This page was most recently updated 5/21/08.
This paper argues that, in contrast to yeast genes, human genes are frequently oriented in the same direction as replication fork movment.
This manuscript describes genes that are necessary for maintenance of an "originless" fragment of chromosome III in budding yeast
This paper demonstrates a phenomenon that was proposed many years ago, but which remained controversial until now: that c-myc can directly stimulate initiation at replication origins, independently of its role as a regulator of gene expression.
This paper shows "that ORC recruitment by TRF2 contributes to telomere integrity by facilitating efficient telomere DNA replication and preventing the generation of telomere-repeat-containing circles"
This interesting paper from Genevieve Almouzni's lab supports the hypothesis that replication fork progression and histone supply are coordinately regulated via a complex consisting of the histone chaperone, Asf1, histones H3 and H4, and the MCM2-7 proteins.
This paper describes a histone modification (methylation of H4K20), catalyzed by the SET8 protein, that is essential for replication fork progression and for avoidance of massive DNA damage during S phase.
This paper suggests that (i) topo1 and topo2 both bind to specific locations at the human lamin B2 replication origin, (ii) they bind at specific times during the cell cycle, and (iii) topo1 is essential for origin firing. However, previous studies indicate that neither topo1 nor topo2 is essential for origin firing in budding yeast. Does this paper provide convincing evidence for a real difference between human and yeast origin-topoisomerase interactions?
This interesting paper characterizes the ways in which yeast and mammalian cells respond to the presence of O6-methyl guanine in their DNA, and the consequences of abortive attempts to repair this lesion by mismatch repair.
This paper shows that a human Sir2 homologue, SIRT6, specifically deacetylates histone H3-K9 in telomeres and that loss of SIRT6 leads to telomere dysfunction and cellular senescence.