More Functional V1R Genes Occur in Nest-Living and Nocturnal Terricolous Mammals

Size of the vomeronasal type 1 receptor (V1R) gene repertoire may be a good indicator for examining the relationship between animal genomes and their environmental niche specialization, especially the relationship between ecological factors and the molecular evolutionary history of the sensory system. Recently, Young et al. (Young JM, Massa HF, Hsu L, Trask BJ. 2009. Extreme variability among mammalian V1R gene families. Genome Res.) concluded that no single ecological factor could explain the extreme variability of the V1R gene repertoire in mammalian genomes. In contrast, we found a significant positive correlation between the size and percentage of intact V1R genes in 32 species that represent the phylogenetic diversity of terricolous mammals and two ecological factors: spatial activity and rhythm activity. Nest-living species possessed a greater number of intact V1R genes than open-living species, and nocturnal terricolous mammals tended to possess more intact V1R genes than did diurnal species. Moreover, our analysis reveals that the evolutionary mechanisms underlying these observations likely resulted from the rapid gene birth and accelerated amino acid substitutions in nest-living and nocturnal mammals, likely a functional requirement for exploiting narrow, dark environments. Taken together, these results reveal how adaptation to divergent circadian rhythms and spatial activity were manifested at the genomic scale. Size of the V1R gene family might have indicated how this gene family adapts to ecological factors

Adaptation to acetaminophen exposure elicits major changes in expression and distribution of the hepatic proteome.

Acetaminophen overdose is the leading cause of acute liver failure. One dose of 10-15 g causes severe liver damage in humans, whereas repeated exposure to acetaminophen in humans and animal models results in autoprotection. Insight of this process is limited to select proteins implicated in acetaminophen toxicity and cellular defence. Here we investigate hepatic adaptation to acetaminophen toxicity from a whole proteome perspective, using quantitative mass spectrometry. In a rat model, we show the response to acetaminophen involves the expression of 30% of all proteins detected in the liver. Genetic ablation of a master regulator of cellular defence, NFE2L2, has little effect, suggesting redundancy in the regulation of adaptation. We show that adaptation to acetaminophen has a spatial component, involving a shift in regionalisation of CYP2E1, which may prevent toxicity thresholds being reached. These data reveal unexpected complexity and dynamic behaviour in the biological response to drug-induced liver injury