Although these terms may be appropriate for the relations between genes and organisms, they interfere with a more general analysis of replication and selection.
Thus, the effect might not be completely related to the promoter controlling the replication, but a more general phenomenon in viral replication might be also involved.
Indeed, the adverse effect on early differentiation into cholinergic neurons appears to be among the most sensitive effects, independent of the more general inhibition of cell replication or axonogenesis.
Gene clusters, formed based on similarity of expression-pattern across either all tissues or the immune tissues only, had highly significant associations both with immunological processes such as chemokine-mediated response, antigen processing, receptor-related signal transduction, and transcriptional regulation, and also with more general processes such as replication and cell cycle control.
Thus, we decided to test our model first on report of actual behavior (i.e., missed school and missed family/friend activities), followed by testing model replication using more general perceptions of disability (i.e., FDI).
The studies from yeast to mammals show that Rif1 function has evolved from a protein that specifically participated in replication of the special DNA sequences present at the telomeres to a more general role in DNA damage response and reinitiation of replication at stalled replication forks.
(For a more general study of gene context of archaeal DNA replication proteins, we refer the interested reader to Ref. [30]).
Do these more general concepts facilitate the formation of a general analysis of replication that applies at the very least to gene-based biological evolution but also to selection in other contexts?
We propose here a more general kinetic formalism for early enantioselection, based on our previously described Graded Autocatalysis Replication Domain (GARD) model for prebiotic evolution in molecular assemblies.
Moreover, as various alterations in Mcm expression or function are linked to oncogenic DNA replication (e.g., [ 57]), Mcm2-7 is a promising drug target for the development of both general replication inhibitors that stem cellular proliferation, as well as potentially more sophisticated inhibitors that specifically target Mcm2-7 in tumor cells (discussed below).
