Owen Hamill, Ph.D.
Associate Professor

  • Affiliations:

    Neuroscience and Cell Biology

    Route: 1069, Room 2.202 Basic Science Building

    Tel:  409-772 5464

    Fax: 409-772-3381

    ohamill@utmb.edu

    Hamill CV

Education: 

BSc, Monash University, Melbourne, 1973

PhD, University New South Wales, Sydney, 1977

Post-Doctoral training: Max Planck Institute Gattingen, 1979-1984. 

Stanford University, 1984-1986.

ohamill@utmb.edu

Hamill Lab Webpage

Dr. Hamill's Publications

Dr. Hamill's CV

Owen Hamill, Ph.D.

Education

BSc, Monash University, Melbourne, 1973

PhD, University New South Wales, Sydney, 1977

Post-Doctoral training: Max Planck Institute Gattingen, 1979-1984.

Stanford University, 1984-1986.

About the Lab

Our research focuses on how cells sense and transduce mechanical forces into biological signals. We study two processes one involving mechanosensitive membrane trafficking and the other involving mechanosensitive membrane ion channels and Ca2+ signaling. Both mechanisms are involved in regulating a wide range of cellular functions including cell growth, proliferation, differentiation and migration.  Our studies indicate that most animal cells possess an exquisitely sensitive integrin-dependent mechanism that regulates constitutive membrane trafficking.  It is this regulated trafficking of membrane and secretory proteins that allows cells to adjust their set point for growth according to their prevailing mechanical environment.  In the presence of increased mechanical stimulation the set point is adjusted towards hypertrophy, while in absence it is adjusted downwards resulting in tissue atrophy. Increased understanding of the molecular mechanisms that control this set point offers the opportunity to control the growth of mechanosensitive tissues including bone and muscle.

We are also interested in the concept that the mechanical forces that develop within an proliferating tumor actually play a causative role in promoting cancer progression. In particular, we have identified a specific mechanosensitive membrane ion channel in prostate cancer cells that transduces intrinsic mechanical forces into Ca2+ influx and in this way regulates prostate tumor cell migration and invasion. Furthermore, the gating mode of the channel displays plasticity with motile and nonmotile tumor cells showing different gating modes. Most significantly external mechanical forces can switch gating from a “nonmotile” to a “motile” gating mode.  Our current research efforts are focused on identifying the specific molecular mechanisms that underlie this mechanosensory switch in MscCa gating.

Select Publications

Zhang, Y.; Gao, F.; Popov, V., Wan, J.; Hamill, O.P. Mechanically-gated channel activity in cytoskeleton deficient blebs and vesicles from Xenopus oocytes. J. Physiol. (Lond) 523.1: 117-129; 2000.

Maroto, R.; Hamill, O.P. Brefeldin A block of integrin-dependent mechanosensitive ATP release from Xenopus oocytes reveals a novel mechanism of mechanotransduction. J.Biol.Chem.276: 23867-23872; 2001.

Hamill, O.P.; Martinac, B.A  Molecular Basis of Mechanotransduction in Living Cells. Physiol. Revs. 81: 685-740; 2001. 

Martinac, B., Hamill, O.P. Gramicidin channels switch between stretch activation and stretch inactivation depending upon bilayer thickness Proc. Natl. Acad. Sci. USA, 99: 4308-4312; 2002.

Maroto, R., Raso, A., Wood, T.G., Kurosky, A., Martinac, B., Hamill, O.P. TRPC1 forms the stretch-activated cation channel in vertebrate cells. Nature Cell Biol. 7, 1443-1446, 2005.

Hamill, O.P. Twenty odd years of stretch-sensitive channels. Pflagers Archives. 453, 333-351, 2006.

Hamill, O.P., Maroto, R. TRPCs as MS channels. Current Topics in Membrane Transport. 59; 191-231, 2007.

Maroto, R., Hamill, O.P. MscCa regulation of tumor cell migration and metastastis. Current Topics in  Membrane Transport. 485-509, 2007.