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Rpd3 regulates single-copy origins independently of the rDNA array by opposing origin stimulation by Fkh1 [ChIP-seq]

ABSTRACT: Rpd3 regulates single-copy origins independently of the rDNA array by opposing origin stimulation by Fkh1 [ChIP-seq]

PROVIDER: PRJNA821254 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18530512.fastq.gz	Fastqsanger.gz
	SRR18530513.fastq.gz	Fastqsanger.gz
	SRR18530514.fastq.gz	Fastqsanger.gz
	SRR18530515.fastq.gz	Fastqsanger.gz
	SRR18530516.fastq.gz	Fastqsanger.gz

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Rpd3 regulates single-copy origins independently of the rDNA array by opposing origin stimulation by Fkh1

Project description:Rpd3 regulates single-copy origins independently of the rDNA array by opposing origin stimulation by Fkh1

| PRJNA824145 | ENA

Rpd3 regulates single-copy origins independently of the rDNA array by opposing origin stimulation by Fkh1 [BrdU-IP-seq]

Project description:Rpd3 regulates single-copy origins independently of the rDNA array by opposing origin stimulation by Fkh1 [BrdU-IP-seq]

| PRJNA824142 | ENA

Rpd3 regulates single-copy origins independently of the rDNA array by opposing origin stimulation by Fkh1 [ChIP-seq]

Project description:The replication of eukaryotic genomes is highly regulated to ensure faithful transmission of all genetic information through cell divisions. In addition to stringent control of origin initiation by cell cycle controls and DNA damage checkpoints, spatial and temporal control of origins serves to stage and balance replication of different genomic regions, with potential implications for development and genome stability. Replication of highly repetitive sequences creates stressful competition between genomic regions for sufficient replication resources. Here, we examined histone deacetylases Rpd3 and Sir2 in balancing replication between unique sequences and the multi-copy ribosomal DNA gene cluster(s), which has emerged as an evolutionarily conserved node of genomic instability. We elucidate Rpd3's mechanism of origin regulation, which is distinct and independent of Sir2.

2022-04-01 | GSE199728 | GEO

Rpd3 regulates single-copy origins independently of the rDNA array by opposing Fkh1-mediated origin stimulation.

Project description:Eukaryotic chromosomes are organized into structural and functional domains with characteristic replication timings, which are thought to contribute to epigenetic programming and genome stability. Differential replication timing results from epigenetic mechanisms that positively and negatively regulate the competition for limiting replication initiation factors. Histone deacetylase Sir2 negatively regulates initiation of the multicopy (∼150) rDNA origins, while Rpd3 histone deacetylase negatively regulates firing of single-copy origins. However, Rpd3's effect on single-copy origins might derive indirectly from a positive function for Rpd3 in rDNA origin firing shifting the competitive balance. Our quantitative experiments support the idea that origins compete for limiting factors; however, our results show that Rpd3's effect on single-copy origin is independent of rDNA copy-number and of Sir2's effects on rDNA origin firing. Whereas RPD3 deletion and SIR2 deletion alter the early S phase dynamics of single-copy and rDNA origin firings in opposite fashion, unexpectedly only RPD3 deletion suppresses overall rDNA origin efficiency across S phase. Increased origin activation in rpd3Δ requires Fkh1/2, suggesting that Rpd3 opposes Fkh1/2-origin stimulation, which involves recruitment of Dbf4-dependent kinase (DDK). Indeed, Fkh1 binding increases at Rpd3-regulated origins in rpd3Δ cells in G1, supporting a mechanism whereby Rpd3 influences initiation timing of single-copy origins directly through modulation of Fkh1-origin binding. Genetic suppression of a DBF4 hypomorphic mutation by RPD3 deletion further supports the conclusion that Rpd3 impedes DDK recruitment by Fkh1, revealing a mechanism of Rpd3 in origin regulation.

| S-EPMC9546531 | biostudies-literature

Rpd3 regulates single-copy origins independently of the rDNA array by opposing origin stimulation by Fkh1 [BrdU-IP-seq]

2022-04-06 | GSE200349 | GEO

Rpd3 regulates single-copy origins independently of the rDNA array by opposing origin stimulation by Fkh1

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

2022-04-06 | GSE200351 | GEO

The Fkh1 Forkhead Associated Domain promotes ORC binding to a cohort of DNA replication origins in budding yeast

Project description:Fkh1 is a transcription factor with multiple roles in chromosomal biology in budding yeast.

2021-02-28 | GSE165464 | GEO

FKH1 phosphoproteomics TMT LC-MS

Project description:Phosphoproteomics of FKH1 in comparison to U937 cells as negative control

2022-10-14 | PXD031429 | Pride

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)

2015-12-18 | GSE71050 | GEO