ROSA26 mice carry a modifier of Min-induced mammary and intestinal tumor development

• Published in: Mammalian genome Vol. 11; no. 12; pp. 1058 - 1062
• Main Authors: Kohlhepp, R L, Hegge, L F, Nett, J E, Moser, A R
• Format: Journal Article
• Language: English
• Published: United States Springer-Verlag 01.12.2000; Springer Nature B.V
• Subjects: Animals; Base Sequence; DNA Primers; Ethylnitrosourea - toxicity; Female; Genes, APC; Genetic Predisposition to Disease; Intestinal Neoplasms - genetics; Male; Mammary Neoplasms, Experimental - chemically induced; Mammary Neoplasms, Experimental - genetics; Mammary Neoplasms, Experimental - pathology; Mice; Mice, Mutant Strains; Min gene; Rodents; Tumors
• ISSN: 0938-8990; 1432-1777
• DOI: 10.1007/s003350010208

B6.129S7-Gtrosa26 (B6.R26) mice carry a LacZ-neoR insertion on Chromosome (Chr) 6, made by promoter trapping with 129 ES cells. Female C57BL/6J Apc ᴹⁱⁿ /+ (B6Min/+) mice are highly susceptible to intestinal tumors and to the induction of mammary tumors after treatment with ethylnitrosourea (ENU). However, B6.R26/+Min/+ females develop fewer mammary and intestinal tumors after ENU treatment than do B6 Min/+ mice. B6.R26/+ mice from two independently derived congenic lines show this modifier effect. Each of these congenic lines carries approximately 20 cM of 129-derived DNA flanking the insertion, raising the possibility that the resistance is due to a linked modifier locus. To further map the modifier locus, we have generated several lines of mice carrying different regions of the congenic interval. We have found that resistance to mammary and intestinal tumors in ENU-treated Min/+ mice maps to a minimum 4-cM interval that includes the ROSA26 LacZ-neoR insertion. Therefore, the resistance to tumor development is due to either the ROSA26 insertion or a very tightly linked modifier locus.