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.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Aug 29, 2018
- Source ID
- 10.1002/1873-3468.13221
Entities
People
- Jianfeng Xiao
- Jun Tian
- Mark S LeDoux
- Mohammad Moshahid Khan
- Satya R Vemula
Organizations
- National Institutes of Health
- United States Department of Defense
- University of Tennessee Health Science Center
- Zhejiang University