Accelerated pathway evolution in XXXX -like rodents involves cell cycle control.

@entity1 @entity5 @entity19 @entity840 @entity35 @entity4334 @entity25095
UNASSIGNED: Rodents include both the @entity5 -susceptible short-lived @entity19 and the two unrelated @entity5 -resistant long-lived mole- @entity35 . In this work, their genomes were analyzed with the goal to reveal pathways enriched in genes, which are more similar between the mole- @entity35 than between the @entity19 and the @entity25095 . The pathways related to cell cycle control were prominent. They include external signal transduction and all cell cycle stages. There are several stem cell pathways among them. The other enriched pathways involve ubiquitin-dependent protein degradation, immunity, mRNA splicing, and apoptosis. The ubiquitin-dependent protein degradation is a core of network of enriched pathways. However, this phenomenon is not specific for the @entity19 and the mole- @entity35 . The other muroid species  show features similar to the @entity19 , whereas the non-muroid rodents and the @entity1 show features similar to the mole- @entity35 . The higher ratio of non-synonymous to synonymous @entity4334 substitutions (dN/dS) indicates the accelerated evolution of revealed pathways in the muroid rodents (except the blind mole- @entity35 ). Paradoxically, the dN/dS averaged over the whole genome is lower in the muroids, i.e., the purifying selection is generally stronger in them. In practical sense, these data suggest caveat for using muroid rodents ( @entity19 , @entity35 , and hamsters) as biomedical models of @entity1 conditions involving cell cycle and show the network of pathways where muroid genes are most different (compared with non-muroid) from @entity1 genes. The @entity840 is emphasized as a more suitable rodent model for biomedical research involving cell cycle.
