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MBC in Press, published online ahead of print May 24, 2006
Mol. Biol. Cell 10.1091/mbc.E06-02-0122

A more recent version of this article appeared on August 1, 2006
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Submitted on February 9, 2006
Revised on May 11, 2006
Accepted on May 12, 2006

Cingulin Regulates Claudin-2 Expression and Cell Proliferation through the Small GTPase RhoA

Laurent Guillemot* and Sandra Citi*{dagger}

*Department of Molecular Biology, University of Geneva, CH-1211 Geneva, Switzerland; {dagger}Department of Biology, University of Padova, I-35121 Padova, Italy

Monitoring Editor: Asma Nusrat

In mouse embryoid bodies, mutation of the tight junction protein cingulin results in changes in gene expression. Here, we studied the function of cingulin using a gene silencing approach in MDCK cells. Cingulin-depleted cells show higher protein and mRNA levels of claudin-2 and ZO-3, increased RhoA activity, activation of G1/S phase transition, and increased cell density. The effects of cingulin depletion on claudin-2 expression, cell proliferation and density are reversed by coexpression of either a dominant-negative form of RhoA (RhoAN19), or the Rho-inhibiting enzyme C3 transferase. However, the increase in ZO-3 protein and mRNA levels is not reversed by inhibition of either RhoA, p38, ERK or JNK, suggesting that cingulin modulates ZO-3 expression by a different mechanism. JNK is implicated in the regulation of claudin-2 levels independently of cingulin depletion and RhoA activity, indicating distinct roles of RhoA- and JNK-dependent pathways in the control of claudin-2 expression. Finally, cingulin depletion does not significantly alter the barrier function of monolayers, and the overall molecular organization of tight junctions. These results provide novel insights about the mechanisms of cingulin function, and the signaling pathways controlling claudin-2 expression in MDCK cells.

Address correspondence to: Sandra Citi (sandra.citi{at}molbio.unige.ch)




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