Identification and Linkage Analyses of a Gene, <italic>Rcs-1</italic>, Suppressing Spontaneous SJL/J Lymphoma Expression<xref ref-type="fn" rid="FN2">2</xref>

Abstract

Populations of SJL/J (SJL), A.SW/SnJ (A.SW), F1, and backcross mice were followed over 2 years for the spontaneous development of reticulum cell sarcoma (RCS). A.SW, F1, and SJL mice demonstrated cumulative RCS incidences of 0, 9, and greater than 95%, respectively. The incidence of RCS in SJL X (SJL X A.SW), SJL X (A.SW X SJL), and (SJL X A.SW) X SJL backcross mice was 58%, a rate consistent (P less than .001) with a single dominant A.SW gene, termed "Rcs-1," suppressing disease. Rcs-1 is not an H-2 gene nor is it on the X- or Y-chromosome. Rcs-1 abrogates tumor initiation relatively early rather than later by affecting tumor growth; its effect is not transmitted by (SJL X A.SW)F1 females to their offspring by non-Medelian maternal factors. No linkage was detected between Rcs-1 and the marker genes Igh-1 (chromosome 12), Pgm-1 (chromosome 5), Hbb (chromosome 7), Idh-1 (chromosome 1), or Gr-1 (chromosome 8). Thus Rcs-1 is different from three genes linked to these markers and known to influence murine leukemia virus, Fv-4 (chromosome 12), Cv (chromosome 5), and Fgv-1 (chromosome 7).