Schizosaccharomyces pombe
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA360247 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5146320.fastq.gz | Fastqsanger.gz | |||
| SRR5146314.fastq.gz | Fastqsanger.gz | |||
| SRR5146315.fastq.gz | Fastqsanger.gz | |||
| SRR5146316.fastq.gz | Fastqsanger.gz | |||
| SRR5146317.fastq.gz | Fastqsanger.gz |
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Project description:Mrc1 is a conserved checkpoint mediator protein that transduces replication-stress signal to downstream effector kinase. Loss of mrc1 checkpoint activity results in aberrant activation of late/dormant origins in the presence of hydroxyurea. Mrc1 was also suggested to regulate orders of early-origin firing in a checkpoint-independent manner, but its mechanism was unknown. Here we identify HBS (Hsk1 Bypass Segment) on Mrc1. ∆HBS does not suppress late/dormant origin firing in the presence of hydroxyurea but causes precocious and enhanced activation of weak early-firing origins during normal S-phase progression, and bypasses the requirement of Hsk1 for growth. This may be caused by disruption of intramolecular binding between HBS and NTHBS (N-terminal-Target-of-HBS). Hsk1 binds to Mrc1 through HBS and phosphorylates a segment adjacent to NTHBS, disrupting intramolecular interaction. We propose that Mrc1 exerts “brake” on initiation (through intra-molecular interaction) and this brake can be released (upon loss of intra-molecular interaction) by either Hsk1-mediated phosphorylation of Mrc1 or deletion of HBS (or phosphomimic mutation) which can bypass the function of Hsk1 for growth. The “brake” mechanism may explain the checkpoint-independent regulation of early origin firing in fission yeast.
2017-01-06 | GSE93178 | GEO
Project description:How early- and late-firing origins are selected on eukaryotic chromosomes is largely unknown. Here we show that Mrc1, a conserved factor required for stabilization of stalled replication forks, selectively binds to the early-firing origins in a manner independent of Cdc45 and Hsk1 kinase in fission yeast. In mrc1∆ (and in swi1∆ to some extent), efficiency of firing is stimulated and its timing is advanced selectively at those origins that are normally bound by Mrc1. In contrast, the late or inefficient origins which are not bound by Mrc1 are not activated in mrc1∆. The enhanced firing and precocious Cdc45 loading at Mrc1-bound early-firing origins are not observed in a checkpoint mutant of mrc1, suggesting that non-checkpoint function is involved in maintaining the normal program of early-firing origins. We propose that pre-firing binding of Mrc1 is an important marker of early-firing origins which are precociously activated by the absence this protein. Mrc1 binding profiles at G1/S boundary or early S-phase in wild type vs hsk1-89 mutant.
2011-03-26 | GSE28182 | GEO
Project description:Mrc1 marks early-firing origins and coordinates timing and efficiency of initiation in fission yeast
| PRJNA139537 | ENA
Project description:Establishing the program of origin firing during S phase in fission yeast
| PRJNA112031 | ENA
Project description:Cdc7/Hsk1 is a conserved kinase required for initiation of DNA replication that potentially regulates timing and locations of replication origin firing. Here, we show that viability of fission yeast hsk1∆ cells can be restored by loss of mrc1, which is required for maintenance of replication fork integrity, by cds1∆, or by a checkpoint-deficient mutant of mrc1. In these mutants, normally inactive origins are activated in the presence of HU and binding of Cdc45 to MCM is stimulated. mrc1∆ bypasses hsk1∆ more efficiently because of its checkpoint-independent inhibitory functions. Unexpectedly, hsk1∆ is viable at 37°C. More DNA is synthesized, and some dormant origins fire in the presence of HU at 37°C. On the other hand, hsk1∆ bypass strains grow poorly at 25°C compared to at higher temperatures. Our results show that Hsk1 functions for DNA replication can be bypassed by different genetic backgrounds as well as under varied physiological conditions, providing additional evidence for plasticity of the replication program in eukaryotes. BrdU incorporation profiles at early S-phase in mrc1∆, cds1∆ and hsk1-89 mutants.
2011-08-26 | GSE31650 | GEO
Project description:Rif1 is a global regulator of timing of replication origin firing in fission yeast
| PRJNA151423 | ENA
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
Project description:Yeast Sen1Senataxin is a RNA/DNA helicase that preserves replication forks across RNA Polymerase II-transcribed genes by counteracting RNA:DNA hybrids accumulation. We show that in Sen1-depleted cells early forks clashing head-on with transcription halt, and impair progression of sister forks within the same replicon. Unsolved replication-transcription collisions trigger the local firing of dormant origins that rescue arrested forks. In sen1 mutants the MRX and Mrc1/Ctf4-complexes protect those forks clashing with transcription by preventing genotoxic fork-resection events mediated by the Exo1 nuclease. Hence, sister forks within the same replicon remain coupled when one of the two forks halts. This is different when forks encounter double strand breaks. Moreover, the local firing of dormant origins is not prevented by checkpoint activation but depends on delayed adjacent forks. Furthermore, a productive head-on clash between replication and transcription requires the tuning of origin firing and coordination between Sen1, the MRX and Mrc1/Ctf4-complexes and Exo1.
2017-10-11 | GSE97046 | GEO
Project description:Post-transcriptional regulation of cell-cell interaction protein-encoding transcripts by Zfs1p in S. pombe
| PRJNA151061 | ENA