Tight junction modulation and biochemical characterisation of the zonula occludens toxin C-and N-termini

FEBS Lett. 2007 Jun 26;581(16):2974-80. doi: 10.1016/j.febslet.2007.05.051. Epub 2007 May 29.

Abstract

The ZOT N-terminal domain was expressed and refolded, yielding a soluble protein with defined secondary structure. Although distantly related to protein I of filamentous phages, no evidence of ATPase activity was found. It is therefore unlikely that the ZOT N-terminal domain is involved in cholera toxin phage packaging in Vibrio cholerae. The ZOT C-terminal domain caused delocalisation of occludin and ZO-1 from Caco-2 cell-cell contacts, irrespective of disulfide bridge formation in its putative binding domain. However, the C-terminal domain did not cause actin reorganisation and this may explain the absence of a concomitant reduction in the transepithelial electrical resistance across cell monolayers.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Adenosine Triphosphatases / metabolism
  • Amino Acid Sequence
  • Caco-2 Cells
  • Cholera Toxin / chemistry*
  • Cholera Toxin / pharmacology*
  • Endotoxins
  • Humans
  • Membrane Proteins / metabolism
  • Molecular Sequence Data
  • Occludin
  • Phosphoproteins / metabolism
  • Protein Structure, Tertiary
  • Sequence Homology, Amino Acid
  • Tight Junctions / drug effects*
  • Zonula Occludens-1 Protein

Substances

  • Actins
  • Endotoxins
  • Membrane Proteins
  • OCLN protein, human
  • Occludin
  • Phosphoproteins
  • TJP1 protein, human
  • Zonula Occludens-1 Protein
  • zonula occludens toxin, Vibrio cholerae
  • Cholera Toxin
  • Adenosine Triphosphatases