Christopher Quinn

Associate Professor, Biological Sciences

Education

Postdoctoral Fellow, Rutgers University, 2009
PhD, Yale University, 2001
BA, Rutgers University, 1996

Research Interests

We are investigating the genetic causes of neuropsychiatric and neurodevelopmental disorders. Genetic studies have identified many human variants that are associated with these disorders. In addition, imaging studies have revealed that these disorders are associated with alterations in axonal projections within the human brain. Despite these advances, we currently lack an understanding of how the disorder-associated genetic variants alter neuronal cell biology to give rise to the alterations in axonal projections that underlie the neurodevelopmental and neuropsychiatric disorders.

To address these questions, we are using C. elegans as a model organism to ask how specific patient-derived variants affect the development and maintenance of axons. Our approach has been to use CRISPR to create edits within the C. elegans genome that are orthologous to human variants associated with neuropsychiatric and neurodevelopmental disorders. We can than ask how these variants affect neuronal cell biology, axonal connectivity, axonal maintenance, and behavior. For example, in one project we have found that variants within the ortholog of the CACNA1C neuropsychiatric risk gene can disrupt axonal connectivity and alter behavior. In another project we have found that variants in the ortholog of the RBM27 autism candidate gene can cause mitochondrial dysfunction and axonal degeneration. For both projects we are currently investigating the mechanisms of how these variants disrupt neuronal cell biology and how these disruptions lead to alterations in connectivity and axon degeneration.

This work has been funded by the National Institute of Mental Health (NIMH), the National Institute of Neurological Disorders and Stroke (NINDS), the University of Wisconsin-Milwaukee (UWM), and by the Greater Milwaukee Foundation (GMF). The information presented here does not represent the views of these funding agencies.

For a full publication list please visit the National Center for Biotechnology Information (NCBI) biblography page.

Selected Publications

Chowdhury TA, Luy DA, Farache D, Lee ASY, Quinn CC (2024). Ortholog of autism candidate gene RBM27 regulates mitoribosomal assembly factor MALS-1 to protect against mitochondrial dysfunction and axon degeneration during neurodevelopment. PLoS Biology 22(10): e3002876.

Drozd CJ, Chowdhury TC, Quinn CC. (2024) UNC-16 interacts with LRK-1 and WDFY-3 to regulate the termination of axon growth. Genetics, iyae053.

Drozd CJ, Quinn CC (2023) UNC-116 and UNC-16 function with the NEKL-3 kinase to promote axon targeting.Development, 150(18): dev201654.

Fischer NC, Friedman V, Martinez-Reyes MA, Hao H, Chowdhury TA, Starr DA, Quinn CC (2022) The ANC-1(Nesprin-1/2) organelle-anchoring protein functions through mitochondria to polarize axon growth in response to SLT-1.PLoS Genetics, 18(11): e1010521.

Buddell T, Friedman V, Drozd CJ, Quinn CC (2019) An autism-causing calcium channel variant functions with selective autophagy to alter axon targeting and behavior. PLoS Genetics, 15(12): e1008488.

Xu Y, Quinn CC (2016) Transition between synaptic branch formation and synaptogenesis is regulated by the lin-4microRNA. Developmental Biology, 420:60-66.

Xu Y, Taru H, Jin Y, Quinn CC (2015) SYD-1C, UNC-40 (DCC) and SAX-3 (Robo) function interdependently to promote axon guidance by regulating the MIG-2 GTPase. PLoS Genetics, 11(4): e1005185.

Xu Y, Quinn CC (2012) MIG-10 functions with ABI-1 to mediate the UNC-6 and SLT-1 axon guidance signaling pathways. PLoS Genetics, 8(11): e1003054.