DNA Replication Profiling Using Deep Sequencing

Saayman, Xanita; Ramos-Pérez, Cristina; Brown, Grant W.

doi:10.1007/978-1-4939-7306-4_15

Cited by 6 publications

(6 citation statements)

References 20 publications

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“…DNA copy number analysis DNA copy number in wild-type and rad5D cells was analyzed during synchronous progression through S phase in the presence of HU, as described (Saayman et al, 2018).…”

Section: Chip Sequencing Data Analysismentioning

confidence: 99%

Rad5 Recruits Error-Prone DNA Polymerases for Mutagenic Repair of ssDNA Gaps on Undamaged Templates

et al. 2019

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Section: Chip Sequencing Data Analysismentioning

confidence: 99%

Rad5 Recruits Error-Prone DNA Polymerases for Mutagenic Repair of ssDNA Gaps on Undamaged Templates

et al. 2019

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“…We asked how Rec8 altered genome replication and how individual adaptive mutations restored the tempo of genome replication to that of wild-type cells. We constructed a whole genome replication profile by genome sequencing multiple time points of a synchronized yeast population proceeding through S phase [50]. By analyzing changes in read depth during S phase, we calculated T rep , the time at which 50% of cells in a population complete replication at a given genomic locus.…”

Section: Adaptive Genetic Changes Delay the Timing Of Genome Replicatmentioning

confidence: 99%

“…The analysis of genome replication profile was done as described [36,50]. Reads mapping and CNVs detection were processed as in [61].…”

Section: Whole Genome Replication Profilementioning

confidence: 99%

Evolutionary repair: Changes in multiple functional modules allow meiotic cohesin to support mitosis

et al. 2020

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The role of proteins often changes during evolution, but we do not know how cells adapt when a protein is asked to participate in a different biological function. We forced the budding yeast, Saccharomyces cerevisiae, to use the meiosis-specific kleisin, recombination 8 (Rec8), during the mitotic cell cycle, instead of its paralog, Scc1. This perturbation impairs sister chromosome linkage, advances the timing of genome replication, and reduces reproductive fitness by 45%. We evolved 15 parallel populations for 1,750 generations, substantially increasing their fitness, and analyzed the genotypes and phenotypes of the evolved cells. Only one population contained a mutation in Rec8, but many populations had mutations in the transcriptional mediator complex, cohesin-related genes, and cell cycle regulators that induce S phase. These mutations improve sister chromosome cohesion and delay genome replication in Rec8-expressing cells. We conclude that changes in known and novel partners allow cells to use an existing protein to participate in new biological functions.

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“…The analysis of genome replication profile was done as described (Saayman et al, 2018); 811 (Fumasoni and Murray, 2019). Reads mapping and CNVs detection were processed as 812 (Koschwanez et al, 2013).…”

Section: Whole Genome Sequencing and Analysis 767mentioning

confidence: 99%

“…We asked how Rec8 altered genome replication and how individual adaptive mutations 399 restored the tempo of genome replication to that of wild-type cells. We constructed a whole 400 genome replication profile by genome sequencing multiple time points of a synchronized yeast 401 population proceeding through S phase (Saayman et al, 2018). By analyzing changes in read depth 402 during S phase, we calculated Trep, the time at which 50% of cells in a population complete 403 replication at a given genomic locus.…”

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confidence: 99%

Evolutionary repair: changes in multiple functional modules allow meiotic cohesin to support mitosis

Hsieh

Makrantoni

Robertson

et al. 2019

Preprint

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Different members of the same protein family often perform distinct cellular functions. How much are these differing functions due to changes in a protein’s biochemical activity versus changes in other proteins? We asked how the budding yeast, Saccharomyces cerevisiae, evolves when forced to use the meiosis-specific kleisin, Rec8, instead of the mitotic kleisin, Scc1, during the mitotic cell cycle. This perturbation impairs sister chromosome linkage and reduces reproductive fitness by 45%. We evolved 15 populations for 1750 generations, substantially increasing their fitness, and analyzed their genotypes and phenotypes. We found no mutations in Rec8, but many populations had mutations in the transcriptional mediator complex, cohesin-related genes, and cell cycle regulators that induce S phase. These mutations improve sister chromosome cohesion and slow genome replication in Rec8-expressing cells. We conclude that changes in known and novel partners allow proteins to improve their ability to perform new functions.

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DNA Replication Profiling Using Deep Sequencing

Abstract: Profiling of DNA replication during progression through S phase allows a quantitative snap-shot of replication origin usage and DNA replication fork progression. We present a method for using deep sequencing data to profile DNA replication in S. cerevisiae.

Cited by 6 publications

References 20 publications

Rad5 Recruits Error-Prone DNA Polymerases for Mutagenic Repair of ssDNA Gaps on Undamaged Templates

Rad5 Recruits Error-Prone DNA Polymerases for Mutagenic Repair of ssDNA Gaps on Undamaged Templates

Evolutionary repair: Changes in multiple functional modules allow meiotic cohesin to support mitosis

Evolutionary repair: changes in multiple functional modules allow meiotic cohesin to support mitosis

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