Early postnatal lethality of mice lacking mitochondrial protein p13

Abstract

p13 is mitochondrial protein widely expressed in central and peripheral tissues. Recently, we generated mice lacking p13 (p13-/- mice), and found that p13-/- genotype was smaller than the expected Mendelian ratio at 3 weeks of age (approx. 40% of the expected ratio). Here, we investigated the possible mechanisms underlying the loss of p13-/- mice. At postnatal day 0 (P0), Mendelian segregation of pup genotypes from heterozygous breeding was observed (n = 294, P = 0.25, χ² analysis), suggesting a significant loss of p13-/- pups specifically during the postnatal period. Kaplan-Meier survival analysis demonstrated that more than half of p13-/- mice died during the first 2 postnatal days. At P0, we observed the presence of milk in p13-/- pups stomach, however, their blood glucose levels were significantly lower than that of wild-type littermates. Taken together, the present results suggest that p13 contributes to early postnatal survival and maintenance of the normal blood glucose levels.