Live-cell imaging of enzyme-substrate interaction reveals spatial regulation of PTP1B

Science. 2007 Jan 5;315(5808):115-9. doi: 10.1126/science.1134966.

Abstract

Endoplasmic reticulum-localized protein-tyrosine phosphatase PTP1B terminates growth factor signal transduction by dephosphorylation of receptor tyrosine kinases (RTKs). But how PTP1B allows for RTK signaling in the cytoplasm is unclear. In order to test whether PTP1B activity is spatially regulated, we developed a method based on Förster resonant energy transfer for imaging enzyme-substrate (ES) intermediates in live cells. We observed the establishment of a steady-state ES gradient across the cell. This gradient exhibited robustness to cell-to-cell variability, growth factor activation, and RTK localization, which demonstrated spatial regulation of PTP1B activity. Such regulation may be important for generating distinct cellular environments that permit RTK signal transduction and that mediate its eventual termination.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • COS Cells
  • Catalysis
  • Cell Line, Tumor
  • Chlorocebus aethiops
  • Epidermal Growth Factor / metabolism
  • Epidermal Growth Factor / pharmacology
  • ErbB Receptors / metabolism*
  • Fluorescence Resonance Energy Transfer
  • Humans
  • Kinetics
  • Mathematics
  • Microscopy, Fluorescence
  • Models, Biological
  • Phosphorylation
  • Protein Tyrosine Phosphatase, Non-Receptor Type 1
  • Protein Tyrosine Phosphatases / metabolism*
  • Receptor Protein-Tyrosine Kinases / metabolism*
  • Recombinant Fusion Proteins / metabolism

Substances

  • Recombinant Fusion Proteins
  • Epidermal Growth Factor
  • ErbB Receptors
  • Receptor Protein-Tyrosine Kinases
  • PTPN1 protein, human
  • Protein Tyrosine Phosphatase, Non-Receptor Type 1
  • Protein Tyrosine Phosphatases