Amama Asif, Mounia Khalil, Alan Rozenblit, Tayler Williams
Department of Biology, Rutgers University, Camden NJ 08102
Download Article as pdf
Abstract
Pan-neuronal knockdown of Ca-α1T, a T-type calcium channel in Drosophila melanogaster, increases sleep. However, researchers do not know which specific neuronal circuit is responsible for this effect. Circadian pacemaker neurons (CPNs) are one of many cell types that contain this T-type calcium channel, and these neurons take part in establishing normal circadian behaviors. We identified certain CPNs as possible candidates in narrowing down which neuronal circuit is responsible for the increase in sleep. We hypothesize that the knockdown of Ca-α1T in these certain CPNs will cause an increase in sleep, with an increase more pronounced in tim-expressing CPNs. To test this hypothesis, we utilized the GAL4-UAS system to target specific CPNs with RNA interference of Ca-α1T. An ethoscope, a computer-mediated apparatus, was paired with rethomics, a set of R packages, to track and analyze the activity of Drosophila through their movement. The data demonstrates that the tim-CaRrnai and pdf-CaRrnai lines exhibit less activity when compared to the tim-GAL4 line. However, no significant difference in sleep exists between the experimental and control groups. Thus, our experiment suggests that the knockdown of Ca-α1T in tim– and pdf-expressing CPNs does not have a significant effect on sleep.