Mutability, sterility and suppression in P—M hybrid dysgenesis: The influence of P subline, cross, chromosome, sex and P-element structure

Abstract

Three Harwich P sublines with different P-element activity potential were used to investigate the influence of P-derived chromosomes on snω mutability and vg suppression and to relate the induction of these dysgenic traits to the number and structure of P elements. Destabilization of the snω allele, a measure of P transposase activity, was differentially influenced by the major autosomes. Chromosome 2 of the standard Harwich subline, Hw, induced only 60% of the level of mutability relative to chromosome 3, whereas chromosome 3 of the weakest Harwich subline, Hf, induced only 50% of the mutability relative to chromosome 2. In somatic suppression of the vg21–3 allele, chromosome 3 of the Hf subline produced a lower level of complete suppression as compared to chromosome 3 of the Hw or the Hs subline (the high hybrid-dysgenesis-inducing subline). The level of these dysgenic traits and GD sterility, was not correlated with the number of P elements per individual (67–68) or per chromosome arm which was very similar among the sublines. The number of complete P elements per genome, based on Southern blot analysis of the X and major autosomes, ranged from 15 to 19. Destabilization of the snω allele and vg suppression by chromosome 3 was correlated with a greater number of complete P elements. Two novel unexpected observations emerged from these studies: both snω mutability and vg suppression data demonstrated high P-element activity in hybrids derived from non-dysgenic crosses irrespective of Harwich subline, indicating a lack of P-cytotype regulation. Mutability in non-dysgenic males ranged from 40 to 60% of the level found in dysgenic males. The high snω mutability and low GD sterility in non-dysgenic hybrids suggests that these traits may arise by a different mechanism. © 1993, Cambridge University Press. All rights reserved.