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. An analysis of two independent unf alleles revealed that unf mutants are characterized by one of two phenotypes. A proportion of the mutants eclosed but failed to expand their wings and were poorly coordinated. The remainder completed wing expansion but displayed severely compromised fertility. Consistent with the restricted neural expression of fax-1 and PNR, unf expression was detected in situ only in mushroom body neurons and a small number of other cells of the central nervous system (CNS). These data support the hypothesis that the wing expansion failure and the compromised fertility of unf mutants are the result of underlying neural defects.

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. Flies that lack the neuropeptide eclosion hormone (EH), or in which its release is inhibited by the tetanus toxin light chain, lack the response. Optic photoreceptors in both the ocelli and the compound eyes appear to be required for the response. The LOn signal has two effects: (1) it drastically reduces the interval between EH release and eclosion, presumably by suppressing a transient descending inhibition that immediately follows EH release, and (2) it stimulates premature EH release. The LOn signal does not influence the latency of wing spreading, an EH-regulated post-ecdysis behavior.

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. Using partial sequences obtained from purified cockroach bursicon, we identified the Drosophila melanogaster gene CG13419 as a candidate bursicon gene. CG13419 encodes a peptide with a predicted final molecular weight of 15 kDa, which likely functions as a dimer. This predicted bursicon protein belongs to the cystine knot family, which includes vertebrate transforming growth factor-beta (TGF-beta) and glycoprotein hormones. Point mutations in the bursicon gene cause defects in cuticle sclerotization and wing expansion behavior. Bioassays show that these mutants have decreased bursicon bioactivity. In situ hybridization and immunocytochemistry revealed that bursicon is co-expressed with crustacean cardioactive peptide (CCAP). Transgenic flies that lack CCAP neurons also lacked bursicon bioactivity. Our results indicate that CG13419 encodes bursicon, the last of the classic set of insect developmental hormones. It is the first member of the cystine knot family to have a defined function in invertebrates. Mutants show that the spectrum of bursicon actions is broader than formerly demonstrated.