Genetic and genomic analysis of oxygen consumption in mice.

Abstract

We estimated genetic parameters for oxygen consumption (OC), OC per metabolic body weight (OCMBW) and body weight at three through 8 weeks of age in divergently selected mice populations, with an animal model considering maternal genetic, common litter environmental and cytoplasmic inheritance effects. Cytoplasmic inheritance was considered based on maternal lineage information. With respect to OC, estimated direct heritability was moderate (0.32) and the estimated proportion of the variance of cytoplasmic inheritance effects to the phenotypic variance was very low (0.01), implying that causal genes for OC could be located on autosomes. To assess this hypothesis, we attempted to identify possible candidate causal genes through selective signature detection with the results of pooled whole-genome resequencing using pooled DNA samples from high and low OC mice. We made a list of possible candidate causal genes for OC, including those relating to electron transport chain and ATP-binding proteins (Ndufa12, Sdhc, Atp10b, etc.), Prr16 encoding Largen protein, Cry1 encoding a key component of the circadian core oscillator and so on. The results, although careful interpretation must be required, could contribute to elucidate the genetic mechanism of OC, an indicator for maintenance energy requirement, and therefore feed efficiency.