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Quantitative BrdU immunoprecipitation method demonstrates that Fkh1 and Fkh2 are rate-limiting activators of replication origins that reprogram replication timing in G1 phase

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE71052 | GEO | 2015/12/18

SECONDARY ACCESSION(S): PRJNA290188

REPOSITORIES: GEO

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Quantitative BrdU immunoprecipitation method demonstrates that Fkh1 and Fkh2 are rate-limiting activators of replication origins that reprogram replication timing in G1 phase.

Project description: Not available

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Quantitative BrdU immunoprecipitation method demonstrates that Fkh1 and Fkh2 are rate-limiting activators of replication origins that reprogram replication timing in G1 phase (BrdU)

Project description:The S. cerevisiae Forkhead Box (FOX) proteins, Fkh1 and Fkh2, regulate diverse cellular processes including transcription, long-range DNA interactions during homologous recombination, and replication origin timing and long-range origin clustering. As stimulators of early origin activation, we hypothesized that Fkh1 and Fkh2 abundance limits the rate of origin activation genome-wide. Existing methods, however, were not well suited to quantitative, genome-wide measurements of origin firing between strains and conditions. To overcome this limitation, we developed qBrdU-seq, a quantitative method for BrdU incorporation analysis of replication dynamics, and applied it to show that overexpression of Fkh1 and Fkh2 advance the initiation timing of many origins throughout the genome resulting in a higher total level of origin initiations in early S phase. The higher initiation rate is accompanied by slower replication fork progression, thereby maintaining a normal length of S phase without causing detectable Rad53 checkpoint kinase activation. The advancement of origin firing time, including that of origins in heterochromatic domains, was established in late G1 phase, indicating that origin timing can be reset subsequently to origin licensing. These results provide novel insights into the mechanisms of origin timing regulation by identifying Fkh1 and Fkh2 as rate-limiting factors for origin firing that determine the ability of replication origins to accrue limiting factors and have the potential to reprogram replication timing late in G1 phase. 5 total experiments with replicates

2015-12-18 | E-GEOD-71050 | biostudies-arrayexpress

Quantitative BrdU immunoprecipitation method demonstrates that Fkh1 and Fkh2 are rate-limiting activators of replication origins that reprogram replication timing in G1 phase (BrdU)

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Quantitative BrdU immunoprecipitation method demonstrates that Fkh1 and Fkh2 are rate-limiting activators of replication origins that reprogram replication timing in G1 phase (ChIP)

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Fkh1 and Fkh2 associate with Sir2 to control CLB2 transcription under normal and oxidative stress conditions.

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CDK12 catalytic activity is rate-limiting for RNAPII processivity on core DNA replication genes and G1/S progression

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-07-22 | GSE120072 | GEO

CDK12 catalytic activity is rate-limiting for RNAPII processivity on core DNA replication genes and G1/S progression (nuclear RNA)

Project description:In this study we characterized the importance of CDK12-kinase activity in cell cycle regulation, using CDK12 anolog-sentive cells. Inhibition of analog-sensitive CDK12 reveals its catalytic activity is necessary for optimal G1/S progression. Mechanistically, CDK12 regulates transcription of core DNA replication genes and affects timely assembly of pre-replication DNA complex on chromatin. We have performed 3’-end RNA-sequencing after CDK12 inhibition and identified that the expression of core DNA replication genes were affected. To investigate further, we carried out nuclear RNA-seq coupled with ChIP-seq, and demonstrated that CDK12 regulates RNAPII processivity of core DNA replication genes and optimal G1/S progression.

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Fkh1 and Fkh2 bind multiple chromosomal elements in the S. cerevisiae genome with distinct specificities and cell cycle dynamics.

Project description: Not available

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