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

Abstract

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 different Ldh3 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.