Format

Send to

Choose Destination
PLoS One. 2011;6(7):e22489. doi: 10.1371/journal.pone.0022489. Epub 2011 Jul 22.

Pathogenic LRRK2 mutations do not alter gene expression in cell model systems or human brain tissue.

Author information

1
Department of Molecular Neuroscience, UCL Institute of Neurology, London, United Kingdom.

Erratum in

  • PLoS One. 2012;7(1). doi:10.1371/annotation/c12e4f9e-5aae-424b-a69f-fddf16976dc5.. Healey, Daniel [corrected to Healy, Daniel].

Abstract

Point mutations in LRRK2 cause autosomal dominant Parkinson's disease. Despite extensive efforts to determine the mechanism of cell death in patients with LRRK2 mutations, the aetiology of LRRK2 PD is not well understood. To examine possible alterations in gene expression linked to the presence of LRRK2 mutations, we carried out a case versus control analysis of global gene expression in three systems: fibroblasts isolated from LRRK2 mutation carriers and healthy, non-mutation carrying controls; brain tissue from G2019S mutation carriers and controls; and HEK293 inducible LRRK2 wild type and mutant cell lines. No significant alteration in gene expression was found in these systems following correction for multiple testing. These data suggest that any alterations in basal gene expression in fibroblasts or cell lines containing mutations in LRRK2 are likely to be quantitatively small. This work suggests that LRRK2 is unlikely to play a direct role in modulation of gene expression, although it remains possible that this protein can influence mRNA expression under pathogenic cicumstances.

PMID:
21799870
PMCID:
PMC3142158
DOI:
10.1371/journal.pone.0022489
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Public Library of Science Icon for PubMed Central
Loading ...
Support Center