SUMMARYThe availability of restriction fragment length polymorphisms (RFLPs) would be useful for studying the extent of diversity among morpholgically indistinguishable populations of filarial parasites. Such polymorphisms may be useful in correlating various physiological and clinical differences with parasite heterogeneity. In order to identify such RFLPs, we isolated DNA from microfilaria of 6 filarial species (Acanthocheilonema viteae, Brugia malayi, Brugia pahangi, Dirofilaria immitis, Litomosoides carinii and Setaria digitatum), digested the DNA with several restriction endonucleases, prepared Southern blots and probed with 32 P-labelled DSA probes. The patterns of fragments generated using two restriction endonucleases, Mbo I and Taq I, in combination with two probes, rDNA from the free-living soil nematode Caenorhabditis elegans, and pBM103, an anonymous DNA probe from B. malayi, unequivocally distinguish between all 6 of the species. To ensure that the differences we observed between the species represent true interspecies variation rather than fortuitous individual variations we analysed DNA from several individual B. malayi and B. pahangi worms. The individual B. malayi worms demonstrated restriction profiles that were invariant, as did the individual B. pahangi worms, demonstrating that the differences we observed were true interspecies variations.

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In a companion study, a number of P element insertions into the singed locus were characterized. Here is reported a detailed analysis of the structure and mutability of another P element insertion at sn, known as sncm. Under conditions which mobilize P elements, sncm mutates at high frequency to both wild-type (sn+) and to a much more extreme allele (snext). Wild-type revertants appear to represent precise or nearly precise excisions of the P element. Certainly two, and most likely all five, of the snext alleles studied result from the insertion of a duplicate copy of this P element into a nearby site in an inverted orientation. We propose a model in which both the sn+ and snext mutational events can be explained by excision of the P element from one chromatid followed by reintegration into the sister chromatid at a nearby site (intracistronic transposition). Finally, it is shown that the snext alleles are themselves unstable and the structure of a resulting chromosome aberration is examined.