Department of Chemistry

Mathematics and Science Center,
Room 260
146 Library Drive
Rochester, MI 48309-4479
(location map)
(248) 370-2320
fax: 370-2321

Adam Avery, Ph.D.

A headshot of Adam Avery outside.

Title: Assistant Professor
Office: 291 Mathematics and Science Center
Phone: (248) 370-3088

Research Interests

I am interested in understanding the molecular mechanisms that control morphogenesis and maintenance of neuronal structures, and how these mechanisms are disrupted to cause neurological disorders. My lab employs protein biochemical techniques, together with genetic and live cell imaging approaches using the model organism Drosophila melanogaster. Students in my lab have the unique opportunity to explore questions in neurobiology at both the single molecule and whole organism level.

A focus of my lab is to understand how the cytoskeleton supports the unique morphologies adopted by neurons. Neuronal morphology is intimately tied to proper functioning of the nervous system. In particular we are currently studying the mechanisms by which the spectrin-actin cytoskeleton supports neuron form and function, and how the spectrin cytoskeleton is disrupted in disease. Mutations in β-III-spectrin cause the neurodegenerative disease, spinocerebellar ataxia type 5 (SCA5). In prior biochemical studies we found that a SCA5 mutation causes β-III-spectrin to binds actin with a striking 1000-fold increased affinity. This high-affinity interaction enabled generation of a cryo-EM structure of mutant β-III-spectrin bound to an actin filament. This structure led to the discovery of a novel motif, an N-terminal helix, required for spectrin actin-binding activity. This cryo-EM structure also confirmed our model that high-affinity actin binding by mutant spectrin results from a specific conformational change within the actin-binding domain of spectrin.

The target neuron in SCA5 pathogenesis is the cerebellar Purkinje cell, which extends a large and highly branched dendritic arbor. To gain insight into how SCA5 mutations impact the dendritic arbors extended by human cerebellar Purkinje cells, we developed an SCA5 model using the fruit fly Drosophila melanogaster. Drosophila sensory neurons expressing SCA5 mutant β-spectrin exhibit a pronounced arbor phenotype. The reduced size of the SCA5 arbor reflects both a degenerative defect, in which distal dendrites are lost, and a developmental defect, in which arbor outgrowth is restricted. Our data suggest the spectrin-actin cytoskeleton functions in neurons to stabilize dendrites and support arbor outgrowth.

Education and Research Experience

  • 2012 – 2018 - Postdoctoral Research Fellow, University of Minnesota, Minneapolis, MN
  • 2006 – 2012 - Research Scientist, Originus, Inc., Ann Arbor, MI
  • 2001 – 2006 - Ph.D. in Biological Chemistry, University of Michigan, Ann Arbor, MI
  • 1997 – 2001 - B.S. in Biochemistry, Oakland University, Rochester, MI

Honors and Awards

  • 2016 – 2018 - Minnesota Muscle Training Program Fellow, University of Minnesota
  • 2018 - Michael B. O'Connor Award, Outstanding Postdoc, Department of Genetics, Cell Biology and Development, University of Minnesota
  • 2014 - Post-doctoral Fellow, National Ataxia Foundation and Bob Allison Ataxia Research Center, University of Minnesota
  • 2002-2005 - Pre-doctoral Fellow, Cellular Biotechnology Training Program, University of Michigan


  1. Amanda L. Neisch, Adam W. Avery, Min-gang Li, Thomas S. Hays. Drosophila cytoplasmic dynein: mutations, tools and developmental functions. 2017. In King, S.M., ed. Dyneins: Structure, Biology and Disease. 2nd
  2. Adam W. Avery, Michael E. Fealey, Fengbin Wang, Albina Orlova, Andrew Thompson, David D. Thomas, Thomas S. Hays, Edward H. Egelman. Structural basis for high-affinity actin binding revealed by a β-III-spectrin SCA5 missense mutation. 2017. Nature Communications. PMID: 29116080.
  3. Adam W. Avery, David. D. Thomas, Thomas. S. Hays. β-III-spectrin spinocerebellar ataxia type 5 mutation reveals a dominant cytoskeletal mechanism that underlies dendritic arborization. 2017. PNAS. PMID: 29078305
  4. Adam W. Avery, Jonathan Crain, David D. Thomas, Thomas S. Hays. A human β-III-spectrin spinocerebellar ataxia type 5 mutation causes high-affinity F-actin binding. 2016. Scientific Reports. 6: 21375. PMID: 26883385
  5. Amanda L. Neisch*, Adam W. Avery*, James B. Machamer, Min-gang Li, Thomas S. Hays Methods to identify and analyze gene products involved in neuronal intracellular transport using Drosophila. 2016. Methods in Cell Biology. 131: 277-309. PMID: 26794520 *Co-first authors.
  6. Jennifer Taylor, Kwan-Ho Chung, Claudia Figueroa, Jonathan Zurawski, Heather M. Dickson, E. J. Brace, Adam W. Avery, David L. Turner and Anne B. Vojtek. The scaffold protein POSH regulates axon outgrowth. 2008. Molecular Biology of the Cell. 19(12): 5181-5192. PMID: 18829867
  7. Adam W. Avery, Claudia Figueroa and Anne Vojtek. UNC-51-like kinase regulation of fibroblast growth factor receptor substrate 2/3. 2007. Cellular Signaling. 19(1): 177-184. PMID: 16887332
  8. Kwan-Ho Chung, Christopher C. Hart, Sarmad Al-Bassam, Adam Avery, Jennifer Taylor, Paresh D. Patel, Anne B. Vojtek, and David L. Turner. Polycistronic RNA polymerase II expression vectors for RNA interference based on BIC/miR-155. 2006. Nucleic Acids Research. 34(7): e53. PMID: 16614444