The proportion of pseudogenes in NWMs is significantly different from other primates (P < 0.01, Fisher's exact test), which is consistent with previous reports that NWMs have a relatively lower fraction of pseudogenes (Rouquier et al. 2000; Gilad et al. 2004).
Also, we discovered that NWMs may have maintained additional, functional steroid-hormone receptor binding sites in the AluSx SINE that could confer retinoic acid (RA) and thyroid hormone (TH) responsiveness; however, these sites were less highly conserved during human, ape and OWM evolution.
Prior to generating divergence estimates, we pruned the family-scale dataset so that each NWM genus was represented by no more than five nominal member species.
These data indicate that the NWM gene has retained the ability to respond to ATRA while the OWM, apes and humans have not.
The lack of response to T3 suggests that the NWM CAMP gene may not respond to this hormone or that other cell types or tissues need to be examined.
The NWMs are naturally resistant to 1,25(OH)2duedue to the over expression of VDRE-binding proteins (VDRE-BP) that requires NWMs to maintain high levels of 1,25(OH)2D3 to displace it from binding sites [ 39, 40].
The analysis of optical density of affected tissue revealed significant reduction of mitochondrial immunoreactive signal for COX-I in both EA (P < 0.01) and LA lesional stages (P < 0.001) in comparison to that in NWM.
Our analyses also estimated the tMRCA of SFVmar and SFVspm (~23.40 Myr) and that of NWM FVs (~40.81 Myr) to be greater than those of their hosts (~22.76 Myr, [ 38]).
Within the cellular profiles, however, mitochondrial density is not reduced in comparison to that seen in the NWM of controls.
In fact, the numbers of functional OR genes in human and chimpanzee are similar to that in NWMs and OWMs.
