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Article: Function of Arl4aa in the Initiation of Hematopoiesis in Zebrafish by Maintaining Golgi Complex Integrity in Hemogenic Endothelium

TitleFunction of Arl4aa in the Initiation of Hematopoiesis in Zebrafish by Maintaining Golgi Complex Integrity in Hemogenic Endothelium
Authors
KeywordsArl4aa
Golgi complex
Notch signaling
definitive hematopoietic stem cells
zebrafish
Issue Date2020
PublisherElsevier (Cell Press): OAJ. The Journal's web site is located at http://stemcellreports.cell.com
Citation
Stem Cell Reports, 2020, v. 14 n. 4, p. 575-589 How to Cite?
AbstractADP-ribosylation factor-like 4aa (Arl4aa) is a member of the ADP-ribosylation factor family. It is expressed in hematopoietic tissue during embryonic development, but its function was unknown. Zebrafish arl4aa is preferentially expressed in the ventral wall of the dorsal aorta (VDA) at 24 and 36 hpf and in caudal hematopoietic tissue at 48 hpf. Morpholino knockdown and transcription activator-like effector nuclease (TALEN) knockout of arl4aa significantly reduced expression of genes associated with definitive hematopoietic stem cells (HSCs). Golgi complex integrity in VDA was disrupted as shown by transmission electron microscopy and immunostaining of Golgi membrane Giantin. Mechanistically, arl4aa knockdown reduced Notch signaling in the VDA and its target gene expression. Protein expression of NICD was also reduced. Effects of arl4aa knockdown on definitive hematopoiesis could be restored by NICD expression. This study identified arl4aa as a factor regulating initiation of definitive HSCs by maintaining the integrity of Golgi complex and, secondarily, maturation of the Notch receptor.
Persistent Identifierhttp://hdl.handle.net/10722/288412
ISSN
2020 Impact Factor: 7.765
2015 SCImago Journal Rankings: 5.523
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorGuo, Y-
dc.contributor.authorCheng, BYL-
dc.contributor.authorWANG, D-
dc.contributor.authorMa, ACH-
dc.contributor.authorHe, BL-
dc.contributor.authorMan, TK-
dc.contributor.authorCheung, MPL-
dc.contributor.authorShi, X-
dc.contributor.authorNg, NKL-
dc.contributor.authorLeung, AYH-
dc.date.accessioned2020-10-05T12:12:30Z-
dc.date.available2020-10-05T12:12:30Z-
dc.date.issued2020-
dc.identifier.citationStem Cell Reports, 2020, v. 14 n. 4, p. 575-589-
dc.identifier.issn2213-6711-
dc.identifier.urihttp://hdl.handle.net/10722/288412-
dc.description.abstractADP-ribosylation factor-like 4aa (Arl4aa) is a member of the ADP-ribosylation factor family. It is expressed in hematopoietic tissue during embryonic development, but its function was unknown. Zebrafish arl4aa is preferentially expressed in the ventral wall of the dorsal aorta (VDA) at 24 and 36 hpf and in caudal hematopoietic tissue at 48 hpf. Morpholino knockdown and transcription activator-like effector nuclease (TALEN) knockout of arl4aa significantly reduced expression of genes associated with definitive hematopoietic stem cells (HSCs). Golgi complex integrity in VDA was disrupted as shown by transmission electron microscopy and immunostaining of Golgi membrane Giantin. Mechanistically, arl4aa knockdown reduced Notch signaling in the VDA and its target gene expression. Protein expression of NICD was also reduced. Effects of arl4aa knockdown on definitive hematopoiesis could be restored by NICD expression. This study identified arl4aa as a factor regulating initiation of definitive HSCs by maintaining the integrity of Golgi complex and, secondarily, maturation of the Notch receptor.-
dc.languageeng-
dc.publisherElsevier (Cell Press): OAJ. The Journal's web site is located at http://stemcellreports.cell.com-
dc.relation.ispartofStem Cell Reports-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectArl4aa-
dc.subjectGolgi complex-
dc.subjectNotch signaling-
dc.subjectdefinitive hematopoietic stem cells-
dc.subjectzebrafish-
dc.titleFunction of Arl4aa in the Initiation of Hematopoiesis in Zebrafish by Maintaining Golgi Complex Integrity in Hemogenic Endothelium-
dc.typeArticle-
dc.identifier.emailMa, ACH: alvinma@hku.hk-
dc.identifier.emailCheung, MPL: mplcheun@hku.hk-
dc.identifier.emailLeung, AYH: ayhleung@hku.hk-
dc.identifier.authorityMa, ACH=rp01810-
dc.identifier.authorityLeung, AYH=rp00265-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1016/j.stemcr.2020.02.012-
dc.identifier.pmid32220330-
dc.identifier.pmcidPMC7160373-
dc.identifier.scopuseid_2-s2.0-85082778717-
dc.identifier.hkuros315796-
dc.identifier.volume14-
dc.identifier.issue4-
dc.identifier.spage575-
dc.identifier.epage589-
dc.identifier.isiWOS:000526941200007-
dc.publisher.placeUnited States-
dc.identifier.issnl2213-6711-

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