Consequences of Cre‐mediated deletion of Ciz1 exon 5 in mice

Abstract

CIZ1 plays a role in DNA synthesis at the G1/S checkpoint. Ciz1 gene-trap null mice manifest motor dysfunction, cell-cycle abnormalities, and DNA damage. In contrast, it has previously been reported that mouse embryonic fibroblasts derived from presumed Ciz1 knock-out mice (Ciz1 ) generated by crossing Cre-expressing mice with exon 5-floxed mice (Ciz1 ) do not exhibit evidence of enhanced DNA damage following γ-irradiation or cell-cycle defects. Here, we report that Ciz1 mice show loss of Ciz1 exon 5 but are neurologically normal and express abnormal transcripts (Ciz1 mice) that are translated into one or more proteins of approximate wild-type size. Therefore, Ciz1 mice (Ciz1 ) lose residues encoded by exon 5 but may gain function from novel amino acid sequences.