Developmental Control of Foraging and Social Behavior by the Drosophila Neuropeptide Y-like System

Abstract

Animals display stereotyped behavioral modifications during development, but little is known about how genes and neural circuits are regulated to turn on/off behaviors. Here we report that Drosophila neuropeptide F (dNPF), a human NPY homolog, coordinates larval behavioral changes during development. The brain expression of npf is high in larvae attracted to food, whereas its downregulation coincides with the onset of behaviors of older larvae, including food aversion, hypermobility, and cooperative burrowing. Loss of dNPF signaling in young transgenic larvae led to the premature display of behavioral phenotypes associated with older larvae. Conversely, dNPF overexpression in older larvae prolonged feeding, and suppressed hypermobility and cooperative burrowing behaviors. The dNPF system provides a new paradigm for studying the central control of cooperative behavior.

Discrete pulses of molting hormone, 20‐hydroxyecdysone, during late larval development of Drosophila melanogaster: Correlations with changes in gene activity

“…Similarly, ecdysone receptor signaling has been implicated in PI3K-regulated programmed autophagy in the mid-third instar fat body (Rusten et al, 2004). Finally, at the level of the whole animal, we consider wandering (Denlinger and Zdá rek, 1994), which represents a cessation of feeding and a switch in phototropism as well as altered social behavior (Sawin-McCormack et al, 1995;Wu et al, 2003). In our study, larvae wandered at 32 hr after ecdysis, several hours after the third 20E peak.…”

The role of neuropeptide F in a transition to parental care

“…For example, npf can have sex-specific expression [23] and influences locomotor and circadian activity [24]. npf acting within the larval brain is developmentally controlled and influences the transition to wandering [25]. npf also serves as a neurohormone and influences the production of ecdysteroids [26], and ovarian [27] and testicular physiology [28].…”

Lack of association between polymorphism of the human cyclic GMP-dependent protein kinase gene and obesity

“…4,16 The conserved role of PKG in food-related behavior has been demonstrated in the honey bee Apis mellifera 5 and in the nematode Caenorhabditis elegans. 6 Wu et al (2003) 17 speculated that the product of the for gene might be a component of the Drosophila Neuropeptide F (dNPF) signaling pathway, which regulates food-related behaviors. 18 The dNPF, a homolog of human NPY, is a conserved hypothalamic neuromodulator that strongly increases food intake.…”