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Microsatellites, repetitive simple sequences of 1–6 nt in length, are abundant in eukaryotic genomes (Weber 1990a). Because of extensive variability in the number of repeat units for any one locus among members of a population, microsatellite loci exhibit high polymorphism. Microsatellite variation has become a useful class of genetic markers in population assessment for numerous species for questions of genetic identification, parentage, kinship, and population variability assessment (Jarne and Lagoda 1996; Goldstein and Pollock 1997). The high level of polymorphism at microsatellite loci is believed to result from slipped-strand mispairing during DNA replication (Levinson and Gutman 1987; Weber 1990b; Weber and Wong 1993; Krugylak et al. 1998), most commonly causing the gain or loss of one or more repeat units. This mutation mechanism would be expected to generate allelic homoplasy, i.e., comigrating allele size fragments which are not identical by descent or in DNA sequence among different individuals. Because mutational slippage does not conform to the infinite-alleles model (Kimura and Crow 1964), a stepwise mutation model (SMM) (Ohta and Kimura 1973; Chakraborty and Nei 1982) has been invoked to explain allele frequency distributions and population variability at microsatellite loci (Valdez, Slatkin, and Freimer 1993; Kimmel et al. 1996). A distinguishing feature of the two models is that homoplasy is not considered under the infinite-alleles model, while it is an expectation of the stepwise mutation model (Viard et al. 1998). The SMM (but not the infinite-alleles model) makes the assumption that differences in allelic length are due to variation in the number of repeat units and not to insertions and deletions in the flanking sequences. Allelic size homoplasy, a condition under which comigrating alleles represent different sequence motifs, has been demonstrated through sequence analysis of electromorphs of compound or imperfect repeats of primates (Blanquer-Maumont and Crouau-Roy 1995), several fish species (Angers and Bernatchez 1997), invertebrates (Viard et al. 1998), and the fungus Candida albicans (Metzgar et al. 1998). Insertion and deletion events in genomic regions flanking microsatellites confer allelic size homoplasy in several marine turtle species (FitzSimmons et al. 1995) and humans (Homo sa-

Patterns of Size Homoplasy at 10 Microsatellite Loci in Pumas (Puma concolor)