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Article: Hypoxia impairs primordial germ cell migration in zebrafish (danio rerio) embryos
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TitleHypoxia impairs primordial germ cell migration in zebrafish (danio rerio) embryos
 
AuthorsLo, KH2
Hui, MNY2
Yu, RMK3
Wu, RSS2 1
Cheng, SH2
 
Issue Date2011
 
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
CitationPlos One, 2011, v. 6 n. 9 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0024540
 
AbstractBackground: As a global environmental concern, hypoxia is known to be associated with many biological and physiological impairments in aquatic ecosystems. Previous studies have mainly focused on the effect of hypoxia in adult animals. However, the effect of hypoxia and the underlying mechanism of how hypoxia affects embryonic development of aquatic animals remain unclear. Methodology/Principal Findings: In the current study, the effect of hypoxia on primordial germ cell (PGC) migration in zebrafish embryos was investigated. Hypoxic embryos showed PGC migration defect as indicated by the presence of mis-migrated ectopic PGCs. Insulin-like growth factor (IGF) signaling is required for embryonic germ line development. Using real-time PCR, we found that the mRNA expression levels of insulin-like growth factor binding protein (IGFBP-1), an inhibitor of IGF bioactivity, were significantly increased in hypoxic embryos. Morpholino knockdown of IGFBP-1 rescued the PGC migration defect phenotype in hypoxic embryos, suggesting the role of IGFBP-1 in inducing PGC mis-migration. Conclusions/Significance: This study provides novel evidence that hypoxia disrupts PGC migration during embryonic development in fish. IGF signaling is shown to be one of the possible mechanisms for the causal link between hypoxia and PGC migration. We propose that hypoxia causes PGC migration defect by inhibiting IGF signaling through the induction of IGFBP-1. © 2011 Lo et al.
 
ISSN1932-6203
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
 
DOIhttp://dx.doi.org/10.1371/journal.pone.0024540
 
PubMed Central IDPMC3169607
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLo, KH
 
dc.contributor.authorHui, MNY
 
dc.contributor.authorYu, RMK
 
dc.contributor.authorWu, RSS
 
dc.contributor.authorCheng, SH
 
dc.date.accessioned2012-08-28T01:30:50Z
 
dc.date.available2012-08-28T01:30:50Z
 
dc.date.issued2011
 
dc.description.abstractBackground: As a global environmental concern, hypoxia is known to be associated with many biological and physiological impairments in aquatic ecosystems. Previous studies have mainly focused on the effect of hypoxia in adult animals. However, the effect of hypoxia and the underlying mechanism of how hypoxia affects embryonic development of aquatic animals remain unclear. Methodology/Principal Findings: In the current study, the effect of hypoxia on primordial germ cell (PGC) migration in zebrafish embryos was investigated. Hypoxic embryos showed PGC migration defect as indicated by the presence of mis-migrated ectopic PGCs. Insulin-like growth factor (IGF) signaling is required for embryonic germ line development. Using real-time PCR, we found that the mRNA expression levels of insulin-like growth factor binding protein (IGFBP-1), an inhibitor of IGF bioactivity, were significantly increased in hypoxic embryos. Morpholino knockdown of IGFBP-1 rescued the PGC migration defect phenotype in hypoxic embryos, suggesting the role of IGFBP-1 in inducing PGC mis-migration. Conclusions/Significance: This study provides novel evidence that hypoxia disrupts PGC migration during embryonic development in fish. IGF signaling is shown to be one of the possible mechanisms for the causal link between hypoxia and PGC migration. We propose that hypoxia causes PGC migration defect by inhibiting IGF signaling through the induction of IGFBP-1. © 2011 Lo et al.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationPlos One, 2011, v. 6 n. 9 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0024540
 
dc.identifier.doihttp://dx.doi.org/10.1371/journal.pone.0024540
 
dc.identifier.hkuros203341
 
dc.identifier.hkuros208958
 
dc.identifier.issn1932-6203
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
 
dc.identifier.issue9
 
dc.identifier.pmcidPMC3169607
 
dc.identifier.pmid21931746
 
dc.identifier.scopuseid_2-s2.0-80052541174
 
dc.identifier.urihttp://hdl.handle.net/10722/161499
 
dc.identifier.volume6
 
dc.languageeng
 
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
dc.publisher.placeUnited States
 
dc.relation.ispartofPLoS ONE
 
dc.relation.referencesReferences in Scopus
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subject.meshGene Expression Profiling
 
dc.subject.meshGene Expression Regulation, Developmental
 
dc.subject.meshGerm Cells - cytology
 
dc.subject.meshInsulin-Like Growth Factor Binding Protein 1 - metabolism
 
dc.subject.meshRNA, Messenger - metabolism
 
dc.titleHypoxia impairs primordial germ cell migration in zebrafish (danio rerio) embryos
 
dc.typeArticle
 
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<contributor.author>Hui, MNY</contributor.author>
<contributor.author>Yu, RMK</contributor.author>
<contributor.author>Wu, RSS</contributor.author>
<contributor.author>Cheng, SH</contributor.author>
<date.accessioned>2012-08-28T01:30:50Z</date.accessioned>
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<description.abstract>Background: As a global environmental concern, hypoxia is known to be associated with many biological and physiological impairments in aquatic ecosystems. Previous studies have mainly focused on the effect of hypoxia in adult animals. However, the effect of hypoxia and the underlying mechanism of how hypoxia affects embryonic development of aquatic animals remain unclear. Methodology/Principal Findings: In the current study, the effect of hypoxia on primordial germ cell (PGC) migration in zebrafish embryos was investigated. Hypoxic embryos showed PGC migration defect as indicated by the presence of mis-migrated ectopic PGCs. Insulin-like growth factor (IGF) signaling is required for embryonic germ line development. Using real-time PCR, we found that the mRNA expression levels of insulin-like growth factor binding protein (IGFBP-1), an inhibitor of IGF bioactivity, were significantly increased in hypoxic embryos. Morpholino knockdown of IGFBP-1 rescued the PGC migration defect phenotype in hypoxic embryos, suggesting the role of IGFBP-1 in inducing PGC mis-migration. Conclusions/Significance: This study provides novel evidence that hypoxia disrupts PGC migration during embryonic development in fish. IGF signaling is shown to be one of the possible mechanisms for the causal link between hypoxia and PGC migration. We propose that hypoxia causes PGC migration defect by inhibiting IGF signaling through the induction of IGFBP-1. &#169; 2011 Lo et al.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong
  2. City University of Hong Kong
  3. University of Newcastle, Australia