Of course a parasite (replicase) molecule cannot help its own replication; it needs another replicase in its catalytic neighbourhood for that.
After the virus had infected the cell and begun its usual process of replication, it incorporated the gene into its own genetic material.
Given its importance for mtDNA replication, it is formally possible that TWINKLE might play an active regulatory role in mtDNA replication.
As IE62 is a potent transactivator essential for the viral replication, it is not easy to investigate its potential role in the inhibition of IRF3 in VZV-infected cells.
Again, this is not a requirement for replication; it is merely one form of a replicator.
Since the deletion-circle lacks an origin of replication it is unlikely that it will be replicated during cell-division.
The third protein-encoding gene of the operon, repC, is essential for plasmid replication; it encodes the initiator protein, RepC, which exerts its function by binding the origin of replication located within its own coding sequence [ 1, 2, 6].
However, due to its emphasis on short genomes and error-prone replication, it soon became a standard for RNA virus evolution.
Although the C-terminal AAD is not required for replication, it is interesting to consider that Dpb11 may, by analogy to its role in checkpoints, play roles in the initiation process beyond simple scaffolding.
Even if Mehr followed through with this option, and conducted an exact replication in the original author's lab (which you could say would be a pure exact replication), it wouldn't allow for future situations in which other labs might wish to independently reproduce the study.
If there is no mismatch in replication it resorts to random sampling.
