Drosophila melanogaster p24 trafficking proteins have vital roles in development and reproduction.

p24 proteins comprise a family of type-I transmembrane proteins of ~24kD that are present in yeast and plants as well as metazoans ranging from Drosophila to humans. These proteins are most commonly localized to the endoplasmic reticulum (ER)-Golgi interface and are incorporated in anterograde and retrograde transport vesicles. Little is known about how disruption of p24 signaling affects individual tissue function or whole animals. Drosophila melanogaster express nine p24 genes, grouped into four subfamilies. Based upon our mRNA and protein expression data, Drosophila p24 family members are expressed in a variety of tissues. To identify functions for particular Drosophila p24 proteins, we used RNA interference (RNAi) to reduce p24 expression. Ubiquitous reduction of most p24 genes resulted in complete or partial lethality during development. We found that reducing p24 levels in adults caused defects in female fecundity (egg laying) and also reduced male fertility. We attributed reduced female fecundity to decreased neural p24 expression. These results provide the first genetic analysis of all p24 family members in a multicellular animal and indicate vital roles for Drosophila p24s in development and reproduction, implicating neural expression of p24s in the regulation of female behavior.

Ecdysone signaling in adult Drosophila melanogaster.

The steroid hormone 20-hydroxyecdysone and its EcR/USP receptor are vital during arthropod development for coordinating molting and metamorphosis. Traditionally, little attention has been given to potential post-developmental functions for this hormone signaling system. However, recent studies in Drosophila melanogaster indicate that the hormone and receptor are present and active in adults and that mutations decreasing hormone or receptor levels affect diverse processes such as reproduction, behavior, stress resistance, and lifespan. We review the current state of knowledge regarding adult hormone production and titers and discuss receptor expression and activity in order to identify potential mechanisms which explain the observed mutant phenotypes. Finally, we describe future research directions focused on identifying isoform-specific functions of EcR, distinguishing effects from EcR/USP gene activation and repression, and determining how ecdysone signaling impacts different tissue types.