ミトコンドリア蛋白p13欠損マウスの生後早期の致死性

• Published in: 日本薬理学会年会要旨集 p. 1-LBS-15
• Main Authors: 新谷, 紀人, 植野, 寛貴, 原, さとみ, 小椋, 紗恵, 井上, 直紀, 師田, 洋平, 橋本, 均
• Format: Journal Article
• Language: Japanese
• Published: 公益社団法人 日本薬理学会 2020
• Subjects: glucose; mitochondria; phenotype
• ISSN: 2435-4953
• DOI: 10.1254/jpssuppl.93.0_1-LBS-15

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.