Delayed early embryonic lethality following disruption of the murine cyclin A2 gene (vol 15, pg 83, 1997)

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.