Departments of Neurology, and Anatomy and Neurobiology, University of Tennessee Health Science Center, Memphis, TN, USA.
Department of Neurology, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
FEBS Lett. 2018 Sep;592(18):3101-3110. doi: 10.1002/1873-3468.13221. Epub 2018 Aug 29.
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 ) generated by crossing Cre-expressing mice with exon 5-floxed mice (Ciz1 ) do not exhibit evidence of enhanced DNA damage following γ-irradiation or cell-cycle defects. Here, we report that Ciz1 mice show loss of Ciz1 exon 5 but are neurologically normal and express abnormal transcripts (Ciz1 mice) that are translated into one or more proteins of approximate wild-type size. Therefore, Ciz1 mice (Ciz1 ) lose residues encoded by exon 5 but may gain function from novel amino acid sequences.
CIZ1 在 G1/S 检查点的 DNA 合成中发挥作用。Ciz1 基因捕获缺失小鼠表现出运动功能障碍、细胞周期异常和 DNA 损伤。相比之下，此前有报道称，通过将表达 Cre 的小鼠与外显子 5 敲除的小鼠（Ciz1 ）杂交产生的假定 Ciz1 敲除小鼠（Ciz1 ）的胚胎成纤维细胞在 γ 辐射或细胞周期缺陷后不会表现出增强的 DNA 损伤的证据。在这里，我们报告说 Ciz1 小鼠表现出 Ciz1 外显子 5 的缺失，但神经系统正常，并表达异常转录本（Ciz1 小鼠），这些转录本被翻译成一种或多种大小近似野生型的蛋白质。因此，Ciz1 小鼠（Ciz1 ）丢失了外显子 5 编码的残基，但可能从新的氨基酸序列获得功能。
