Involvement of MAP kinase in insulin signalling revealed by non-invasive imaging of luciferase gene expression in single living cells

Curr Biol. 1995 Aug 1;5(8):890-9. doi: 10.1016/s0960-9822(95)00179-5.

Abstract

Background: Studies of the mechanisms by which signals are transmitted from receptor tyrosine kinases would be facilitated by a way of monitoring events at the single-cell level. We have explored how luciferase imaging can be used to examine the role of specific signalling pathways in insulin-stimulated gene expression. The analysis of luciferase expression in single cells has previously been hampered by the insensitivity of existing methodologies and the lack of a way of monitoring quantitatively, and independently, more than one promoter within the same cell. We have developed a technique for examining the dynamics of insulin-stimulated AP-1-dependent transcription in single living cells, and have explored the signalling pathway involved.

Results: Luciferase and aequorin gene expression were examined in single living cells with a high-sensitivity photon-counting camera. The technique involved the comicroinjection of luciferase- and aequorin-based reporter plasmids directly into the cell nucleus, and the subsequent analysis of luminescence in the presence of luciferin and coelenterazine, respectively. The method is quantitative and allows insulin-stimulated gene expression to be monitored in real time. We found that insulin promoted a substantial increase in the expression of a luciferase gene under the control of the AP-1-binding site from the collagenase gene promoter. Aequorin expression, under the control of a cytomegalovirus promoter, was unaffected by insulin. The effect of insulin on luciferase expression was specifically blocked by overexpression of either the mitogen-activated protein (MAP) kinase phosphatase CL100, or the dominant-negative mutant MAP kinase kinase, MEKS217/221A.

Conclusions: Microinjection coupled with luciferase imaging allows hormone-regulated gene expression from relatively weak promoters to be monitored in single living cells. We have used this method to demonstrate that MAP kinase plays a central role in the ability of insulin to stimulate AP-1-dependent gene transcription.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aequorin / genetics
  • Animals
  • Biological Transport
  • CHO Cells
  • Calcium-Calmodulin-Dependent Protein Kinases / metabolism*
  • Cell Cycle Proteins*
  • Cell Nucleus / metabolism
  • Collagenases / genetics
  • Cricetinae
  • Dual Specificity Phosphatase 1
  • Gene Expression Regulation, Enzymologic / drug effects
  • Image Processing, Computer-Assisted
  • Immediate-Early Proteins / genetics*
  • Insulin / metabolism*
  • Insulin / pharmacology
  • Luciferases / genetics*
  • Microinjections
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinase Kinases
  • Mitogen-Activated Protein Kinases*
  • Phosphoprotein Phosphatases*
  • Promoter Regions, Genetic
  • Protein Kinases / metabolism*
  • Protein Phosphatase 1
  • Protein Tyrosine Phosphatases / genetics*
  • Signal Transduction*
  • Transcription Factor AP-1 / metabolism

Substances

  • Cell Cycle Proteins
  • Immediate-Early Proteins
  • Insulin
  • Transcription Factor AP-1
  • Aequorin
  • Luciferases
  • Protein Kinases
  • Calcium-Calmodulin-Dependent Protein Kinases
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinase Kinases
  • Phosphoprotein Phosphatases
  • Protein Phosphatase 1
  • Dual Specificity Phosphatase 1
  • Protein Tyrosine Phosphatases
  • Collagenases