SUMMARYNeuraminidase‐1 (NEU‐1) is one of two neuraminidase isozymes which can be detected electrophoretically in mouse liver extracts. The inheritance of variation in NEU‐1 and the linkage relationships of the gene controlling this variation were studied through a backcross analysis involving the SM/J and MA/MyJ inbred strains, and by examination of NEU‐1 phenotypes in three congenic strains: Bl0.SM, Bl0.SM(22R) and B10.RVB. The data indicate that NEU‐1 is controlled byNeu‐1, a gene previously identified by its effect on total liver neuraminidase activity in whole tissue homogenates. Analysis of the congenic strains revealed identical low activity (SM/J‐type:Neu‐1α/Neu‐1α) NEU‐1 phenotypes in all three strains. This indicates thatNeu‐Ilies in the segment of the SM/J‐derivedH‐2region that is common to all three strains:H‐2EαtoH‐2D. In addition, we examined the relationship between NEU‐1 and phenotypic variation in liver acid phosphatase (AP; for which a new typing method is described) and linkage order among several other enzyme‐coding genes linked toH‐2. In all animals that could be scored confidently for AP, the NEU‐1 and AP phenotypes were concordant, adding support to the hypothesis that both phenotypes are controlled byNeu‐1. Recombination rates among six H‐2‐Linked marker loci were unexpectedly low, but were sufficient to verify the position ofUpg‐1as the telomeric flanking marker relat
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