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Embryonic lethality of mutant mice deficient in the p116 gene
Rimiko Koyanagi-Katsuta1, Nobuyoshi Akimitsu, Hiroshi Hamamoto
1Graduate School of Pharmaceutical Sciences, The University of Tokyo, Japan.
Insights
Disrupting the p116 gene, a key part of the translation initiation factor eIF3, causes lethal developmental defects in mouse embryos. This essential protein is crucial for early embryonic development and cell survival.
Area of Science:
- Molecular Biology
- Developmental Biology
- Genetics
Background:
- The p116 protein is a subunit of eukaryotic translation initiation factor 3 (eIF3).
- p116 mRNA is widely expressed, suggesting a vital cellular role.
- Mouse p116 shares high homology with human p116 and possesses conserved RNA-binding domains.
Purpose of the Study:
- To investigate the essential role of the p116 protein in mouse development.
- To determine the consequences of p116 gene disruption in vivo.
Main Methods:
- Generation of mice with a disrupted p116 gene.
- Genotyping of offspring from heterozygous intercrosses at various embryonic stages.
- Analysis of embryonic development in p116 knockout models.
Main Results:
- No p116(-/-) pups were observed among 84 neonates.
- No p116(-/-) embryos were found at 13.5 days postcoitum.
- Only one p116(-/-) embryo was identified at the blastocyst stage (3.5 d.p.c.) out of 77 embryos.
Conclusions:
- p116 is essential for early mouse embryonic development.
- Complete loss of p116 function leads to embryonic lethality.
- The p116 protein plays a critical role in cell survival and development from the earliest stages.
Abstract:
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.