Interaction in fitness between lethal genes in heterozygous condition in Drosophila melanogaster.

OST or all individuals of sexually reproducing, diploid and outbreeding species carry in heterozygous condition genetic variants which are deleterious or even lethal in homozygotes. A major open problem of population genetics is to determine how these variants affect the fitness of their heterozygous carriers. Even genes or chromosomes having drastic effects on viability in homozygous condition could be maintained in natural populations for a long time, depending on their heterozygous effects on fitness. Many works (STERN er al. 1952; WALLACE and KING 1952; and others) during the last 25 years have dealt with the heterozygous effects of recessive lethals on the components of fitness (i.e., preadult viability, develolpmental rate, female fertility etc.). Their orientations might be classified into two groups. From the “classical7’ point of view, evidence has accumulated that lethal genes even in a heterozygous state result in a lowering of fitness (STERN et al. 1952; WALLACE and KING 1952; PROUT 1952; SETO 1954; HIRAIZUMI and CROW 1960; GREENBERG and CROW 1960; OSHIMA and KITAGAWA 1961a; TEMIN 1963, 1966; CROW and TEMIN 1964). From the other, “balance,” point of view, the effects of many lethals in a heterozygous state are neutral, or even slightly advantageous when compared with the mean viability of lethal-free organisms (MUKAI and BURDICK 1959; DOBZHANSKY et al 1960; WALLACE and DOBZHAVSKY 1962; OSHIMA 1963; DOBZHANSKY 1964; WALLACE 1965 ; WALLACE and MADDEN 1965 ) . Which of these viewpoints, “classical” or “balance,” more nearly discribes the behavior of lethals, in natural populations? The answer to this important question has implications for our concepts of the genetic load and its role in the evolutionary process ( I~OBZHANSKY 1955). The present study is an attempt to determine the average effects of recessive lethals and ultimately to estimate the interaction in fitness between them, both for natural and for induced recessive lethal mutations, by determining the change in viability with an increase in the number of recessive lethal genes per zygote.