Dr. Cavnar is currently recruiting new graduate students for Fall 2014. Click here for more information.
Peter J. Cavnar
Ph.D., Biological Science - Cell & Molecular Biology, 2008. Florida State University
Fax : 850-474-2749
Cell Biology, General Biology Lab
My research focuses on investigating the molecular mechanisms that regulate cell motility and adhesion, processes that are important to many physiological and pathological mechanisms including cancer invasion and metastasis, embryonic development, wound healing, and the inflammatory response. Cell motility is a dynamic process that relies on the spatiotemporal regulation of signaling mechanisms, and the formation of an actin dendritic network by the Arp2/3 complex and Rho GTPase effector proteins, which lead to the protrusion of pseudopodia.
In response to infection, bacteria secrete chemical signals called chemoattractants. Cells recognize these chemical cues and reorganize their cytoskeleton through a complex network of signaling molecules in order to migrate to, and destroy the bacterial infection.
I utilize a model neutrophil cell line to investigate cell motility mechanisms. Neutrophils are key mediators of the innate immune system, and are the first responders to sites of infection or acute injury. Although the primary function of neutrophils is to protect the host from infection or tissue injury, neutrophils can also contribute to the progression of inflammation and the pathogenesis of autoimmune diseases, such as arthritis and lupus. I am currently working on cytoskeletal adaptor proteins, such as HS1-associated protein X-1 (Hax1), which has been shown to play a role in primary immunodeficiencies such as neutropenia. I am interested how protein-protein interactions with Hax1 and other adaptor proteins regulate neutrophil cell motility and adhesion.
For more information please listen to the following podcast that highlighted my work: http://jcb.rupress.org/site/biobytes/biobytes_may_02_2011.xhtml
Neutrophil chemotaxis to a micropipette needle containing the chemoattractant formyl-Met-Leu-Phe
Neutrophis deficient in HS1-associated protein X-1 (Hax1) display defective chemotaxis towards formyl-Met-Leu-Phe
Subcellular localization of the actin regulatory adaptor protein HS1 fused
to GFP in neutrophils during chemotaxis.
Cavnar, P. J., Mogen, K., Berthier, E., Beebe, D. J., and Huttenlocher, A. (2012) The Actin Regulatory Protein HS1 Interacts with Arp2/3 and Mediates Efficient Neutrophil Chemotaxis. J Biol Chem 287, 25466-25477
Deng, Q., Yoo, S. K., Cavnar, P. J., Green, J. M., and Huttenlocher, A. (2011) Dual roles for Rac2 in neutrophil motility and active retention in zebrafish hematopoietic tissue. Dev Cell 21, 735-745
Cavnar, P. J., Berthier, E., Beebe, D. J., and Huttenlocher, A. (2011) Hax1 regulates neutrophil adhesion and motility through RhoA. J Cell Biol 193, 465-473
Yoo, S. K., Deng, Q., Cavnar, P. J., Wu, Y. I., Hahn, K. M., and Huttenlocher, A. (2010) Differential regulation of protrusion and polarity by PI3K during neutrophil motility in live zebrafish. Dev Cell 18, 226-236
Cavnar, P. J., Olenych, S. G., and Keller, T. C. S. (2007) Molecular identification and localization of cellular titin, a novel titin isoform in the fibroblast stress fiber. Cell Motil Cytoskeleton 64, 418-433