Hybrid Dysgenesis

Hybrid dysgenesis is a syndrome observed in Drosophila that results from the high-frequency germline transposition of a particular Drosophila transposable element called the P element (1). The phenotypes associated with hybrid dysgenesis include a high frequency of mutation and sterility. Hybrid dysgenesis results when males from a strain that contains P elements in its genome are crossed with females from a non-P strain. The lack of high-frequency transposition when P+ (or P– )  strains are crossed among themselves results from the fact that the P element encodes, in addition to a transposase, an inhibitor of transposition. Thus, hybrid dysgenesis occurs only when the egg is from a P– strain, lacking the P element and its inhibitor, and when the P-element-containing DNA arrives via sperm without the inhibitor.

Regulation at several levels can account for hybrid dysgenesis. Transposition of the P element is restricted to the germ line because an intact transposase protein is produced only in the germ line. Transposase is encoded by four separate exons whose messenger RNA needs to be assembled by RNA splicing. This splicing event can occur only in the germ line because a somatic protein that binds to Exon 2 RNA near the 5′ splice site inhibits splicing in somatic tissue (2, 3). Another level of control of P element transposition is the transposition inhibitor encoded by the P element itself (1). This inhibitor derives from the P element mRNA, so the transposition inhibitor is related to, but is not identical to, transposase. The mechanism of inhibition appears to involve repression of transcription, which decreases the amount of available transposase.

The high-frequency P-element transposition in the germline that leads to hybrid dysgenesis thus results from the germline-specific synthesis of transposase from the DNA of the sperm of a P+ male in the absence of a transposition inhibitor; the inhibitor is lacking in the maternal cytoplasm because this fly lacks a P element to generate the inhibitor.

References

1. W. R. Engels (1996) Curr. Top. Microbiol. Immunol. 204, 103–124.

2. F. A. Laski, D. C. Rio, and G. M. Rubin (1986) Cell 44, 7–19. 

3. C. W. Siebel and D. C. Rio (1990) Science 248, 1200–1208.