Arnaud-Dabernat S, Bourbon P M, Dierich A, Le Meur M, Daniel J Y
Biologie de la Différenciation et du Développement, Université Victor Segalen-Bordeaux2, Bordeaux, France.
J Bioenerg Biomembr. 2003 Feb;35(1):19-30. doi: 10.1023/a:1023561821551.
Mice carrying a homozygous germ-line mutation in the nm23-M1 gene that eliminates its protein expression and drives expression of beta-galactosidase by nm23-M1 promoter have been generated. nm23-M1 gene inactivation is not teratogenic and the pups can grow to adult age without apparent health problems. However, they undergo a growth retardation and knocked out females cannot feed their pups. Both effects are background dependent. Beta-galactosidase mapping of nm23-M1 promoter activation during embryogenesis shows that the nm23-M1 gene is principally expressed in epithelial layer of tissues which require inductive epithelial-mesenchymal interactions for their formation. In conclusion, invalidated mice could be interesting models to analyze the role of nm23-M1 on signal transduction pathway regulation, or cancer induction and proliferation.
已培育出在nm23-M1基因中携带纯合种系突变的小鼠，该突变消除了其蛋白质表达，并通过nm23-M1启动子驱动β-半乳糖苷酶的表达。nm23-M1基因失活不会致畸，幼崽能够成长至成年，且无明显健康问题。然而，它们会出现生长迟缓，基因敲除的雌性小鼠无法哺育幼崽。这两种效应均依赖于遗传背景。胚胎发育过程中nm23-M1启动子激活的β-半乳糖苷酶定位显示，nm23-M1基因主要在那些形成需要诱导性上皮-间充质相互作用的组织的上皮层中表达。总之，基因无效小鼠可能是分析nm23-M1在信号转导通路调控、癌症诱导和增殖中作用的有趣模型。
