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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 simila...

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Detalles Bibliográficos
Autores principales: Ren, Guiqi, Xin, Shengchang, Li, Song, Zhong, Hanbing, Lin, Shuo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3116841/
https://www.ncbi.nlm.nih.gov/pubmed/21698186
http://dx.doi.org/10.1371/journal.pone.0020630
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author Ren, Guiqi
Xin, Shengchang
Li, Song
Zhong, Hanbing
Lin, Shuo
author_facet Ren, Guiqi
Xin, Shengchang
Li, Song
Zhong, Hanbing
Lin, Shuo
author_sort Ren, Guiqi
collection PubMed
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.
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spelling pubmed-31168412011-06-22 Disruption of LRRK2 Does Not Cause Specific Loss of Dopaminergic Neurons in Zebrafish Ren, Guiqi Xin, Shengchang Li, Song Zhong, Hanbing Lin, Shuo PLoS One Research Article 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. Public Library of Science 2011-06-16 /pmc/articles/PMC3116841/ /pubmed/21698186 http://dx.doi.org/10.1371/journal.pone.0020630 Text en Ren et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Ren, Guiqi
Xin, Shengchang
Li, Song
Zhong, Hanbing
Lin, Shuo
Disruption of LRRK2 Does Not Cause Specific Loss of Dopaminergic Neurons in Zebrafish
title Disruption of LRRK2 Does Not Cause Specific Loss of Dopaminergic Neurons in Zebrafish
title_full Disruption of LRRK2 Does Not Cause Specific Loss of Dopaminergic Neurons in Zebrafish
title_fullStr Disruption of LRRK2 Does Not Cause Specific Loss of Dopaminergic Neurons in Zebrafish
title_full_unstemmed Disruption of LRRK2 Does Not Cause Specific Loss of Dopaminergic Neurons in Zebrafish
title_short Disruption of LRRK2 Does Not Cause Specific Loss of Dopaminergic Neurons in Zebrafish
title_sort disruption of lrrk2 does not cause specific loss of dopaminergic neurons in zebrafish
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3116841/
https://www.ncbi.nlm.nih.gov/pubmed/21698186
http://dx.doi.org/10.1371/journal.pone.0020630
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