Microevolution in a philopatric rodent: MHC variation, bottleneck recovery, and fine-scale genetic structure in Dipodomys spectabilis

Joseph D Busch, Purdue University

Abstract

In my dissertation, I investigated microevolution in free-living populations of a philopatric rodent, the banner-tailed kangaroo rat (Dipodomys spectabilis). Because individuals reside in permanent mounds and can be trapped repeatedly, D. spectabilis is an excellent model species for inquiries of dispersal and genetic variation. In Chapter 1, I characterized molecular variation among class II loci of the major histocompatibility complex (MHC). I found D. spectabilis has at least five DRB-like loci that are expressed in the spleen, which demonstrates a level of class II duplication 2-3 times greater than that in muroid rodents such as Mus, Rattus, and Peromyscus. I also determined the complete nuclear sequence (∼10kb including introns) of a putative DRB pseudogene (Disp-DRB*07) and found it had a conventional exon/intron structure. The intron sequences of this locus contain microsatellite loci and short interspersed nuclear elements (SINEs) of the B4, Alu and IDL-Geo subfamilies. BLASTn searches against D. ordii genomic sequences (unassembled reads) showed 90-97% nucleotide similarity between the two kangaroo rat species. Collectively, these data suggest that class II diversity in heteromyid rodents is based on polylocism and departs from the muroid architecture. In addition to studying adaptive variation in this species, I used neutral genetic markers (microsatellites) to investigate the role of dispersal in genetic recovery from demographic bottlenecks (Chapter 2) and the influence of dispersal on fine-scale genetic structure (Chapter 3). I performed an empirical evaluation of the three “single-sample” tests (heterozygosity excess, mode-shift, and M-ratio methods) widely used in conservation genetics. Despite severe demographic bottlenecks in two Arizona populations (Rucker and Portal), a genetic bottleneck signature was not observed using any of the three bottleneck detection methods. While I estimated a relatively high mutation rate in D. spectabilis using genetic parentage (0.0081 mutants/generation/locus), mutation alone is unlikely to explain the rapid bottleneck recovery. Dispersal leading to gene flow is a more likely explanation, despite prior mark-recapture analyses that rarely observed interpopulation dispersal. We interpret our kangaroo rat data in light of the broader literature and conclude that demographic bottlenecks may often be obscured in populations connected by migration. The philopatry displayed by both kangaroo rat sexes is expected to result in fine-scale spatial genetic structure (SGS). In Chapter 3, I used a 14-year temporal series (1994-2007) to track changes in SGS at low, medium, and high population densities. Individual-based spatial genetic autocorrelation detected fine-scale SGS in both Rucker (<800m) and Portal (<400m). Density was negatively associated with SGS (low density>medium density>high density). With regard to sex-bias, I found a small but significant increase in the SGS level of males over females, which matches the greater dispersal distances observed in females. I observed variation in SGS over the ecological timescale of this study, which indicates fine-scale genetic structure is temporally labile. I infer that the decrease in SGS at higher densities is due to the overlap of kin clusters, and that the spatial arrangement of relatives is a key factor in determining SGS patterns. Because few organisms maintain discreet kin clusters, I predict that density will be negatively associated with SGS in many other species.

Degree

Ph.D.

Advisors

DeWoody, Purdue University.

Subject Area

Genetics|Evolution and Development|Organismal biology

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