Consequences of Cre-mediated deletion of Ciz1 exon 5 in mice.

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^{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.

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