Mid-facial developmental defects caused by the widely used LacZ reporter gene when expressed in neural crest-derived cells.
Mid-facial developmental defects caused by the widely used LacZ reporter gene when expressed in neural crest-derived cells.
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由广泛使用的 LacZ 报告基因在神经嵴衍生细胞中表达时引起的中面部发育缺陷
DOI：
10.1007/s11248-018-0091-0
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发表时间：
2018-12
影响因子：
3
通讯作者：
Liu F
中科院分区：
文献类型：
--
作者：
Wei X;Hu M;Liu F
报告基因在转基因研究中起着重要作用。LacZ是一种广泛使用的报告基因，其编码大肠杆菌β-半乳糖苷酶，该酶以其将X-gal水解成蓝色产物的能力而闻名。目前还不清楚转基因LacZ是否有任何副作用。R26R报告小鼠，含有LacZ报告基因，产生监测体内重组活性的各种转基因Cre重组酶通过X-gal染色。P0-Cre在神经嵴来源的细胞中表达，这些细胞产生大部分颅面骨。在此，我们报告说，12%的R26R报告小鼠窝藏P0-Cre有意想不到的面中部发育缺陷，表现为一些面骨的不对称生长，从而导致倾斜的面中部结构，较短的头骨长度，和咬合不正。组织学检查显示额上颌缝的紊乱，这至少可以部分解释受影响的转基因小鼠的形态缺陷。我们的数据要求考虑转基因β-半乳糖苷酶引起的潜在体内不良反应。
Reporter genes play important roles in transgenic research. LacZ is a widely used reporter gene that encodes Escherichia coli β-galactosidase, an enzyme that is well known for its ability to hydrolyze X-gal into a blue product. It is unknown whether transgenic LacZ has any adverse effects. R26R reporter mice, containing a LacZ reporter gene, were generated to monitor the in vivo recombination activity of various transgenic Cre recombinase via X-gal staining. P0-Cre is expressed in neural crest-derived cells, which give rise to the majority of the craniofacial bones. Herein, we report that 12% of the R26R reporter mice harboring P0-Cre had unexpected mid-facial developmental defects manifested by the asymmetrical growth of some facial bones, thus resulting in tilted mid-facial structure, shorter skull length, and malocclusion. Histological examination showed a disorganization of the frontomaxillary suture, which may at least partly explain the morphological defect in affected transgenic mice. Our data calls for the consideration of the potential in vivo adverse effects caused by transgenic β-galactosidase.
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