Axons connect neurons across great distances in the nervous system, and this distance is a fundamental vulnerability for neurons. Maintenance of functional connectivity requires robust mechanisms for transporting proteins and organelles, in addition to mechanisms for local synthesis of proteins distant from the cell body. Glial cells also provide important local support to axons and synapses. Axons are therefore vulnerable to stressors that impair energy metabolism, cytoskeleton, axonal transport machinery and glial support as well as acute physical injury.
The Collins lab is particularly interested in cellular mechanisms of plasticity that allow the nervous system to adapt to impairments in axons. These include cell autonomous signaling pathways that become triggered in damaged axons, and neuron-glial interactions that mediate circuit adaptations to axonal damage.
Our lab uses both Drosophila melanogaster and mice as model organisms, when enables us to combine molecular genetics approaches with cell biology, biochemistry and primary cell culture to study conserved pathways of axonal damage response.