Genetic control of MuLV-gs expression in crosses between high and low leukemia incidence strains

✍ Scribed by Jo Hilgers; Jan Galesloot

• Book ID: 102865841
• Publisher: John Wiley and Sons
• Year: 1973
• Tongue: French
• Weight: 911 KB
• Volume: 11
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/ijc.2910110329

✦ Synopsis

Abstract

A newly developed test for MuLV‐gs antigen, based on disappearance rate (DR) of injected rat anti‐MuLV antibody in mice, has been used in combination with a previously described quantitative immunofluorescence adsorption (IFA) technique for the antigen in spleens, in order to classify inbred strains of mice of European and American origin. The following groups could be distinguished: (1) low leukemia incidence strains, mice which were MuLV‐gs negative in their spleens and sera; (2) low leukemia incidence strains, of which young adult mice were generally MuLV‐gs negative, whereas old mice were occasionally positive, levels of the antigen being invariably low in the spleens of positive animals; (3) one low leukemia strain (NZB, a mouse strain with auto‐immune disease), of which young adult mice were generally MuLV‐gs negative, whereas all older mice were highly positive, levels in spleens reaching those in spleens of high leukemia strain mice; and (4) high leukemia strains, mice of which were always MuLV‐gs positive, levels of the antigen in spleens and sera being invariably high, even in young adult mice. Spleens and sera of adult animals of the F~1~ hybrid between a high (AKR) and a low (C57BL) leukemia incidence strain contain intermediate amounts of MuLV‐gs. In this heterozygote, the antigen was generally found at an earlier age than in all low leukemia incidence strains, but at a later age than in the high leukemia incidence strain. Typing for MuLV‐gs in spleens and sera of normal segregants between mice of high and low leukemia strains revealed that: (1) one semidominant host gene, presumably Fv‐1, controls MuLV‐gs levels as shown in back‐crosses to the high incidence strain, and (2) two additional dominant genes are involved in all‐or‐none expression of MuLV‐gs as shown in backcrosses to the low incidence strain and in F~2~ generations.