PLK2 modulates α-synuclein aggregation in yeast and mammalian cells

Mol Neurobiol. 2013 Dec;48(3):854-62. doi: 10.1007/s12035-013-8473-z. Epub 2013 May 17.

Abstract

Phosphorylation of α-synuclein (aSyn) on serine 129 is one of the major post-translation modifications found in Lewy bodies, the typical pathological hallmark of Parkinson's disease. Here, we found that both PLK2 and PLK3 phosphorylate aSyn on serine 129 in yeast. However, only PLK2 increased aSyn cytotoxicity and the percentage of cells presenting cytoplasmic foci. Consistently, in mammalian cells, PLK2 induced aSyn phosphorylation on serine 129 and induced an increase in the size of the inclusions. Our study supports a role for PLK2 in the generation of aSyn inclusions by a mechanism that does not depend directly on serine 129 phosphorylation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Humans
  • Inclusion Bodies / metabolism
  • Mice
  • Phosphorylation / drug effects
  • Phosphoserine / metabolism
  • Protein Serine-Threonine Kinases / metabolism*
  • Protein Structure, Quaternary
  • Saccharomyces cerevisiae / cytology*
  • Saccharomyces cerevisiae / metabolism
  • Tumor Suppressor Proteins
  • alpha-Synuclein / chemistry*
  • alpha-Synuclein / metabolism
  • alpha-Synuclein / toxicity

Substances

  • Tumor Suppressor Proteins
  • alpha-Synuclein
  • Phosphoserine
  • PLK3 protein, human
  • PLK2 protein, human
  • Protein Serine-Threonine Kinases