Faculty    |   Research Faculty    |   Joint Appointments    |   Adjunct Appointments

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

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), demyelinating neuropathies, and lens cataracts. In addition, gene targeting of connexins in mice has provided new insights into connexin function and revealed a variety of unexpected phenotypes.

We are interested in how different members of the connexin family fulfill unique functions in tissue homeostasis. For example, the lens expresses three connexins Cx43, Cx46 and Cx50. Mutations in either the human Cx46 or Cx50 genes lead to congenital cataract. Using genetically engineered mice with targeted disruption of these connexins, we have found that connexin diversity is not required for embryonic development of the lens but is essential for normal postnatal growth and function.

Selected Publications

G. Meşe, 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 [Epub ahead of print]

N.A. Levit, G. Meşe, M.-G. R. Basaly and T.W. White (2011). Pathological hemichannels associated with human Cx26 mutations causing Keratitis-Ichthyosis-Deafness syndrome. Biochim. Biophys. Acta [Epub ahead of print]

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. Ebihara, J.J. Tong, B. Vertel, T.W. White, and T.L. Chen (2011). Properties of connexin 46 hemichannels in dissociated lens fiber cells. Invest. Ophthalmol. Vis. Sci. 52:882-889

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

L. Tao, A.M. DeRosa, T.W. White and G. Valdimarsson (2010). Zebrafish Cx30.3: Identification and characterization of a gap junction gene highly expressed in the skin. Dev. Dyn. 239:2627-2636

H.A. Sánchez, G. Meşe, 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

M. Tekin, X.-J. Xia, R. Erdenetungalag, F.B. Cengiz, T.W. White, J. Radnaabazar, B. Dangaasuren, H. Tastan, W.E. Nance, A. Pandya (2010). GJB2 mutations in Mongolia: Complex alleles, low frequency, and reduced fitness of the deaf. Ann. Hum. Genet. 74:155-164

R.T Mathias, T.W White and X. Gong (2010). Lens gap junctions in growth, differentiation and homeostasis. Physiol. Rev. 90:179-206

J.R. Lee and T.W. White (2009). Connexin26 mutations in deafness and skin disease. Expert Rev. Mol. Med. 11:e35

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

A.M. DeRosa, G. Meşe, L. Li, C. Sellitto, P.R. Brink, X. Gong and T.W. White (2009). The cataract causing Cx50-S50P mutant inhibits Cx43 and intercellular communication in the lens epithelium. Exp. Cell Res. 315:1063-1075

H. Wang, J. Gao, X. Sun, F.J. Martinez- Wittinghan, L. Li, K. Varadaraj, M. Farrel, V.N. Reddy, T.W. White, R.T. Mathias (2009). The effects of GPX-1 knockout on membrane transport and intracellular homeostasis in the lens. J. Mem. Biol. 227:25-37

G. Meşe, 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:C966–C974

C. Cheng, C.H. Xia, L. Li, T.W. White, J. Niimi and X. Gong (2008) Gap junction communication influences intercellular protein distribution in the lens. Exp. Eye Res. 86:966-974

G. Kanaporis, G. Meşe, L. Valiuniene, T.W. White, P.R. Brink and V. Valiunas (2008). Gap junction channels exhibit connexin-specific permeability to cyclic nucleotides. J. Gen. Physiol. 131:293-305

T.W. White, Y. Gao, L. Li, C. Sellitto, and M. Srinivas (2007). Changes in lens epithelial cell proliferation are correlated with changes in 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

G. Meşe, G. Richard and T.W. White (2007). Gap junctions: basic structure and function. J. Invest. Derm. 127:2516-2524

S.W. Yum, J. Zhang, V. Valiunas, G. Kanaporis, P.R. Brink, T.W. White, and S.S. Scherer (2007). Human connexin26 and connexin30 form functional heteromeric hemichannels and heterotypic channels. Am. J. Physiol. Cell Physiol. 293:C1032-C1048

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.D. Hoptak, K.A. Klein, A.M. DeRosa, T.W. White, and M.K. Iovine (2007). Zebrafish short fin mutations in connexin43 lead to aberrant gap junctional intercellular communication. FEBS Letters 581:3297-3302



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