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Consequences of Cre‐mediated deletion of Ciz1 exon 5 in mice
Author(s) -
Xiao Jianfeng,
Khan Mohammad Moshahid,
Vemula Satya,
Tian Jun,
LeDoux Mark S.
Publication year - 2018
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.13221
Subject(s) - exon , biology , microbiology and biotechnology , dna damage , gene , dna , genetics
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.