Giovanna

doi:10.1007/978-3-642-76988-7_26

Cited by 1 publication

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References 23 publications

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“…However, this is different in a large number of other DNA-damaging backgrounds tested, such as the temperature-sensitive cdc17-1 mutant, in which abrogation of the checkpoint results in a decrease in cell viability as temperature increases [37]; CDC17 codes for the catalytic subunit of the DNA polymerase alpha-primase complex; ref. 42,43). Interestingly, while the ddc1 mutation and the rfa1-t11 mutations, both abrogating the DNA-damage checkpoint, decreased cdc17-1 cell survival at the semi-permissive temperature of 32°C, the rfa1-12 mutation had no effect, further suggesting that this mutant is not deficient in DNA-damage checkpoint ( Figure 2D).…”

Section: Simple Observation Of the Checkpoint-deficient Cdc13-1 Rad24mentioning

confidence: 93%

RPA provides checkpoint-independent cell cycle arrest and prevents recombination at uncapped telomeres of Saccharomyces cerevisiae

Grandin

Charbonneau

2013

DNA Repair

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Replication Protein A (RPA) is an evolutionary conserved essential complex with single-stranded DNA binding properties that has been implicated in numerous DNA transactions. At damaged telomeres, Saccharomyces cerevisiae RPA recruits the Mec1-Ddc2 module of the DNA damage checkpoint network, its only known function in DNA damage signaling. Here, we describe rfa1 mutants (rfa1-1, rfa1-9, rfa1-10, rfa1-11 and rfa1-12) that are proficient in this checkpoint but nevertheless exhibit deregulation of cell cycle control upon telomere uncapping induced by the cdc13-1 mutation. Overriding of this damage-induced checkpoint-independent cell cycle block in the rfa1 mutants was suppressed following genetic inactivation of either TEL1 or EST2/telomerase. Altogether, our results suggest that a previously non-suspected function of RPA is to block cell cycle progression upon telomere uncapping using a yet unidentified pathway that functions in a Mec1-Ddc2-independent manner. We propose that in the rfa1 mutants, ill-masking of uncapped telomeres provokes inappropriate access of Tel1 and inappropriate functioning of telomerase, which, by yet unknown mechanisms, allows cell division to take place in spite of the block established by the DNA damage checkpoint. In the present study, we also observed that upon telomere uncapping, rfa1-12, but not the other studied rfa1 mutants, triggered telomeric recombination in the presence of functional telomerase. In conclusion, the present study identifies a novel pathway of telomere end protection that utilizes a previously unsuspected function of RPA at the telomeres.

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Section: Simple Observation Of the Checkpoint-deficient Cdc13-1 Rad24mentioning

confidence: 93%

RPA provides checkpoint-independent cell cycle arrest and prevents recombination at uncapped telomeres of Saccharomyces cerevisiae

Grandin

Charbonneau

2013

DNA Repair

View full text Add to dashboard Cite

show abstract

Genetic Control of the DNA Polymerase α-Primase complex in the Yeast Saccharomyces cerevisiae

Cited by 1 publication

References 23 publications

RPA provides checkpoint-independent cell cycle arrest and prevents recombination at uncapped telomeres of Saccharomyces cerevisiae

RPA provides checkpoint-independent cell cycle arrest and prevents recombination at uncapped telomeres of Saccharomyces cerevisiae

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