ZFIN ID: ZDB-PUB-110629-31
Disruption of LRRK2 Does Not Cause Specific Loss of Dopaminergic Neurons in Zebrafish
Ren, G., Xin, S., Li, S., Zhong, H., and Lin, S.
Date: 2011
Source: PLoS One   6(6): e20630 (Journal)
Registered Authors: Lin, Shuo
Keywords: none
MeSH Terms:
  • Animals
  • Base Sequence
  • DNA Primers
  • Dopamine/metabolism*
  • Gene Knockdown Techniques
  • In Situ Hybridization
  • Neurons/cytology*
  • Neurons/metabolism
  • Protein-Serine-Threonine Kinases/genetics
  • Protein-Serine-Threonine Kinases/physiology*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Zebrafish/embryology
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/physiology*
PubMed: 21698186 Full text @ PLoS One
Mutations in LRRK2 are genetically linked to Parkinson's disease (PD) but its normal biological function is largely unknown. Sheng et al. recently reported that deletion of the WD40 domain of LRRK2 in zebrafish specifically causes PD-like loss of neurons and behavior defect. However, our similar early study and recent confirming experiments using the same reagents reported by Sheng et al. failed to reproduce the phenotype of the loss of dopaminergic neurons, although the mRNA of LRRK2 was molecularly disrupted. Our study suggests that function of LRRK2 and its usefulness to generate zebrafish PD model needs further evaluation.