I googled them, but as I was reading about them, I realised that I skipped high school biology.

Care to give a laymans' explanation?

Don't worry, that's definitely above high school biology level. Here's the most readable article I could find:

https://www.ncbi.nlm.nih.gov/books/NBK21254/

In summary (me: CS background, biology family), there are self-mobile genetic sequences (in that they themselves encode the molecular machinery necessary to move their string of DNA to a different location in the genome) in some fruit fly populations.

Additionally, the implementation of this also gives rise to a phenomenon called hybrid dysgenesis whereby the sexed cross of one type (female without, male with) causes rampant mutations in offspring. Whereas the oppositely sexed cross (female with, male without) has much of the P activity suppressed and therefore able to live.

Presumably this terrifies parent poster because one could hypothetically create a situation where only a population with the genetic secret contained in their females would be able to successfully reproduce.

The short version is that it's a gene that causes mutations and that in somatic and egg cells is turned off. A P-positive female can have offspring with a P-negative male (because the egg cell carries the repressor), but a P-positive male cannot have offspring with a P-negative female. It's easy to see why the P-element would spread through the population.

Yes, it seems to be a common fly-only lab tool over the last 30 years for making some gene (test) pop into more and more genes of the lab population (generation by generation) until either the mutations caused or the overabundance of testRNA wreck the clade. So if MVS II fork{} gave you nightmares more than breeding flies, I guess? [crosses fingers for enjoyable and apt youtube link]