The recent discoveries of a Fe-S cluster binding domain in Pri2 and three major replicative DNA polymerases raise the possibility that DNA replication may be subjected to redox regulation.
Of course in nature so many variables are beyond the control of researchers that no study can ever be perfectly replicated, and in some cases, as with critically endangered species, replication may be infeasible and even unethical [ 12].
Whether other types of replicators exist is an empirical matter, and viewing various biological processes as replication may be scientifically productive according to Sterelny et al. (1996).
Our data also suggest that the initial step of DNA replication may be modulated by oxidative stress.
Furthermore, under optimal growth conditions accelerated proliferation (also called 'multifork DNA-replication') can be monitored: new rounds of DNA replication may be initiated before a previous round is completed, putatively providing another source of heterogeneity (Bley [1990]; Müller [2007]).
In Clouds, the replication may be achieved either by copying the state of a system (checkpoint) or by replaying input to all replicas (lock-step based) [16] (see Fig. 9).
This suggests that point mutations that reduce fitness and in vivo replication may be more stable than initially anticipated, which may alleviate some concerns regarding rationally designed MD vaccines based upon point mutations.
The Chinese equine infectious anemia virus (EIAV) donkey-leukocyte attenuated vaccine (DLV) provides a unique natural model system by which attenuated mechanism and immunological control of lentivirus replication may be studied.
Although P27 was rationally designed to block dimerization of the mature HIV-1 protease, the effects of P27 on HIV-1 replication may be related to partial inhibition of Gag-Pol processing leading to a disruption in virus release.
Therefore, no tradeoff between virulence and replication may be at play in our pathosystem.
Possibly, replication may be defective due to reduced PCNA levels upon anti-estrogen treatment of cells in S-phase.
