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

我们对经氯胺丁苯(CHL)处理的G1小鼠进行了筛选中发现的突变体的深入表型鉴定。我们鉴定的突变株是；菌株ID号，CHL0106和CHL0225。前者表现出较低的血糖水平，后者表现为快速凝血。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，我们分析了血小板凝集和计数，以检查功能的异常和血小板的数量。此外，我们还测定了活化的凝血酶原时间、凝血酶原时间。此外，还测定了纤维单体复合体、抗凝血酶-凝血酶复合体的含量，以检测抗凝血因子的作用。因此，我们没有发现CHL0225的所有参数都有异常。提示突变株CHL0225对已知凝血因子、抗凝血因子和血小板功能无明显影响，但凝血级联反应中未知基因发生突变。

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.