This inhibitor reduces the disruption to the genome caused by the movement of P elements, allowing fertile progeny.
Evidence for this comes from crosses of laboratory females (which lack the P transposase inhibitor) with wild-type males (which have P elements).
In the absence of the inhibitor, the P elements can proliferate throughout the genome, disrupting many genes and often proving lethal to progeny or rendering them sterile.
The P element is a class II transposon, and moves by a DNA-based "cut and paste" mechanism.
The hybrid dysgenesis syndrome is marked by temperature-dependent sterility, elevated mutation rates, and increased chromosomal rearrangement and recombination.
The eggs of P strain females contain high amounts of a repressor protein that prevents transcription of the transposase gene.
The eggs of M strain mothers, which do not contain the repressor protein, allow for transposition of P elements from the sperm of fathers.
[3] This effect contributes to piRNAs being inherited only in the maternal line, which provides a defense mechanism against P elements.
Transposase regulates and catalyzes the excision of a P element from the host DNA, cutting at the two recognition sites, and then reinserting randomly.
To use this as a useful and controllable genetic tool, the two parts of the P element must be separated to prevent uncontrolled transposition.
Several lines of flies are required so comparison can take place and ensure that no additional genes have been knocked out.