title: Regulation of autophagy by LRRK2 in Caenorhabditis elegans.
abstract: BACKGROUND
  Mutations in LRRK2 (leucine-rich repeat kinase 2) are a common cause of familial Parkinson's disease. However, the mechanisms through which LRRK2 mutations contribute to neurodegeneration are poorly understood.
  
  
  OBJECTIVE
  We investigated the effects of WT, G2019S (GS), R1441C (RC) and kinase dead LRRK2 across multiple different cellular compartments in order to gain insight into the breadth of LRRK2 effects on cellular function.
  
  
  METHODS
  Nematodes expressing lgg-1::RFP, hsp1::GFP, hsp4::GFP and hsp6::GFP were crossed to nematode lines expressing WT, GS, RC or kinase dead LRRK2.
  
  
  RESULTS
  We observed that GS and RC LRRK2 inhibited autophagy, while WT, GS and RC LRRK2 increased the response of the mitochondrial hsp6 reporter to stress. The response of the hsp reporters under basal conditions was more nuanced.
  
  
  CONCLUSIONS
  These results support a putative role of LRRK2 in the autophagic and mitochondrial systems.
authors.affiliation: Departments of Pharmacology and Neurology, Boston University School of Medicine, Boston, Mass., USA.
authors.forename: Shamol
authors.initials: S
authors.lastname: Saha
authors.forename: Liqun
authors.initials: L
authors.lastname: Liu-Yesucevitz
authors.forename: Benjamin
authors.initials: B
authors.lastname: Wolozin
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D001343:Autophagy / Q000235:genetics*; D017173:Caenorhabditis elegans / Q000235:genetics*; D000090263:Leucine-Rich Repeat Proteins; D011506:Proteins / Q000235:genetics*
chemical_list: D000090263:Leucine-Rich Repeat Proteins; D011506:Proteins