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Characterization of transgenic insertional mutant mice with agenesis of corpus caliosum

机译:call体发育不全的转基因插入突变小鼠的表征

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摘要

Here we report a novel mutant mouse line with agenesis of corpus caliosum. We produced the transgenic mice carrying Ted-on expression systems and named a line of the mice TAS. Twenty percentage of heterozygous TAS mice exhibited abonormal circling behavior. Yypical histological abnormality was the agenesisi of corpus caliosum and anterior commissure, the formation of Probst bundle, and the hypoplasia of hippocampus and its commissure, resembling callosal dysgenesis in human, The frequency of the cerebral abnormality was 50% and 100% in heterozygous and homozygous TAS mice, respectively. Sinece it is well-known that Tet-on expression systems do not affect mouse development, the cerebral malformation may be due to transgene insertional/ or deletion mutation. FISH and SNPs analyses revealed that TAS transgene is integrated into 19.4 Mb downstream so the centromere on chromosome 18 somewhere. Our findings demonstrated thet TAS mouse line is a useful model for the investigation of pathogenesis on callosal dysgenesis.
机译:在这里,我们报告一种新的突变小鼠品系的发生。我们生产了携带Ted-on表达系统的转基因小鼠,并命名了TAS小鼠系。 20%的杂合TAS小鼠表现出异常的盘旋行为。典型的组织学异常是人的cal体和前连合的年龄缺失,Probst束的形成以及海马及其连合的发育不全,类似于人的call体发育不全。在杂合子和纯合子中,脑部异常的发生率分别为50%和100%。 TAS小鼠。众所周知,Tet-on表达系统不会影响小鼠的发育,大脑畸形可能是由于转基因插入/缺失突变引起的。 FISH和SNPs分析表明,TAS转基因已整合到下游的19.4 Mb中,因此18号染色体上的着丝粒位于某处。我们的发现表明,TAS小鼠系是用于研究骨s发育不全的发病机理的有用模型。

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