Mous Saturation mutagenesis project:Construction of sperm bank for chromosome deletion mutants and development of screening system for the mutations

我们对筛选氯霉素（CHL）处理的Gl小鼠中发现的小鼠突变体进行了深入的表型表征。我们描述的突变体是；菌株ID号，CHL0106和CHL0225。前者突变体表现出较低的血清葡萄糖水平，后者表现出快速的血液凝固。通过与野生型小鼠杂交，证实了这两个突变体的遗传。对于CHL0225，我们分析血小板凝固，计数血小板数量，以检查功能异常和血小板数量。此外，我们还测定了活化凝血活素时间、凝血酶原时间。此外，测定抗凝血素-抗凝血素复合物纤维单体的数量，以检测抗凝血因子的功能。因此，我们没有发现CHL0225的所有参数都有异常。说明突变体CHL0225不影响已知凝血因子、抗凝血因子和血小板功能，而是发生了凝血级联中未知基因的突变。

We carried out in-depth phenotype characterization of mouse mutants identified in screening for chlorambucil (CHL) treated Gl mice. The mutants that we characterized were ; strain ID numbers, CHL0106 and CHL0225. The former mutant showed lower glucose level in serum, and the latter showed rapid blood clotting. Inheritance of these two mutants was confirmed by cross of the mutants with wild-type mice. For the CHL0225, we analyzed platelet coagulation and counted the number of the platelets in order to examine abnormalities of the function and the amount of the platelets. In addition, we assayed activated thromboplastin time, prothrombin time. Moreover, Amount of fibrimonomer complex antithromobin-thromobin complex was measured in order to examine the function of anti-coagulation factors. As a result, we could not find abnormalities in the all parameters of the CHL0225. It indicated that the mutant CHL0225 is not affected in the known coagulation factors, the anti-coagulation factors and the platelet function, but rather unknown gene in the blood clotting cascade is mutated.