Nature Genet. 15, 83–86 (1997).
Maternally derived cyclin A2 was suggested to ensure normal cell division cycles in Ccna2–/– mouse embryos. This hypothesis was based on immunofluorescence studies at the blastocyst stage. The one-step fixation and permeabilization procedure followed by incubation with the anti-cyclin A2 antiserum has since been shown to result in a high background staining of the embryo. Given that maternal cyclin A2 is undetectable in Ccna2–/– blastocysts using other fixation and permeabilization procedures, we feel that maternal cyclin A2 cannot be considered to persist to the blastocyst stage during early mouse development. This point does not change any of the other conclusions presented in the article.
Author information
Authors and Affiliations
Additional information
The online version of the original article can be found at 10.1038/ng0197-83
Rights and permissions
About this article
Cite this article
Murphy, M. Correction: Delayed early embryonic lethality following disruption of the murine cyclin A2 gene. Nat Genet 23, 481 (1999). https://doi.org/10.1038/70612
Issue Date:
DOI: https://doi.org/10.1038/70612
