PUBLICATION
Disruption of LRRK2 Does Not Cause Specific Loss of Dopaminergic Neurons in Zebrafish
- Authors
- Ren, G., Xin, S., Li, S., Zhong, H., and Lin, S.
- ID
- ZDB-PUB-110629-31
- 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
Citation
Ren, G., Xin, S., Li, S., Zhong, H., and Lin, S. (2011) Disruption of LRRK2 Does Not Cause Specific Loss of Dopaminergic Neurons in Zebrafish. PLoS One. 6(6):e20630.
Abstract
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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping