Director of Undergraduate Studies in Neurobiology / Associate Professor of Instruction in Neurobiology
- Hogan 2-162
- BIOL SCI 302 Fundamentals of Neurobiology I
- NEUROSCI 360 Neuroscience of Brain Disorders
- NEUROBIO 402 Advanced Neurobiology
Molecular Genetics of Sleep
We all sleep and we spend a lot of time doing it. Humans spend 1/3 of their lives in this unconscious state, unable to eat, mate, or protect young. In fact, without sleep a human being will die within weeks. Yet, it is not at all clear why we sleep. Is it to help form memories? Restore daily damage? Clean away accumulated toxins? Perhaps all of these or maybe none are the real underlying function of sleep. And it’s not just us. Every animal examined to date sleeps, including the fruit fly Drosophila. That’s lucky, because Drosophila have proven to be one of the best, fastest, most versatile systems in which to discover the genetic roots of conserved biological processes, including those important to human health and disease.
I am interested in asking why it is that we sleep, at a fundamental level. We are using the molecular-genetic tools and behavioral assays available in flies to ask what genes, what networks of neurons, are involved in sleep regulation. What happens to learning and memory in flies when their sleep is altered? What happens to repair and restoration (like in neurodegeneration below)? What is the relationship between metabolism and sleep? My ultimate goal is to understand how sleep affects human health and provide insight into ways to lead a healthy life and mitigate disease.
Neurodegeneration and the Circadian Clock
Disruption of daily rhythms has wide-ranging health consequences. We have begun to explore the links between the circadian clock and neurodegeneration. Human neurodegenerative disease such as Alzheimer’s, ALS, and Huntington’s disease frequently involves symptoms of circadian disruption. Remarkably, normalization of circadian rhythms and sleep cycles can stave off the progression of disease. We are using fruit fly models of human neurodegenerative disease to test the hypothesis that normal circadian function can protect against neurodegenerative decline, and to discover the genetic bases of these links in hopes of providing novel pharmaceutical targets and protective strategies.
- Seluzicki A, Flourakis M, Kula-Eversole E, Zhang L, Kilman V, Allada R. (2014). Dual PDF signaling pathways reset clocks via TIMELESS and acutely excite target neruons to control circadian behavior. PLoS Biology, 12(3):e1001810.
- Lim C, Lee J, Choi C, Kilman VL, Kim J, Park SM, Jang SK, Allada R* and Choe J* (*co-corresponding authors). (2014). The novel gene twenty-four defines a critical translational step in the Drosophila clock. Nature, 470: 399-403.
- Zhang L, Chung B, Lear B, Kilman VL, Liu Y, Mahesh G, Meissner R, Hardin P, Allada R. (2010). DN1p circadian neurons coordinate acute light and PDF inputs to produce robust daily behavior in Drosophila. Curr Biol, 20:591-9.
- Kilman VL and Allada R. (2009). Genetic analysis of ectopic circadian clock induction in Drosophila. J Biol Rhythms, 24: 368-378.
- Kilman VL, Zhang L, Meissner RA, Burg E, Allada R. (2009). Perturbing dynamin reveals potent effects on the Drosophila circadian clock. PLoS ONE, 4(4): e5235.
- Chung BY, Kilman VL, Keath JR, Pitman JL, Allada R. (2009). The GABA(A) receptor RDL acts in peptidergic PDF neurons to promote sleep in Drosophila. Curr Biol, 9(5): 386-90.