piRNA-mediated transposon regulation and the germ-line mutation rate in Drosophila melanogaster males.

Transposons, especially retrotransposons, are abundant in the genome of Drosophila melanogaster. These mobile elements are regulated by small RNAs that interact with the Piwi family of proteins-the piwi-interacting or piRNAs. The Piwi proteins are encoded by the genes argonaute3 (ago3), aubergine (aub), and piwi.

Transposon regulation in Drosophila: piRNA-producing P elements facilitate repression of hybrid dysgenesis by a P element that encodes a repressor polypeptide.

The transposons of Drosophila melanogaster are regulated by small RNAs that interact with the Piwi family of proteins. These piRNAs are generated from transposons inserted in special loci such as the telomere-associated sequences at the left end of the X chromosome. Drosophila's P transposons can also be regulated by a polypeptide encoded by the KP element, a 1.

Genetic interactions between P elements involved in piRNA-mediated repression of hybrid dysgenesis in Drosophila melanogaster.

Previous studies have shown that telomeric P elements inserted at the left end of the X chromosome are anchors of the P cytotype, the maternally inherited state that regulates P-element activity in the germ line of Drosophila melanogaster. This regulation is mediated by small RNAs that associate with the Piwi family of proteins (piRNAs). We extend the analysis of cytotype regulation by studying new combinations of telomeric and nontelomeric P elements (TPs and non-TPs).

Maternal enhancement of cytotype regulation in Drosophila melanogaster by genetic interactions between telomeric P elements and non-telomeric transgenic P elements.

The X-linked telomeric P elements (TPs) TP5 and TP6 regulate the activity of the entire P element family because they are inserted in a major locus for the production of Piwi-interacting RNAs (piRNAs). The potential for this cytotype regulation is significantly strengthened when either TP5 or TP6 is combined with a non-telomeric X-linked or autosomal transgene that contains a P element. By themselves, none of the transgenic P elements have any regulatory ability.

Maternal impairment of transposon regulation in Drosophila melanogaster by mutations in the genes aubergine, piwi and Suppressor of variegation 205.

TP5, a P element inserted in the telomere-associated sequences of the X chromosome, represses the excision of other P elements in the germ line through a combination of maternal and zygotic effects. The maternal component of this repression is impaired by heterozygous mutations in the aubergine and Suppressor of variegation 205 genes; one mutation in the piwi gene also appears to impair repression. In the female germ line, the level of TP5 mRNA is increased by these impairing mutations.

Cytotype regulation in Drosophila melanogaster: synergism between telomeric and non-telomeric P elements.

The X-linked telomeric P elements TP5 and TP6 interact synergistically with non-telomeric P elements to repress hybrid dysgenesis. In this repression, the telomeric P elements exert maternal effects, which, however, are not sufficient to establish synergism with the non-telomeric P elements. Once synergism is established, the capacity to repress dysgenesis in the offspring of a cross persists for at least two generations after removing the telomeric P element from the genotype.

Cytotype regulation by telomeric P elements in Drosophila melanogaster: variation in regulatory strength and maternal effects.

Strains carrying the X-linked telomeric P elements TP5 or TP6 varied in their ability to repress hybrid dysgenesis. The rank ordering of these strains was consistent across different genetic assays and was not related to the type of telomeric P element (TP5 or TP6) present. Strong repression of dysgenesis was associated with weak expression of mRNA from the telomeric P element and also with a reduced amount of mRNA from a transposase-producing P element contained within a transgene inserted on an autosome.