Laura Duvall, PhD
Columbia University
Biography:
Laura received her B.A. in Biochemistry and Biological Basis of Behavior from the University of Pennsylvania in 2007. She then went on to complete a PhD with Paul Taghert at Washington University in St. Louis studying the neuropeptide regulation of circadian behavior in Drosophila. She conducted postdoctoral research with Leslie Vosshall at the Rockefeller University where she switched her studies to the Aedes aegypti mosquito. She started her own lab at Columbia University in 2019 where she is a member of the Department of Biological Sciences and an affiliate of the Zuckerman Institute. Her research focuses on understanding the biological basis of host-seeking and mating behaviors in mosquitoes. She is the recipient of a Beckman Young Investigator Award, a Klingenstein-Simons Fellowship Award in Neuroscience, and she is Pew Scholar in Biomedical Sciences.

Abstract:
Female Aedes aegypti mosquitoes, the primary vector of dengue, Zika, and yellow fever, require a blood meal to reproduce and are strongly attracted seek human hosts to obtain it. After blood feeding, they temporarily suppress their attraction to humans while they convert ingested nutrients into eggs. Understanding how mosquitoes sense a completed blood meal and switch off host-seeking behavior could reveal new strategies to interrupt disease transmission. However, the biological mechanisms linking nutritional state to behavior and reproduction have remained poorly understood. In many animals, including humans, Neuropeptide Y (NPY) signaling is a key regulator of hunger, satiety, and feeding behavior. We previously found that loss of a related receptor in Aedes aegypti, NPYLR7, prevents mosquitoes from properly suppressing host-seeking after a blood meal, but where and how this receptor acts was unknown. We recently found a surprising answer. Although we initially expected it to be expressed in the brain, instead NPYLR7 is expressed only in a specialized population of non-neuronal cells in the mosquito hindgut, similar to the proximal colon in mammals. Although this tissue is traditionally associated with fluid and ion balance, mutant mosquitoes that lack NPYLR7 show normal fluid regulation but they fail to properly load their eggs with yolk protein, and they continue seeking human hosts even after taking a complete blood meal. Although they are not neurons, these cells display some neuron-like features: they respond to NPYLR7 actvation via calcium signaling, and they express the molecular machinery for neurotransmitter synthesis and vesicle-mediated secretion. Critically, vesicle recruitment in these cells is triggered by blood feeding in wild-type females but is absent in npylr7 mutants. Together, these findings reveal an unexpected gut-brain circuit in mosquitoes: peripheral sensory cells in the hindgut detect nutritional cues from a blood meal and communicate with the nervous system to coordinate reproductive physiology and behavior. This parallels gut-brain axes in mammals, where enteroendocrine cells lining the intestine sense nutrients and signal to the brain via neuropeptides and neurotransmitters, and suggests these circuits are more ancient and conserved than previously appreciated. Beyond basic biology, these results identify a mosquito-specific cell population as a potential target for new vector control strategies aimed at breaking the cycle of blood feeding and disease transmission.
Laura Duvall, PhD