Compensation of Inositol 1,4,5-Trisphosphate Receptor Function by Altering Sarco-Endoplasmic Reticulum Calcium ATPase Activity in theDrosophilaFlight Circuit

Inositol 1,4,5-Trisphosphate Receptor and dSTIM Function inDrosophilaInsulin-Producing Neurons Regulates Systemic Intracellular Calcium Homeostasis and Flight

“…1, available at www.jneurosci.org as supplemental material). Differences in temporal and spatial levels of pan-neuronal GAL4 expression coupled with a differential requirement for InsP 3 R function at multiple steps of flight circuit formation are a likely explanation for these data (see Discussion and Banerjee et al, 2006).…”

“…Pan-neuronal expression of wild-type itpr, dOrai and dSTIM however do not rescue itpr mutants to the same extent as rescue from the subneuronal domains, suggesting a developmental hierarchy for itpr mutant phenotypes beginning with wing posture. The rescue of individual phenotypes depends upon the level of pan-neuronal GAL4 expression at different stages of pupal development; normal wing posture is necessary but insufficient for restoration of flight physiology (Banerjee et al, 2004(Banerjee et al, , 2006. Thus, unlike complete rescue, which requires GAL4 driven expression throughout flight circuit development, pan-neuronal knock-down at an early stage of pupal development produces wing posture defects, which abrogate normal flight.…”

“…The importance of neuronal InsP 3 R-mediated Ca 2ϩ signaling for neural circuit function is well recognized (Banerjee and Hasan, 2005;Mikoshiba, 2006). We have previously shown that flight and associated defects observed in itpr gene (which encodes the only Drosophila InsP 3 R) mutants can be rescued by restoring InsP 3 R function in aminergic neurons (Banerjee et al, 2004) and that InsP 3 R-mediated Ca 2ϩ signaling is required at multiple steps for generating the neural circuit responsible for air-puff stimulated Drosophila flight (Banerjee et al, 2006). We also recently identified a requirement for SOCE in Drosophila neurons for regulating flight behavior (Venkiteswaran and Hasan, 2009).…”

Reduced Odor Responses from Antennal Neurons of Gqα, Phospholipase Cβ, andrdgAMutants inDrosophilaSupport a Role for a Phospholipid Intermediate in Insect Olfactory Transduction

“…Mutations were verified by their failure of complementation with Df(2R)vg-C, which uncovers the dgq locus and subsequent molecular analysis. GqGAL4 and UASdgq␣3 stocks were provided by Sonal Srikanth [National Centre for Biological Sciences (NCBS), Bangalore, India] and Neha Agrawal (NCBS); details of the RNAi construct for dgq (UASGq 1F1 ) and UASAcGq transgenics are published (Ratnaparkhi et al, 2002;Banerjee et al, 2006). plc21C insertion allele ( plc21C P319 ) and the deficiency Df(2L)p60A, which uncovers plc21C, were obtained from S. Leevers (Cancer Research Institute, London, UK) (Weinkove et al, 1999).…”

Dynamin- and Rab5-dependent endocytosis is required to preventDrosophilaphotoreceptor degeneration

“…This is particularly important, as it has been estimated that 1% Rh1 expression is sufficient to achieve proper rhabdomere morphogenesis (Leonard et al, 1992). To address this issue, we made use of an embryonic lethal null allele for Gqe, dgq 221c (Banerjee et al, 2006). Generating whole mutant eyes for this null allele did not reveal any detectable phenotype in 1-day-old flies ( Fig.…”