Models of repression of transposition in P-M hybrid dysgenesis by P cytotype and by zygotically encoded repressor proteins.

By analytical theory and computer simulation the expected evolutionary dynamics of P transposable element spread in an infinite population are investigated. The analysis is based on the assumption that, unlike transposable elements which move via RNA intermediates, the harmful effects of P elements arise primarily in the act of transposition, and that this causes their evolutionary dynamics to be unusual. It is suggested that a situation of transposition-selection balance will be superceded by the buildup of a cytoplasmically inherited repression or by the elimination of active transposase-encoding elements from the chromosomes, a process which may be accompanied by the evolution of elements which encode proteins which repress transposition.

Somatic reversion of P transposable element insertion mutations in the singed locus of Drosophila melanogaster requiring specific P insertions and a trans- acting factor

SummaryDestabilization in somatic cells of P-element insertions in the X-linked singed gene of Drosophila melanogaster has been studied. We have shown that some but not all unstable P-element insertions in singed can form mosaics. The cause of this variation is not clear from studies of the restriction maps of the mutations tested. The transposable element movements occur early in development and require, in addition to an appropriate P-element insertion in singed, a trans-acting maternal effect component. Movements appear to occur preferentially in attached-X stocks. However, the maternal effect component maps to the central region of chromosome 2.