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 (Ciz1tm1.1Homy/tm1.1Homy) generated by crossing Cre-expressing mice with exon 5-floxed mice (Ciz1tm1Homy/tm1Homy) do not exhibit evidence of enhanced DNA damage following γ-irradiation or cell-cycle defects. Here, we report that Ciz1tm1.1Homy/tm1.1Homy mice show loss of Ciz1 exon 5 but are neurologically normal and express abnormal transcripts (Ciz1ΔE5/ΔE5 mice) that are translated into one or more proteins of approximate wild-type size. Therefore, Ciz1tm1.1Homy/tm1.1Homy mice (Ciz1ΔE5/ΔE5) lose residues encoded by exon 5 but may gain function from novel amino acid sequences.
Publication Title
FEBS Letters
Recommended Citation
Xiao, J., Khan, M., Vemula, S., Tian, J., & LeDoux, M. (2018). Consequences of Cre-mediated deletion of Ciz1 exon 5 in mice. FEBS Letters, 592 (18), 3101-3110. https://doi.org/10.1002/1873-3468.13221
