Embryonic lethality of mutant mice deficient in the p116 gene
Embryonic lethality of mutant mice deficient in the p116 gene
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DOI：
10.1093/oxfordjournals.jbchem.a003172
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发表时间：
2002-06-01
影响因子：
2.7
通讯作者：
Sekimizu, K
中科院分区：
文献类型：
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作者：
Koyanagi-Katsuta, R;Akimitsu, N;Sekimizu, K
我们报告了一种致死表型的小鼠胚胎与破坏的基因编码p116，翻译起始因子，eIF 3的亚基。小鼠p116的氨基酸序列与人p116的同源性高达97%，并含有保守的RNA结合位点RNP 1和RNP 2。p116 mRNA在各种器官中普遍表达，表明p116蛋白具有管家功能。为了获得p116蛋白在小鼠细胞中的重要作用的遗传证据，我们构建了p116基因中断的小鼠。将杂合子p116（+/-）小鼠进行杂交，并确定后代的基因型。结果表明，84名新生儿中没有p116（-/-）幼崽。此外，没有p116（-/-）胚胎后13.5天（d.p.c.）。在77个胚胎中，只有一个p116（-/-）胚胎在囊胚期（3.5 d.p.c.）。这些结果表明，p116在小鼠发育的早期阶段起着至关重要的作用。
We report a lethal phenotype of mouse embryo with a disruption in the gene encoding p116, a subunit of the translation initiation factor, eIF3. The amino acid sequence of mouse p116, as deduced from the cDNA, shows high homology (97%) with human p116, and contains the conserved RNA binding sites, RNP1 and RNP2. The p116 mRNA is ubiquitously expressed in various organs, suggesting a house-keeping function of the p116 protein. To obtain genetic evidence for the essential role of the p116 protein in mouse cells, we constructed mice with a disruption in the p116 gene. Heterozygous p116(+/-) mice were intercrossed, and the genotypes of the offspring were determined. The results indicated no p116(-/-) pups among 84 neonates. Also, there were no p116(-/-) embryos 13.5 days postcoitum (d.p.c.). Among 77 embryos, there was only one p116(-/-) embryo at the blastocyst stage (3.5 d.p.c.). These results indicate that p116 plays an essential role in the early stages of mouse development.