We conclude that Pif1 and Rrm3 are detrimental to the integrity of replicating chromosomes in the absence of Rad53 following replication stress.
Every nucleosome across the genome must be disrupted and reformed when the replication fork passes, but how chromatin organization is re-established following replication is unknown.
We then discuss chromatin reassembly following replication fork passage, where the incorporation of a combination of newly synthesized histones and parental histones can impact the inheritance of lysine methylation marks on the daughter strands.
CtrA is re-synthesized following replication initiation.
We provide evidence that recombination-like X structures form at OriP following replication pausing and origin activation.
XerC/D recombinases act at the dif site to resolve chromosome dimers following replication termination [35], [36].
Association of UNG2 with centromeres during late S-phase would suggest a role for UNG2 during or immediately following replication of centromeric DNA.
However, ATR, which is responsible for H2AX phosphorylation following replication inhibition [7], appears to have access to heterochromatin at least during S-phase.
These results indicate that either the products of viral replication are not required for ISG stimulation, or that the virus can efficiently antagonize innate immune responses following replication, thus inhibiting ISG activation.
Deamination of cytosine (C) results in the formation of uracil (U) in DNA which will code for adenine in the following replication cycle, thus giving rise to a C to T (thymine) transition [1], [2].
We propose the following replication cycle (Figure 8), composed of an early phase between 0 3 h p.i. (steps 1 4) and of a late phase thereafter (steps 5 8).
