The Simmons lab is studying transposable genetic elements -- transposons --
in Drosophila melanogaster. These elements are structurally and functionally
diverse, and constitute approximately 15% of the Drosophila genome. Collectively,
they are responsible for a large fraction of spontaneous mutations and chromosome
rearrangements, and some are related to the vertebrate retroviruses, including those
that cause human disease. Although a few transposons may perform useful functions
in a genome, most seem to be little more than genetic parasites.

The principal focus of Simmons' research is the regulation of the P family of transposons
in Drosophila. This transposon family is present in all natural populations, where it is
essentially quiescent. However, in crosses between wild and laboratory strains, the P family
is activated by a P-encoded enzyme called the transposase. This enzyme recognizes
sequences near the ends of each element and catalyzes movement. A basic question
is why this movement does not occur in natural populations. Recent analyses have indicated
that P elements inserted near the ends of chromosomes play an important role in the regulation
of the P transposon family, possibly by transferring a repressive chromatin imprint to other
P elements or by triggering an RNA interference pathway that destroys P element RNA.
These possibilities are being investigated using a combination of molecular and genetic
techniques.


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