Gould K A, Dietrich W F, Borenstein N, Lander E S, Dove W F
McArdle Laboratory for Cancer Research, University of Wisconsin, Madison 53706, USA.
Genetics. 1996 Dec;144(4):1769-76. doi: 10.1093/genetics/144.4.1769.
The intestinal tumor multiplicity in mice heterozygous for ApcMin is strongly modulated by genetic background. On the sensitive C57BL/6J (B6) background, mice develop large numbers of intestinal adenomas. The AKR/J (AKR) strain carries alleles that correlate with a strong reduction in tumor multiplicity. To study the effect of one of these modifiers, Mom1, we have generated a mouse line in which the AKR allele of Mom1 is carried on the sensitive B6 genetic background. This strain was produced by using a marker-assisted selection method to eliminate unlinked AKR alleles more rapidly. The application and efficiency of this method are discussed. We used this strain to determine that Mom1 affects both tumor multiplicity and tumor size in a semi-dominant fashion.
ApcMin杂合子小鼠的肠道肿瘤多发性受到遗传背景的强烈调控。在敏感的C57BL/6J(B6)背景下,小鼠会产生大量肠道腺瘤。AKR/J(AKR)品系携带的等位基因与肿瘤多发性的显著降低相关。为了研究其中一个修饰基因Mom1的作用,我们培育了一个小鼠品系,其Mom1的AKR等位基因位于敏感的B6遗传背景上。该品系是通过使用标记辅助选择方法更快地消除不连锁的AKR等位基因而产生的。本文讨论了该方法的应用及效率。我们使用这个品系确定Mom1以半显性方式影响肿瘤多发性和肿瘤大小。