Targeted Inactivation of p12Cdk2ap1, CDK2 Associating Protein 1, Leads to Early Embryonic Lethality
2009

The Role of Cdk2ap1 in Early Embryo Development

Sample size: 399 publication 10 minutes Evidence: high

Author Information

Author(s): Kim Yong, McBride Jim, Kimlin Lauren, Pae Eung-Kwon, Deshpande Amit, Wong David T.

Primary Institution: University of California Los Angeles

Hypothesis

Cdk2ap1 is essential for early embryonic development and craniofacial morphogenesis.

Conclusion

The study demonstrates that the targeted disruption of Cdk2ap1 leads to early embryonic lethality and craniofacial defects.

Supporting Evidence

  • The knockout of Cdk2ap1 resulted in a high rate of embryonic lethality.
  • Surviving homozygous knockout mice exhibited craniofacial defects.
  • Transgenic rescue improved the survival rate of homozygous knockout mice.
  • Analysis showed that Cdk2ap1 is essential for proper embryonic development.

Takeaway

Cdk2ap1 is a gene that helps embryos grow properly, and when it's missing, the embryos can die or have facial problems.

Methodology

The study used knockout mice to investigate the role of Cdk2ap1 in embryonic development through timed pregnancy analysis and transgenic rescue experiments.

Potential Biases

Potential bias due to the selective breeding and genotyping processes involved in generating knockout mice.

Limitations

The study was limited by the low number of surviving homozygous knockout mice, which may affect the generalizability of the findings.

Participant Demographics

Mice were used in the study, specifically Cdk2ap1 knockout and transgenic mice.

Statistical Information

P-Value

0.5%

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0004518

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