Cap-Gly proteins at microtubule plus ends: is EB1 detyrosination involved?

PLoS One. 2012;7(3):e33490. doi: 10.1371/journal.pone.0033490. Epub 2012 Mar 14.

Abstract

Localization of CAP-Gly proteins such as CLIP170 at microtubule+ends results from their dual interaction with α-tubulin and EB1 through their C-terminal amino acids -EEY. Detyrosination (cleavage of the terminal tyrosine) of α-tubulin by tubulin-carboxypeptidase abolishes CLIP170 binding. Can detyrosination affect EB1 and thus regulate the presence of CLIP170 at microtubule+ends as well? We developed specific antibodies to discriminate tyrosinated vs detyrosinated forms of EB1 and detected only tyrosinated EB1 in fibroblasts, astrocytes, and total brain tissue. Over-expressed EB1 was not detyrosinated in cells and chimeric EB1 with the eight C-terminal amino acids of α-tubulin was only barely detyrosinated. Our results indicate that detyrosination regulates CLIPs interaction with α-tubulin, but not with EB1. They highlight the specificity of carboxypeptidase toward tubulin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies / immunology
  • Antibody Specificity / immunology
  • Brain / metabolism
  • Cattle
  • Fibroblasts / metabolism
  • Mice
  • Microtubule-Associated Proteins / chemistry
  • Microtubule-Associated Proteins / metabolism*
  • Microtubules / chemistry
  • Microtubules / metabolism*
  • Protein Structure, Tertiary
  • Recombinant Proteins / chemistry
  • Recombinant Proteins / metabolism
  • Tubulin / chemistry
  • Tubulin / immunology
  • Tubulin / metabolism
  • Tyrosine / metabolism*

Substances

  • Antibodies
  • EB1 microtubule binding proteins
  • Microtubule-Associated Proteins
  • Recombinant Proteins
  • Tubulin
  • Tyrosine