However, we point out that most H3K9me3 sites are normally in late replicating domains and therefore the reduction must basically "mainly" affect late replication domains.
Telomeres of the fission yeast, Schizosaccharomyces pombe, are known to replicate in late S phase, but the reasons for this late replication are not fully understood.
Specifically, point mutations and copy number losses correlate with late replication, while copy number gains and other rearrangements correlate with early replication.
By overlaying CpG and expression data onto the trained replication-timing map, we also show that supraHex is able to intuitively capture an inherent relationship between late replication, low CpG density promoters and low expression levels.
In this model, a third category is added to separately model early and late replication studies.
Furthermore, in human cells it has been demonstrated that late replication foci contain a HDAC and also that PCNA interacts with the DNA methyltransferase DNMT1, which localizes to both early and late replication foci [49].
Increased histone acetylation in the Δrpd3 mutant shortens S-phase by advancing the timing of Cdc45 binding to late replication origins and causing their earlier activation.
Recruitment of a HAT to a late replication origin advances its association with Cdc45 and its time of firing in yeast [4].
It has recently been demonstrated in the Encode project that the H3K27me3 mark shows a positive correlation with late replication of large DNA segments [53].
In Saccharomyces cerevisiae the deletion of one of the S-phase cyclins, Clb5, causes a strong delay of late replication origins [16].
Deletion of RPD3 had been shown to accelerate S-phase progression by advancing Cdc45 binding and activation of late replication origins [2], [4].
