Abstract
Organismal growth regulation requires the interaction of multiple metabolic, hormonal and neuronal pathways. While the molecular basis for many of these are well characterized, less is known about the developmental origins of growth regulatory structures and the mechanisms governing control of feeding and satiety. For these reasons, new tools and approaches are needed to link the specification and maturation of discrete cell populations with their subsequent regulatory roles. In this study, we characterize a rhomboid enhancer element that selectively labels four Drosophila embryonic neural precursors. These precursors give rise to the hypopharyngeal sensory organ of the peripheral nervous system and a subset of neurons in the deutocerebral region of the embryonic central nervous system. Post embryogenesis, the rhomboid enhancer is active in a subset of cells within the larval pharyngeal epithelium. Enhancer-targeted toxin expression alters the morphology of the sense organ and results in impaired larval growth, developmental delay, defective anterior spiracle eversion and lethality. Limiting the duration of toxin expression reveals differences in the critical periods for these effects. Embryonic expression causes developmental defects and partially penetrant pre-pupal lethality. Survivors of embryonic expression, however, ultimately become viable adults. In contrast, post-embryonic toxin expression results in fully penetrant lethality. To better define the larval growth defect, we used a variety of assays to demonstrate that toxin-targeted larvae are capable of locating, ingesting and clearing food and they exhibit normal food search behaviors. Strikingly, however, following food exposure these larvae show a rapid decrease in consumption suggesting a satiety-like phenomenon that correlates with the period of impaired larval growth. Together, these data suggest a critical role for these enhancer-defined lineages in regulating feeding, growth and viability.
Highlights
Controlled organismal growth involves a delicate balance between nutrient consumption and utilization
While populations of neurons have been identified in the mature brain that are required for regulating growth in Drosophila, the lack of specific genetic tools to match many of these neurons with their precursors of origin has hindered studies linking development to function
Our data addresses each of these issues by tracking a novel set of neural precursors through development and demonstrating that disrupting these precursors via targeted toxin expression produces measurable deficits in feeding and growth
Summary
Controlled organismal growth involves a delicate balance between nutrient consumption and utilization. While food intake may be the easiest to conceptually understand, the factors underlying an organism’s decision to begin or cease feeding are varied and complex These include environmental cues such as food availability, sensory stimuli and social norms, as well as intrinsic states of hunger or satiety, mediated in part by neuroendocrine feedback from metabolic and homeostatic pathways [1,2,3,4]. Many of the signaling pathways that control size in the fly are highly analogous to, but often less redundant than, those found in vertebrates [4,11,12] These include an array of neural and endocrine mechanisms that inextricably link growth control to nervous system development. We characterize a subset of neural precursor cells and correlate their development with control of feeding and growth. Our results suggest that satiation can occur in larvae, and we introduce a paradigm for documenting such effects and define a new neural component in the regulation of feeding, growth and viability
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