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

ABSTRACT: 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.

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE199728 | GEO | 2022/04/01

REPOSITORIES: GEO

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

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HDACs act on ribosomal DNA to control the yeast replication program and the competition between origins for limiting initiation factors [ChIP-seq]

Project description:In S. cerevisiae, replication timing is controlled by epigenetic mechanisms restricting the accessibility of origins to limiting initiation factors. About 30% of these origins are located within repetitive DNA sequences such as the ribosomal DNA (rDNA) array, but their regulation is poorly understood. Here, we have investigated how histone deacetylases (HDACs) control the replication program in budding yeast. This analysis revealed that two HDACs, Rpd3 and Sir2, control replication timing in an opposite manner. Whereas Rpd3 delays initiation at late origins, Sir2 is required for the timely activation of early origins. Moreover, Sir2 represses initiation at rDNA origins whereas Rpd3 counteracts this effect. Remarkably, deletion of SIR2 restored normal replication in rpd3 cells by reactivating rDNA origins. Together, these data indicate that HDACs control the replication timing program in budding yeast by modulating the ability of repeated origins to compete with single-copy origins for limiting initiation factors. BrdU-IP-seq analysis of origin activity in wt, sir2 and rpd3 cells, aligned against genomic DNA (sacCer3) and rDNA sequences Please note that the wt WCE #1 and #2 samples are whole-cell extracts from wild-type cells arrested in HU that were used to calculate the log ratio of the BrdU IP #1 and #2 batches, respectively.

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HDACs act on ribosomal DNA to control the yeast replication program and the competition between origins for limiting initiation factors [Mnase-seq]

Project description:In S. cerevisiae, replication timing is controlled by epigenetic mechanisms restricting the accessibility of origins to limiting initiation factors. About 30% of these origins are located within repetitive DNA sequences such as the ribosomal DNA (rDNA) array, but their regulation is poorly understood. Here, we have investigated how histone deacetylases (HDACs) control the replication program in budding yeast. This analysis revealed that two HDACs, Rpd3 and Sir2, control replication timing in an opposite manner. Whereas Rpd3 delays initiation at late origins, Sir2 is required for the timely activation of early origins. Moreover, Sir2 represses initiation at rDNA origins whereas Rpd3 counteracts this effect. Remarkably, deletion of SIR2 restored normal replication in rpd3 cells by reactivating rDNA origins. Together, these data indicate that HDACs control the replication timing program in budding yeast by modulating the ability of repeated origins to compete with single-copy origins for limiting initiation factors. MNase-seq analysis of nucleosome position in wt, sir2 and rpd3 cells, aligned against genomic DNA (sacCer3; *sorted_s3.bed) and rDNA sequences (*rdna_nucleosomes.bed)

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HDACs act on ribosomal DNA to control the yeast replication program and the competition between origins for limiting initiation factors

Project description:In S. cerevisiae, replication timing is controlled by epigenetic mechanisms restricting the accessibility of origins to limiting initiation factors. About 30% of these origins are located within repetitive DNA sequences such as the ribosomal DNA (rDNA) array, but their regulation is poorly understood. Here, we have investigated how histone deacetylases (HDACs) control the replication program in budding yeast. This analysis revealed that two HDACs, Rpd3 and Sir2, control replication timing in an opposite manner. Whereas Rpd3 delays initiation at late origins, Sir2 is required for the timely activation of early origins. Moreover, Sir2 represses initiation at rDNA origins whereas Rpd3 counteracts this effect. Remarkably, deletion of SIR2 restored normal replication in rpd3 cells by reactivating rDNA origins. Together, these data indicate that HDACs control the replication timing program in budding yeast by modulating the ability of repeated origins to compete with single-copy origins for limiting initiation factors. BrdU-IP-chip analysis of origin usage in different yeast HDAC mutants

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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.

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HDACs act on ribosomal DNA to control the yeast replication program and the competition between origins for limiting initiation factors [Mnase-seq]

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HDACs act on ribosomal DNA to control the yeast replication program and the competition between origins for limiting initiation factors [ChIP-seq]

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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

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

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