Disentangling Self-Avoidance

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Description

SUMMARY Dendrites are the fine, and often highly branched, processes through which neurons receive information from their environment. The morphologies of dendrites are important for connectivity and healthy functioning of the nervous system. Thus, it is critical to understand the genes that control dendrite morphogenesis and maintenance. One key broadly conserved feature of dendrite and axon morphology is their even spreading across territories without overlap. Repulsion between arbors of the same cell, termed self-avoidance, is under the control of two major pathways in Drosophila somatosensory neurons, a powerful model for studies of dendrite morphogenesis. One pathway supports dendrite-dendrite recognition and repulsion and is mediated by Down syndrome cell adhesion molecule 1 (Dscam1). In the absence of this pathway, dendrites cross each other and become tangled, leaving parts of their receptive field uncovered and other parts over-innervated. Another pathway that impacts whether dendritic membranes are available for contact and recognition is mediated by integrin receptors for the extracellular matrix. In the absence of this pathway, dendrite-substrate interactions predominate and dendrites become enclosed by membranes of nearby cells. It is important to discriminate between these two pathways so that the molecular basis for dendrite development can be better understood. However, we still have relatively few insights into how different genes impact these two pathways, so both dendrite-dendrite and dendrites-substrate interactions are not well known. As a result, the potential for these studies to inform our understanding of more complex mammalian systems has not been fully realized. We will use a simple but powerful technique for assaying dendrite-substrate interactions to build a clearer understanding of self-avoidance pathways. We expect that the insights gained can inform us about the development of more complex brains that are more similar to own.
StatutActif
Date de début/de fin réelle6/1/235/31/25

Financement

  • National Institute of Neurological Disorders and Stroke: 164 500,00 $ US

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