Present address: Department of Anatomy and Neurobiology, Washington University Medical School, St. Louis, MO 63110, USA.
Population structure and genetic diversity of metamorphic and paedomorphic populations of the tiger salamander, Ambystoma tigrinum
Version of Record online: 11 DEC 2002
Journal of Evolutionary Biology
Volume 6, Issue 3, pages 329–357, May 1993
How to Cite
Routman, E. (1993), Population structure and genetic diversity of metamorphic and paedomorphic populations of the tiger salamander, Ambystoma tigrinum. Journal of Evolutionary Biology, 6: 329–357. doi: 10.1046/j.1420-9101.1993.6030329.x
- Issue online: 11 DEC 2002
- Version of Record online: 11 DEC 2002
- Received 16 January 1992; accepted 22 September 1992.
- Cited By
- Population structure;
- local adaptation
Genetic relationships, population subdivision and genetic diversity were estimated from mtDNA and allozyme data for two subspecies of tiger salamander, one of which is obligately metamorphic and the other polymorphic for paedomorphosis (larval reproduction). Far greater genetic differentiation exists between subspecies than within subspecies, suggesting that the subspecies have evolved in allopatry. Values of Fst calculated from both mtDNA and allozymes were greater than 0.400 for each subspecies. Significant population subdivision was detected even on a microgeographic scale. This extensive population subdivision indicates that populations can respond to extremely localized selection pressures. In the case of paedomorphosis, populations in permanent water should evolve paedomorphosis as long as the appropriate genes exist. For both mtDNA and allozymes, comparisons of population structure within the polymorphic subspecies and between polymorphic and metamorphic subspecies reveal no discernible effects of paedomorphosis. However, a comparison of paedomorphic and metamorphic populations of the polymorphic subspecies showed significantly higher mtDNA diversity in paedomorphic populations. The discrepancy between the allozyme and mtDNA results may be due to the lower effective population size of mtDNA compared to autosomal genes.