Different patterns of P transposon and blood retrotransposon distribution in Harwich and Canton-S sub-strains do not affect the manifestation of Drosophila melanogaster intraspecific PM hybrid dysgenesis.

Abstract

Intraspecific infertility, the nature of which is not always understood, occurs in many eukaryotes. Intraspecific PM hybrid dysgenesis (PM HD) in Drosophila melanogaster manifests in one cross direction as offspring infertility and other genetic disorders due to incompatibility between the maternal cytoplasm and the paternal genome. PM HD is believed to result from a massive transposition of the P-element when the maternal cytoplasm lacks a repressor to block it. In this work, we have investigated the distribution of the P transposon and blood retrotransposon in the reference PM HD strains (Canton-S and Harwich), which have been maintained in different laboratories for several decades. P-element distribution patterns vary among Harwich sub-strains, indicating that the P-element was translocated in these genomes. The rate of movement of the P-element, which was not induced by crosses, is comparable to the rate of movement of other DNA transposons. The distribution pattern of the low-active blood retrotransposon in Harwich sub-strains is more stable than that of the P-element, indicating genetic relatedness between sub-strains. Derivatives of the P-element detected in some Canton-S sub-strains possibly indicate genetic contamination. The significant difference in the blood transposable element distribution pattern in Canton-S sub-strains also indicates genetic heterogeneity among them. Despite the complex genealogy of the studied sub-strains, including cases of possible genetic contamination, and differences in P-element distribution, the ability to express PM HD symptoms is preserved in the studied sub-strains.