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Thomas White

Thomas W. White

Ph.D. Harvard, 1994

Basic Science Tower, T-5, Room 147
Stony Brook University
Stony Brook, NY, 11794-8661

Phone: 631-444-9683
Fax: 631-444-3432
Email: Thomas.White@stonybrook.edu

White Lab Site




Gap junction functions defined by genetic diseases and gene knockouts.

Intercellular channels present in gap junctions allow cells to share small molecules and thus coordinate a wide range of behaviors. In vertebrates, a large family of genes known as connexins (Cx) encodes these gap junctional channels, and mutations in human connexins underlie a variety of diseases, including deafness, skin diseases (keratodermas), and lens cataracts. We are interested in how different members of the connexin family fulfill unique functions in tissue homeostasis, and in how intercellular channel activity is regulated by intracellular signal transduction cascades. We study the consequences of disease causing mutations on the functional behavior of channels using in vitro assays of channel permeation and gating followed by the generation of genetically engineered mice where genes have been deleted or mutated to create models of human disease.
Selected Publications


C. Sellitto, L. Li, J. Gao, M.L. Robinson, R.Z. Lin, R.T. Mathias and T.W. White (2013). AKT activation promotes PTEN hamartoma tumor syndrome-associated cataract development. J. Clin. Invest. 123:5401-5409
P.V. Mhaske, N.A. Levit, L. Li, H.-Z. Wang, J.R. Lee, Z. Shuja, P.R. Brink, and T.W. White (2013). The human Cx26-D50A and Cx26-A88V mutations causing Keratitis-Ichthyosis-Deafness syndrome display increased hemichannel activity. Am. J. Physiol. Cell Physiol. 304:C1150-C1158
N.A. Levit, G. Mese, M.-G. R. Basaly and T.W. White (2012). Pathological hemichannels associated with human Cx26 mutations causing Keratitis-Ichthyosis-Deafness syndrome. Biochim. Biophys. Acta 1818:2014-2019
G. Mese, C. Sellitto, L. Li, H.-Z. Wang, V. Valiunas, G. Richard, P.R. Brink and T.W. White (2011). The Cx26-G45E mutation displays increased hemichannel activity in a mouse model of the lethal form of keratitis-ichthyosis-deafness syndrome. Mol. Biol. Cell 22:4776-4786
J. Gao, X. Sun, L.C. Moore, T.W. White, P.R. Brink and R.T. Mathias (2011). Lens intracellular hydrostatic pressure is generated by the circulation of sodium and modulated by gap junction coupling. J. Gen. Physiol. 137:507-520
L. Li, C. Cheng, C.H. Xia, T.W. White, D.A. Fletcher and X. Gong (2010). Connexin mediated cataract prevention in mice. PLoS One 5:e12624
H.A. Sanchez, G. Mese, M. Srinivas, T.W. White and V.K. Verselis (2010). Differentially altered Ca2+ regulation and Ca2+permeability in Cx26 hemichannels formed by the A40V and G45E mutations that cause Keratitis-Ichthiosis-Deafness Syndrome. J. Gen. Physiol. 136:47-62
T. Shakespeare, C. Sellitto, L. Li, C. Rubinos, X. Gong, M. Srinivas, and T.W. White (2009). Interaction between connexin50 and mitogen-activated protein kinase signaling in lens homeostasis. Mol. Biol. Cell 20:2582-2592
J.R. Lee, A.M. DeRosa and T.W. White (2009). Connexin mutations causing skin disease and deafness increase hemichannel activity and cell death when expressed in Xenopus oocytes. J. Invest. Derm. 129:870-878
G. Mese, V. Valiunas, P.R. Brink and T.W. White (2008). Connexin26 deafness associated mutations show altered permeability to large cationic molecules. Am. J. Physiol. Cell Physiol. 295:C96-C974
T.W. White, Y. Gao, L. Li, C. Sellitto, and M. Srinivas (2007). Optimal lens epithelial cell proliferation is dependent on the connexin isoform providing gap junctional coupling. Invest. Ophthalmol. Vis. Sci. 48:5630-5637
A.M. DeRosa, C.H. Xia, X. Gong and T.W. White (2007). The cataract inducing Cx50-S50P mutation dominantly alters wild-type lens connexin channel gating. J. Cell Sci. 120:4107-4116
D.A. Gerido, A.M. DeRosa, G. Richard and T.W. White (2007). Aberrant hemichannel properties of Cx26 mutations causing skin disease and deafness. Am. J. Physiol. Cell Physiol. 293:C337-C345
A.M. DeRosa, R. Mui, M. Srinivas and T.W. White (2006). Functional characterization of a naturally occurring Cx50 truncation. Invest. Ophthalmol. Vis. Sci. 47:4474-4481
H.-B. Zhao, T. Kikuchi, A. Ngezahayo and T.W. White (2006). Gap junctions and cochlear homeostasis. J. Mem. Biol. 209:177-186
T.W. White, H. Wang, R. Mui, J. Litteral and P.R. Brink (2004). Cloning and functional expression of invertebrate connexins from Halocynthia pyriformis. FEBS Letters 577:42-48
C. Sellitto, L. Li, and T.W. White (2004). Connexin50 is required for normal postnatal lens cell proliferation. Invest. Ophthalmol. Vis. Sci. 45:3196-3202
G. Mese, E. Londin, R. Mui, P.R. Brink and T.W. White (2004). Altered gating properties of functional Cx26 mutants associated with recessive non-syndromic hearing loss. Hum. Genet. 115:191-199
F.J. Martinez-Wittinghan, C. Sellitto, L. Li, X. Gong, P.R. Brink, R.T. Mathias and T.W. White (2003). Dominant cataracts result from incongruous mixing of wild-type lens connexins. J. Cell Biol. 161: 969-978
T.W. White (2002). Unique and redundant connexin contributions to lens development. Science 295:319-320