Microsatellites, comprising (GT)\dn6 n tandemly repeated arrays, were isolated from a size-selected genomic library of rainbow trout (Oncorhynchus mykiss) DNA. Primers were designed for five microsatellite loci, four of which were variable. Primers for two of these loci were used in conjunction with primers for three microsatellite loci from a related species, Salmo salar, to investigate patterns of differentiation in freshwater migratory populations of rainbow trout in Lake Ontario. The five loci used revealed high levels of polymorphism with heterozygosity estimates ranging from 0.740 to 0.956. Significant differences in allele frequencies among populations were observed for all loci. Heterozygosity and allele number values, at each locus for each population, were used to test two alternative mutation models, the infinite allele model (IAM) and the stepwise mutation model (SMM). The predictions of the IAM proved to be more accurate for the majority of the data and this model was used to calculate estimates of effective population size.

Molecular EcologyVolume 5, Issue 2 p. 311-312 Development of PCR primers for nine polymorphic American mink Mustela vison microsatellite loci M. O'CONNELL, Corresponding Author M. O'CONNELL Marine Gene Probe Laboratory, Department of Biology, Dalhousie University, Halifax, Nova Scotia, Canada B3H 4J1 Tel.: 902 494 2260. Fax: 902 494 3736. E-mail: michaelo@is.dal.caSearch for more papers by this authorJ. M. WRIGHT, J. M. WRIGHT Marine Gene Probe Laboratory, Department of Biology, Dalhousie University, Halifax, Nova Scotia, Canada B3H 4J1Search for more papers by this authorA. FARID, A. FARID *Department of Animal Science, Nova Scotia Agricultural College, Truro, Nova Scotia, Canada B2N 5E3Search for more papers by this author M. O'CONNELL, Corresponding Author M. O'CONNELL Marine Gene Probe Laboratory, Department of Biology, Dalhousie University, Halifax, Nova Scotia, Canada B3H 4J1 Tel.: 902 494 2260. Fax: 902 494 3736. E-mail: michaelo@is.dal.caSearch for more papers by this authorJ. M. WRIGHT, J. M. WRIGHT Marine Gene Probe Laboratory, Department of Biology, Dalhousie University, Halifax, Nova Scotia, Canada B3H 4J1Search for more papers by this authorA. FARID, A. FARID *Department of Animal Science, Nova Scotia Agricultural College, Truro, Nova Scotia, Canada B2N 5E3Search for more papers by this author First published: April 1996 https://doi.org/10.1046/j.1365-294X.1996.00103.xCitations: 45AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume5, Issue2April 1996Pages 311-312 RelatedInformation

The transcriptional enhancers of the Moloney and Friend murine leukemia viruses (MLV) are important determinants of viral pathogenicity. We used electrophoretic mobility shift and methylation interference assays to study nuclear factors which bind to a region of these enhancers whose sequence is identical between Moloney and Friend viruses and particularly highly conserved among 35 mammalian type C retroviruses whose enhancer sequences have been aligned (E. Golemis, N. A. Speck, and N. Hopkins, J. Virol. 64:534-542, 1990). Previous studies identified sites for the leukemia virus factor b (LVb) and core proteins in this region (N. A. Speck and D. Baltimore, Mol. Cell. Biol. 7:1101-1110, 1987) as well as a site, overlapping those for LVb and core, for a third factor (N. R. Manley, M. A. O'Connell, P. A. Sharp, and N. Hopkins, J. Virol. 63:4210-4223, 1989). Surprisingly, the latter factor appeared to also bind two sites identified in the Friend MLV enhancer, Friend virus factor a and b1 (FVa and FVb1) sites, although the sequence basis for the ability of the protein to bind these diverse sites was not apparent. Here we describe the further characterization of this binding activity, termed MCREF-1 (for mammalian type C retrovirus enhancer factor 1), and the identification of a consensus sequence for its binding, GGN8GG. We also identify a factor, abundant in mouse T-cell lines and designated LVt, which binds to two sites in the Moloney MLV enhancer, overlapping the previously identified LVb and LVc binding sites. These sites contain the consensus binding site for the Ets family of proteins. We speculate on how distinct arrays of these factors may influence the disease-inducing phenotype.

Mammalian type C retrovirus enhancer factor 1 (MCREF-1) is a nuclear protein that binds several directly repeated sequences (CNGGN6CNGG) in the Moloney and Friend murine leukemia virus (MLV) enhancers (N. R. Manley, M. O'Connell, W. Sun, N. A. Speck, and N. Hopkins, J. Virol. 67:1967-1975, 1993). In this paper, we describe the partial purification of MCREF-1 from calf thymus nuclei and further characterize the binding properties of MCREF-1. MCREF-1 binds four sites in the Moloney MLV enhancer and three sites in the Friend MLV enhancer. Ethylation interference analysis suggests that the MCREF-1 binding site spans two adjacent minor grooves of DNA.