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Disruption of LRRK2 Does Not Cause Specific Loss of Dopaminergic Neurons in Zebrafish

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 ear... Full description

Journal Title: PLoS ONE 2011, Vol.6(6)
Main Author: Ren, Guiqi
Other Authors: Xin, Shengchang , Li, Song , Zhong, Hanbing , Lin, Shuo
Format: Electronic Article Electronic Article
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ID: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0020630 ; PMCID: 3116841 ; PMID: 21698186
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recordid: pubmed_central3116841
title: Disruption of LRRK2 Does Not Cause Specific Loss of Dopaminergic Neurons in Zebrafish
format: Article
creator:
  • Ren, Guiqi
  • Xin, Shengchang
  • Li, Song
  • Zhong, Hanbing
  • Lin, Shuo
subjects:
  • Research Article
  • Biology
  • Medicine
ispartof: PLoS ONE, 2011, Vol.6(6)
description: 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.
language:
source:
identifier: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0020630 ; PMCID: 3116841 ; PMID: 21698186
fulltext: fulltext
issn:
  • 1932-6203
  • 19326203
url: Link


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descriptionMutations 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.
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titleDisruption of LRRK2 Does Not Cause Specific Loss of Dopaminergic Neurons in Zebrafish
descriptionMutations 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.
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abstractMutations 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.
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