Consequences of Cre‐mediated deletion of Ciz1 exon 5 in mice
| Autor: | Satya R. Vemula, Mohammad Moshahid Khan, Jun Tian, Jianfeng Xiao, Mark S. LeDoux |
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| Rok vydání: | 2018 |
| Předmět: |
Male
0301 basic medicine Cerebellum DNA damage Biophysics Mice Transgenic RNA-Seq Motor Activity Biology Biochemistry Article 03 medical and health sciences Exon Structural Biology Genetics medicine Animals Molecular Biology Cells Cultured Mice Knockout chemistry.chemical_classification Dystonia Integrases DNA synthesis urogenital system Cell Cycle Nuclear Proteins Exons Cell Biology Fibroblasts Embryo Mammalian medicine.disease Embryonic stem cell Molecular biology Amino acid Mice Inbred C57BL 030104 developmental biology medicine.anatomical_structure chemistry Female DNA Damage |
| Zdroj: | FEBS Letters. 592:3101-3110 |
| ISSN: | 1873-3468 0014-5793 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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