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Pathak, H.

Publications and source records attributed to Pathak, H..

2 recordsLinked to original sources

Regulation of starvation-mediated hyperactivity and triglyceride metabolism by Short neuropeptide F and Insulin Like Peptide in Drosophila

The circadian clock regulates various behavioral, metabolic and physiological processes to occur at the most suitable time of the day. Internal energy stores and nutrient availability modulates the most apparent circadian clock mediated locmotor activity rhythm in Drosophila. Although previous studies unraveled the role of circadian clock in metabolism and activity rest rhythm, the precise pathway through which the circadian neuropeptidergic signaling regulates internal energy storage and the starvation-mediated increase in activity resembling foraging remains largely unclear. This study was aimed to elucidate the role of circadian neuropeptide, short neuropeptide F (sNPF) in triglyceride metabolism, starvation resistance and starvation-mediated increased locomotor activity in Drosophila. The results showed that snpf transcripts exhibits significant rhythmicity in wild type flies under 12:12 hour light-dark cycles (LD) and constant darkness (DD) whereas snpf transcript level in period null flies did not exhibit any significant rhythmicity under LD. Knockdown of sNPF in circadian clock neurons reduced the triglyceride level, starvation resistance and increased the starvation-mediated hyperactivity response after 24 hour of starvation. Further studies showed that knock down of sNPF receptors (sNPFR) expressed in insulin producing cells (IPC) increased the starvation resistance and reduced starvation-induced hyperactivity response after 24 hour of starvation. Collectively, our results suggest that transcriptional oscillation of snpf mRNA is endogenously controlled by the circadian clock and elucidate the role of sNPF in modulating locomotor activity in accordance with the nutrient availability in Drosophila.

animal behavior and cognition

Edem1 activity in the fat body regulates insulin signalling and metabolic homeostasis in Drosophila

In Drosophila, nutrient status is sensed by the fat body, a functional homolog of mammalian liver and white adipocytes. The fat body conveys nutrient information to insulin-producing cells (IPCs) through humoral factors which regulate Drosophila insulin-like peptide (DILP) levels and insulin signalling. Insulin signalling has pleiotropic functions, which include the management of growth and metabolic pathways. Here, we report that Edem1 (endoplasmic reticulum degradation-enhancing -mannosidase-like protein 1), an endoplasmic reticulum-resident protein involved in protein quality control, acts in the fat body to regulate insulin signalling and thereby the metabolic status in Drosophila. Edem1 limits the fat body derived Drosophila TNF Eiger activity on IPCs and maintains systemic insulin signalling in fed conditions. During food deprivation, edem1 gene expression levels drop, which aids in the reduction of systemic insulin signalling crucial for survival. Overall we demonstrate that Edem1 plays a vital role in helping the organism to endure a fluctuating nutrient environment by managing insulin signalling and metabolic homeostasis.

developmental biology