Taricha

Abstract: Thirty species of potential predators on Taricha granulosa were tested by injection or force-feeding to determine their susceptibility to adult T. granulosa skin toxin. All species tested were found to be susceptible to Taricha skin toxin. The action of adult T. granulosa skin toxin is identical to that described for tetrodotoxin from the eggs of T. torosa and the puffer fish. Mammals and birds are susceptible to similar relative amounts of toxin; 0.0002 cc of back skin of T. granulosa killed white mice in 10 min. Snakes other than garter snakes were about 200 times more resistant, and garter snakes were 2000 times more resistant than white mice. T. granulosa was self-susceptible to large doses. Garter snakes, Thamnophis sirtalis concinnus, were able to eat adult newts, even though they were killed by injections. Taricha toxin was very stable and did not lose potency over an 11-month period.

Abstract: Where do the genetic variants underlying adaptive change come from? Are currently adaptive alleles recruited by selection from standing genetic variation within populations, moved through introgression from other populations, or do they arise as novel mutations? Here, we examine the molecular basis of repeated adaptation to the toxin of deadly prey in 3 species of garter snakes (Thamnophis) to determine whether adaptation has evolved through novel mutations, sieving of existing variation, or transmission of beneficial alleles across species. Functional amino acid substitutions in the skeletal muscle sodium channel (Nav1.4) are largely responsible for the physiological resistance of garter snakes to tetrodotoxin found in their newt (Taricha) prey. Phylogenetic analyses reject the hypotheses that the unique resistance alleles observed in multiple Thamnophis species were present before the split of these lineages, or that alleles were shared among species through occasional hybridization events. Our results demonstrate that adaptive evolution has occurred independently multiple times in garter snakes via the de novo acquisition of beneficial mutations.