Screening for novel LRRK2 inhibitors using a high-throughput TR-FRET cellular assay for LRRK2 Ser935 phosphorylation

PLoS One. 2012;7(8):e43580. doi: 10.1371/journal.pone.0043580. Epub 2012 Aug 28.

Abstract

Background: Mutations in the leucine-rich repeat kinase-2 (LRRK2) have been linked to Parkinson's disease. Recent studies show that inhibition of LRRK2 kinase activity decreased the level of phosphorylation at its own Ser910 and Ser935, indicating that these sites are prime targets for cellular readouts of LRRK2 inhibition.

Methodology/principal findings: Using Time-Resolved Förster Resonance Energy Transfer (TR-FRET) technology, we developed a high-throughput cellular assay for monitoring LRRK2 phosphorylation at Ser935. LRRK2-Green Fluorescence Protein (GFP) fusions were expressed in cells via BacMam. Phosphorylation at Ser935 in these cells is detected using a terbium labeled anti-phospho-Ser935 antibody that generates a TR-FRET signal between terbium and GFP. LRRK2 wild-type and G2019S are constitutively phosphorylated at Ser935 in cells as measured by TR-FRET. The phosphorylation level is reduced for the R1441C mutant and little could be detected for the kinase-dead mutant D1994A. The TR-FRET cellular assay was further validated using reported LRRK2 inhibitors including LRRK2-IN-1 and our results confirmed that inhibition of LRRK2 can reduce the phosphorylation level at Ser935. To demonstrate the utility of this assay for screening, we profiled a small library of 1120 compounds. Three known LRRK2 inhibitors were identified and 16 hits were followed up in the TR-FRET and a cytotoxicity assay. Interestingly, out of the top 16 hits, five are known inhibitors of IκB phosphorylation, two CHK1 and two CDC25 inhibitors. Thirteen hits were further tested in a biochemical LRRK2 kinase activity assay and Western blot analysis for their effects on the phosphorylation of Ser910, Ser935, Ser955 and Ser973.

Conclusions/significance: We developed a TR-FRET cellular assay for LRRK2 Ser935 phosphorylation that can be applied to the screening for LRRK2 inhibitors. We report for the first time that several compounds such as IKK16, CHK1 inhibitors and GW441756 can inhibit LRRK2 Ser935 phosphorylation in cells and LRRK2 kinase activity in vitro.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line, Tumor
  • Checkpoint Kinase 1
  • Chemistry, Pharmaceutical / methods*
  • Drug Design
  • Drug Evaluation, Preclinical / methods*
  • Fluorescence Resonance Energy Transfer / methods*
  • Gene Library
  • Green Fluorescent Proteins / metabolism
  • Humans
  • Immunoprecipitation / methods
  • Inhibitory Concentration 50
  • Leucine-Rich Repeat Serine-Threonine Protein Kinase-2
  • Models, Genetic
  • Parkinson Disease / drug therapy
  • Parkinson Disease / genetics
  • Phosphorylation
  • Protein Kinases / chemistry
  • Protein Serine-Threonine Kinases / antagonists & inhibitors*
  • Serine / chemistry*

Substances

  • Green Fluorescent Proteins
  • Serine
  • Protein Kinases
  • CHEK1 protein, human
  • Checkpoint Kinase 1
  • LRRK2 protein, human
  • Leucine-Rich Repeat Serine-Threonine Protein Kinase-2
  • Protein Serine-Threonine Kinases

Grants and funding

Support for this work by R. Jeremy Nichols was from grants from the Michael J. Fox Foundation for Parkinson's Research and the benevolence of the Brin/Wojciki foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.