Isolation of a new peroxisome-deficient CHO cell mutant defective in peroxisome targeting signal-1 receptor

Biochem Biophys Res Commun. 1997 Jan 13;230(2):402-6. doi: 10.1006/bbrc.1996.5971.

Abstract

For the study of mechanism of peroxisome biogenesis, we attempted to isolate CHO cell mutants deficient in peroxisome biogenesis. We used as the parent strain a stable CHO transformant of rat PEX2 (formerly named peroxisome assembly factor-1) cDNA, to avoid unusually frequent isolation of Pex2 mutants. Among the three peroxisome-deficient mutants obtained, ZP102 was a new CHO mutant of complementation group 2, and was restored for peroxisome assembly by the transfection of human PEX5 (formerly called PXR1 or PTS1R) cDNA. This approach would facilitate the isolation of new complementation gorups of peroxisome-deficient CHO mutants and the identification of essential genes for peroxisome biogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CHO Cells
  • Catalase / metabolism
  • Cell Fusion
  • Cricetinae
  • DNA Primers
  • Digitonin / pharmacology
  • Genetic Complementation Test
  • Humans
  • Membrane Proteins / biosynthesis*
  • Microbodies / physiology*
  • Microbodies / ultrastructure
  • Mutation
  • Peroxisomal Biogenesis Factor 2
  • Peroxisome-Targeting Signal 1 Receptor
  • Polymerase Chain Reaction
  • Rats
  • Receptors, Cytoplasmic and Nuclear / biosynthesis*
  • Receptors, Cytoplasmic and Nuclear / deficiency
  • Receptors, Cytoplasmic and Nuclear / genetics
  • Recombinant Proteins / biosynthesis
  • Transfection

Substances

  • DNA Primers
  • Membrane Proteins
  • PEX2 protein, human
  • PEX5 protein, human
  • Peroxisome-Targeting Signal 1 Receptor
  • Pex2 protein, rat
  • Receptors, Cytoplasmic and Nuclear
  • Recombinant Proteins
  • Peroxisomal Biogenesis Factor 2
  • Catalase
  • Digitonin