| dc.description.abstract | The organism Drosophila melanogaster, otherwise known as the fruit fly, has proven to be a respectable genetic model for analyzing behavior. Genes function within signaling pathways to regulate a variety of behavioral responses, such as ovulation and egg laying. Our gene family of interest consists of nine p24 genes that encode for 24 kD transmembrane proteins. When the expression of p24 genes logjam, eclair, or baiser is lost, adult females do not oviposit eggs. These genes may be responsible for trafficking cargo vesicles from the endoplasmic reticulum to the Golgi apparatus within cells. Therefore, we hypothesize that the function of p24 proteins is to traffic an ovulation or oviposition signal within a specialized set of cells. Unfortunately specificities regarding the function and localization of p24s remain unidentified.
In order to determine function, we characterized p24 localization in a variety of D. melanogaster tissues using p24-specific antisera. We discovered that p24 proteins are expressed in an assortment of tissues in the fly, especially in the nervous system and reproductive tissues.
Co-immunostaining of p24 proteins and peptidergic cell markers showed an association between p24-expressing and peptide secreting cells, thus supporting the hypothesis that p24s function in the relaying of signals for neuropeptide secretion. If the trafficking of signals is blocked due to the lack of p24 gene function, then neuropeptides controlling ovulation and egg laying would not be secreted, and eggs would not be oviposited as seen in some p24-deficient animals. There is evidence that two specific neurotransmitters, octopamine and glutamate, synergistically control egg laying behavior. It is possible that p24 mutants are deficient in the release of these neurotransmitters. To test this hypothesis, eclair and logjam mutants were fed octopamine and glutamate in order to restore egg-laying behavior. We discovered that feeding mutant females these neurotransmitters did not restore egg laying. Therefore, the defect is most likely not due to the loss of neurotransmitters. However, we have theorized ideas of possible issues with the p24-deficient fly. | en |
