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Genetic diversity in leukemia-prone feral house mice infected with murine leukemia virus
Abstract:
The Lake Casitas (LC) mouse population located in south western Ventura county in California is unusual insofar as 85% of these mice are persistently viremic with congenitally transmitted murine leukemia virus (MuLV). The virus has been identified as the etiological agent responsible for lymphoma and neuromotor paralysis in large numbers of the mice. The majority of other wild mouse populations are generally free of infectious MuLV despite the presence of endogenous cellular DNA sequences homologous to infectious virus isolated from wild mice. Electrophoretic variation in 46 gene-enzyme systems was surveyed using mice from Lake Casitas and from a virus-negative population located in Bouquet Canyon (BC) approximately 40 miles from Lake Casitas. The LC and BC populations are genetically very similar to each other and to feral mouse populations previously studied in California and Europe. In the LC population 24% of the loci are polymorphic compared to 17% in the BC population. The average heterozygosities for the LC and Bc populations are 0.094 and 0.073, respectively. The large amount of genic variation in LC fails to support the concept of the derivation of the colony from a small number of founders. Tests for linkage disequilibrium and/or selective association of viremia and polymorphism at 15 loci located on nine mouse chromosomes did not reveal any nonrandom assortments. The viremic LC population, then, appears indistinguishable within the limits of experimental resolution from the virus-negative BC population in its population genetic structure.
Insights
The Lake Casitas mouse population shows high rates of persistent murine leukemia virus (MuLV) infection. Genetic analysis reveals this viremic population is genetically similar to virus-negative populations, indicating no significant impact of MuLV on population structure.
Area of Science:
- * Virology
- * Population Genetics
- * Mammalian Genetics
Background:
- * The Lake Casitas (LC) mouse population exhibits an unusual persistent congenital infection with murine leukemia virus (MuLV) in 85% of individuals.
- * MuLV is linked to lymphoma and neuromotor paralysis in the LC mice, contrasting with most wild mouse populations that are MuLV-free despite endogenous viral sequences.
- * Understanding the genetic structure of this unique viremic population is crucial for disease ecology and host-pathogen interactions.
Purpose of the Study:
- * To compare the population genetic structure of the viremic LC mouse population with a virus-negative population (BC).
- * To investigate potential genetic associations between MuLV viremia and electrophoretic variation in gene-enzyme systems.
- * To assess the impact of persistent MuLV infection on the genetic diversity and population dynamics of the LC mice.
Main Methods:
- * Surveyed electrophoretic variation across 46 gene-enzyme systems in both LC and BC mouse populations.
- * Analyzed genetic similarity, polymorphism, and heterozygosity between the two populations.
- * Tested for linkage disequilibrium and selective associations between viremia and polymorphisms at 15 loci across nine chromosomes.
Main Results:
- * LC and BC populations are genetically similar to each other and to other studied feral mouse populations.
- * The LC population exhibits higher genetic variation (24% polymorphic loci, 0.094 heterozygosity) compared to the BC population (17% polymorphic loci, 0.073 heterozygosity).
- * No significant nonrandom associations were found between MuLV viremia and polymorphisms at the tested loci.
Conclusions:
- * The substantial genic variation in the LC population does not support a bottleneck event from a small number of founders.
- * Despite persistent MuLV infection, the LC population's genetic structure is indistinguishable from the virus-negative BC population within experimental limits.
- * Congenital MuLV infection does not appear to significantly alter the overall population genetic structure of these mice.