The unfulfilled/DHR51 gene of Drosophila melanogaster modulates wing expansion and fertility.

This is the first functional analysis in Drosophila of unfulfilled (unf; DHR51), the NR2E3 nuclear receptor superfamily ortholog of C. elegans fax-1 and human PNR. Both fax-1 and PNR mutations disrupt developmental events in a limited number of neurons, resulting in behavioral or sensory deficits.

Light and peptidergic eclosion hormone neurons stimulate a rapid eclosion response that masks circadian emergence in Drosophila.

Light signals can entrain circadian clocks, but they can also mask aspects of the circadian output. We have analyzed the masking effects of a lights-on (LOn) signal on Drosophila eclosion. The LOn response results in 12-21% of the flies that emerge on a given day eclosing within 10 min of the LOn signal.

Identification of the gene encoding bursicon, an insect neuropeptide responsible for cuticle sclerotization and wing spreading.

To accommodate growth, insects must periodically replace their exoskeletons. After shedding the old cuticle, the new soft cuticle must sclerotize. Sclerotization has long been known to be controlled by the neuropeptide hormone bursicon, but its large size of 30 kDa has frustrated attempts to determine its sequence and structure.