Abstract
P elements were first discovered in the fruit fly Drosophila melanogaster as the causative agents of a syndrome of aberrant genetic traits called hybrid dysgenesis. This occurs when P element-carrying males mate with females that lack P elements and results in progeny displaying sterility, mutations and chromosomal rearrangements. Since then numerous genetic, developmental, biochemical and structural studies have culminated in a deep understanding of P element transposition: from the cellular regulation and repression of transposition to the mechanistic details of the transposase nucleoprotein complex. Recent studies have revealed how piwi-interacting small RNA pathways can act to control splicing of the P element pre-mRNA to modulate transposase production in the germline. A recent cryo-electron microscopy structure of the P element transpososome reveals an unusual DNA architecture at the transposon termini and shows that the bound GTP cofactor functions to position the transposon ends within the transposase active site. Genome sequencing efforts have shown that there are P element transposase-homologous genes (called THAP9) in other animal genomes, including humans. This review highlights recent and previous studies, which together have led to new insights, and surveys our current understanding of the biology, biochemistry, mechanism and regulation of P element transposition.
Highlights
P elements were first discovered in the fruit fly Drosophila melanogaster as the causative agents of a syndrome of aberrant genetic traits called hybrid dysgenesis
P elements were discovered in the mid-1970s by population geneticists when wild Drosophila melanogaster strains were brought into captivity and mated to laboratory strains that had been in captivity since the early 1900s [1,2]
Alternative pre-mRNA splicing of the third intron in dysgenic germ cells leads to the production of full-length P element mRNAs encoding for the 87 kDa transposase protein. This restricts the deleterious effects of rampant P element transposition and hybrid dysgenesis to germline cells of dysgenic progeny [59]
Summary
An intriguing feature of hybrid dysgenesis that readily captivated the attention of researchers was its temperaturesensitivity [4]. Developmental analyses corroborated results obtained early on from temperature shift experiments, which narrowed the temperature-sensitive window leading to complete sterility to the period between 10 h after egg laying and 4 days of development—a period that spans from mid-embryogenesis until late-larval development [5,43]. It is likely that the germ cell fate transition from PGCs to germline stem cells (GSCs), which occurs during late-larval stages when the somatic niche is formed and becomes active, delineates the end of the temperaturesensitive window that leads to complete sterility. Instead, following a temporary halt in GSC differentiation, fertility is restored to wild-type levels a few days after the beginning of the exposure to restrictive temperatures [5,48] In this case, as well as what was observed in individuals grown at 25°C, halt in germline development in response to non-dysgenic royalsocietypublishing.org/journal/rsob Open Biol. Dysgenesis involves the activity of the chk DNA damage checkpoint kinase [48,49]
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