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

CIZ 1 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 tm1.1Homy/tm1.1Homy ) generated by crossing Cre‐expressing mice with exon 5‐floxed mice ( Ciz1 tm1Homy/tm1Homy ) do not exhibit evidence of enhanced DNA damage following γ‐irradiation or cell‐cycle defects. Here, we report that Ciz1 tm1.1Homy/tm1.1Homy mice show loss of Ciz1 exon 5 but are neurologically normal and express abnormal transcripts ( Ciz1 ΔE5/ΔE5 mice) that are translated into one or more proteins of approximate wild‐type size. Therefore, Ciz1 tm1.1Homy/tm1.1Homy mice ( Ciz1 ΔE5/ΔE5 ) lose residues encoded by exon 5 but may gain function from novel amino acid sequences.