Developmental rate and viability of rainbow trout with a null allele at a lactate dehydrogenase locus

We show that a previously described isozyme polymorphism in rainbow trout(Salmo gairdneri) is the result of an enzymatically inactive (i.e., null) allele(n). Ldh3 null homozygotes(n/n) and heterozygotes(100/n) have reductions of about 20 and 12% in total lactate dehydrogenase (LDH) activity at hatching, respectively. As juveniles,(100/n) fish have reductions in LDH activity of 15, 37, and 21% in brain, heart, and white muscle, respectively. Embryos with differntLdh3 phenotypes from 11 families do not differ significantly in either survival or hatching time. However, a second measure of developmental rate, the amount of malate dehydrogenase (MDH) and phosphoglucomutase (PGM) activity in 33-day-old embryos, suggests that(100/n) embryos develop more slowly than(100/100) embryos. In three of four families examined,(100/n) embryos have significantly lower amounts of total MDH activity (8–10%). In one of these,(100/n) embryos also have significantly lower total PGM activity (15%). These data suggest that the reduction in total LDH activity is associated with small but detectable delays in developmental rate but nondetectable differences in survival to hatching.This research was supported by NSF Grant BSR-8300039 to F. W. Allendorf and a postgraduate scholarship from the NSERC (Canada) to M. M. Ferguson.