Besides epigenetic factors, also availability and abundance of single nucleotides affect activation of origins of replication [34] and could play a role in variations of replication fork rates.
These differences in contribution to disease and function could be caused by regional variations of replication and adipogenic potential.
These comparative analyses demonstrated frequent variation of the replication origins in both chromosomal variable regions and unstable extrachromosomal replicons, while the conserved replication origins were maintained in location which may be promoted by their impacts on surrounding genes or on the stabilization of minireplicons.
However, to which extend this contributes to the overall replication rate remains unclear, and whether these sequence-specific attributes play an active role in the variation of DNA replication rates has, to our knowledge, not been investigated.
Conversely, the frequent reconstruction of P2 resulted in the variation of bearing replication origins.
These distributions were modeled based on the variation of the replication rates as quantified from single cell microfluidic data (unpublished data).
To test whether this intrinsic variation of mtDNA replication is related to cell cycle as recently demonstrated in mammalian cells [ 16], we co-stained EdU-incubated cells with different cell cycle markers: cyclin E for G1, nuclear EdU incorporation for S phase, cyclin A for G2, and phospho-histone H3 (PH3) for mitosis [ 17, 18].
Data reported are the mean values ± standard variation of three replications.(** P<0.01).
Data reported are the mean values ± standard variation of three replications.
Thus, we proposed that the instability of oriC6- and oriC7-containing ARS plasmids might reflect the unstable nature of the minichromosomes in Haloarcula species, which conversely forced the variation of their bearing replication origins, suggesting an association between the evolution of extrachromosomal replicons and the bearing replication origins.
