A C420R gain-of-function mutation in the Pik3ca (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) gene arises somatically in some cancers and vascular malformations.&nbsp; These Pik3ca:C420R conditional mutant mice permit further study of how this mutation alters cell behavior. Exon 8 of the mouse Pik3ca gene carries the C420R aa (T2928C bp) mutation.&nbsp; Exons 7-9 are further flanked by loxP sites, and an FRT-flanked PGK-neomycin cassette in reverse orientation in intron 9 blocks expression of the gene. Pik3ca:C420R heterozygotes are viable and fertile, but animals homozygous for this knock-out allele are embryonic lethal.FLP recombinase-mediated excision of the reverse-oriented FRT-flanked PGK-neomycin cassette in intron 9 enables tissue-specific expression of the C420R mutant form of the gene. Though untested in vivo (October, 2018), subsequent cre recombinase-mediated excision of floxed exons 7-9 is predicted to result in a complete tissue-specific knock-out of Pik3ca.

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FLP recombinase-mediated excision of a reverse-oriented FRT-flanked PGK-neomycin cassette in this conditional knock-in/knock-out allele enables tissue-specific expression of an exon 8 C420R mutant form of Pik3ca that has been associated with cancer and vascular malformations. Subsequent cre recombinase-mediated excision of floxed exons 7-9 is predicted to result in a complete tissue-specific knock-out.

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