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Mutability, sterility and suppression in P—M hybrid dysgenesis: the influence ofPsubline, cross, chromosome, sex and P-element structure

Authors :
Lola Margulies
Howard Balter
Max Levitan
Yuan Wang
Source :
Genetical Research. 62:111-123
Publication Year :
1993
Publisher :
Hindawi Limited, 1993.

Abstract

SummaryThree Harwich P sublines with differentP-element activity potential were used to investigate the influence of P-derived chromosomes on snωmutability andvgsuppression and to relate the induction of these dysgenic traits to the number and structure ofPelements. Destabilization of thesnωallele, a measure ofPtransposase 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 thevg21–3allele, chromosome 3 of the Hfsubline produced a lower level of complete suppression as compared to chromosome 3 of the Hwor the Hssubline (the high hybrid-dysgenesis-inducing subline). The level of these dysgenic traits and GD sterility, was not correlated with the number ofPelements per individual (67–68) or per chromosome arm which was very similar among the sublines. The number of completePelements per genome, based on Southern blot analysis of the X and major autosomes, ranged from 15 to 19. Destabilization of thesnωallele andvgsuppression by chromosome 3 was correlated with a greater number of completePelements. Two novel unexpected observations emerged from these studies: bothsnωmutability andvgsuppression data demonstrated highP-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 highsnωmutability and low GD sterility in non-dysgenic hybrids suggests that these traits may arise by a different mechanism.

Details

ISSN :
14695073 and 00166723
Volume :
62
Database :
OpenAIRE
Journal :
Genetical Research
Accession number :
edsair.doi.dedup.....d111d8d2c87747d6426d2f73f93f8283
Full Text :
https://doi.org/10.1017/s0016672300031700