@article {1231,
	title = {A sleep-inducing gene, nemuri, links sleep and immune function in Drosophila [Transgenic Fly Facility]},
	journal = {Science},
	volume = {363},
	year = {2019},
	month = {2019 02 01},
	pages = {509-515},
	abstract = {<p>Sleep remains a major mystery of biology. In particular, little is known about the mechanisms that account for the drive to sleep. In an unbiased screen of more than 12,000 lines, we identified a single gene, , that induces sleep. The NEMURI protein is an antimicrobial peptide that can be secreted ectopically to drive prolonged sleep (with resistance to arousal) and to promote survival after infection. Loss of increased arousability during daily sleep and attenuated the acute increase in sleep induced by sleep deprivation or bacterial infection. Conditions that increase sleep drive induced expression of in a small number of fly brain neurons and targeted it to the sleep-promoting, dorsal fan-shaped body. We propose that NEMURI is a bona fide sleep homeostasis factor that is particularly important under conditions of high sleep need; because these conditions include sickness, our findings provide a link between sleep and immune function.</p>
},
	keywords = {Animals, Antimicrobial Cationic Peptides, Arousal, Bacterial Infections, Brain, Drosophila melanogaster, Drosophila Proteins, Female, Gain of Function Mutation, Gene Knockout Techniques, Homeostasis, Immune System, Male, Neurons, Sleep},
	issn = {1095-9203},
	doi = {10.1126/science.aat1650},
	author = {Toda, Hirofumi and Williams, Julie A and Gulledge, Michael and Sehgal, Amita}
}
@article {483,
	title = {Inositol 1,4,5-trisphosphate receptor and dSTIM function in Drosophila insulin-producing neurons regulates systemic intracellular calcium homeostasis and flight. [Drosophila facility]},
	journal = {J Neurosci},
	volume = {30},
	year = {2010},
	month = {2010 Jan 27},
	pages = {1301-13},
	abstract = {<p class="rtejustify">Calcium (Ca(2+)) signaling is known to regulate the development, maintenance and modulation of activity in neuronal circuits that underlie organismal behavior. In Drosophila, intracellular Ca(2+) signaling by the inositol 1,4,5-trisphosphate receptor and the store-operated channel (dOrai) regulates the formation and function of neuronal circuits that control flight. Here, we show that restoring InsP(3)R activity in insulin-producing neurons of flightless InsP(3)R mutants (itpr) during pupal development can rescue systemic flight ability. Expression of the store operated Ca(2+) entry (SOCE) regulator dSTIM in insulin-producing neurons also suppresses compromised flight ability of InsP(3)R mutants suggesting that SOCE can compensate for impaired InsP(3)R function. Despite restricted expression of wild-type InsP(3)R and dSTIM in insulin-producing neurons, a global restoration of SOCE and store Ca(2+) is observed in primary neuronal cultures from the itpr mutant. These results suggest that restoring InsP(3)R-mediated Ca(2+) release and SOCE in a limited subset of neuromodulatory cells can influence systemic behaviors such as flight by regulating intracellular Ca(2+) homeostasis in a large population of neurons through a non-cell-autonomous mechanism.</p>
},
	keywords = {Animals, Calcium, Calcium Signaling, Cell Membrane, Cells, Cultured, Central Nervous System, Drosophila, Drosophila Proteins, Flight, Animal, Homeostasis, Inositol 1,4,5-Trisphosphate Receptors, Insulin, Intracellular Fluid, Membrane Proteins, Mutation, Neural Pathways, Neurons, Pupa, Stromal Interaction Molecule 1},
	issn = {1529-2401},
	doi = {10.1523/JNEUROSCI.3668-09.2010},
	author = {Agrawal, Neha and Venkiteswaran, Gayatri and Sadaf, Sufia and Padmanabhan, Nisha and Banerjee, Santanu and Hasan, Gaiti}
}
