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Human Molecular Genetics Advance Access published online on December 1, 2006
Human Molecular Genetics, doi:10.1093/hmg/ddl452
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© The Author 2006. Published by Oxford University Press. All rights reserved

Tissue specific effects of wildtype and mutant Connexin 31: a role in neurite outgrowth

Harriet C. Unsworth*, Trond Aasen*, Suzanne McElwaine{dagger} and David P. Kelsell*,

* Centre for Cutaneous Research, Institute of Cell & Molecular Science, Queen Mary's School of Medicine & Dentistry, University of London, Whitechapel, E1 4AT, UK {dagger} Department of Experimental Haematology, Institute of Cell & Molecular Science, Queen Mary's School of Medicine & Dentistry, University of London, Whitechapel, E1 4AT, UK

Correspondence should be addressed to David P. Kelsell. Centre for Cutaneous Research, Institute of Cell and Molecular Science, Queen Mary's School of Medicine & Dentistry, University of London, 4 Newark Street, Whitechapel, London, UK. , Fax: 44 (0)20 7882 7171. E-mail: d.p.kelsell{at}qmul.ac.uk

Received September 28, 2006; Revised November 16, 2006; Accepted November 24, 2006

Channels formed by connexins (Cx), the major protein subunits of gap junctions, allow passage of ions and molecular messengers between cells to provide a mechanism of synchronised cellular response. Twenty human Cx isoforms have been identified and mutations in the gene GJB3 encoding the 31 kDa isoform, Cx31, can cause dominant or recessive skin disease, dominant or recessive deafness or dominant neuropathy with deafness. Cx31 is expressed in differentiating keratinocytes in skin. Here, we also demonstrate endogenous Cx31 expression in human neuronal cell lines, particularly in differentiated neurones. Exogenous Cx31 expression induced neurite outgrowth in human neuronal cell lines, but not differentiation in primary human keratinocytes. Though neither the neuropathy and hearing loss mutation (66delD)Cx31 nor the skin disease associated mutation (R42P)Cx31 are able to traffic to the plasma membrane, the R42P mutant induced neurite outgrowth to a level equal to wild-type Cx31. In contrast, there was significantly reduced neurite outgrowth after (66delD)Cx31 expression. As well as indicating a potential disease mechanism for the neuropathy/deafness mutation, this work demonstrates a tissue-specific function for Cx31.

The authors wish it to be known that, in their opinion, the first 2 authors should be regarded as joint First Authors


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