Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0176345
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dc.titleImpact of the c-MybE308G mutation on mouse myelopoiesis and dendritic cell development
dc.contributor.authorPapathanasiou P.
dc.contributor.authorPetvises S.
dc.contributor.authorHey Y.-Y.
dc.contributor.authorPerkins A.C.
dc.contributor.authorO'Neill H.C.
dc.date.accessioned2019-11-01T07:53:35Z
dc.date.available2019-11-01T07:53:35Z
dc.date.issued2017
dc.identifier.citationPapathanasiou P., Petvises S., Hey Y.-Y., Perkins A.C., O'Neill H.C. (2017). Impact of the c-MybE308G mutation on mouse myelopoiesis and dendritic cell development. PLoS ONE 12 (4) : e0176345. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0176345
dc.identifier.issn19326203
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/161197
dc.description.abstractBooreana mice carrying the c-Myb308G point mutation were analyzed to determine changes in early hematopoiesis in the bone marrow and among mature cells in the periphery. This point mutation led to increased numbers of early hematopoietic stem and progenitor cells (HSPCs), with a subsequent reduction in the development of B cells, erythroid cells, and neutrophils, and increased numbers of myeloid cells and granulocytes. Myelopoiesis was further investigated by way of particular subsets affected. A specific question addressed whether booreana mice contained increased numbers of dendritic-like cells (L-DC subset) recently identified in the spleen, since L-DCs arise in vitro by direct differentiation from HSPCs co-cultured over splenic stroma. The non-lethal c-Myb mutation in booreana mice was associated with significantly lower representation of splenic CD8- conventional dendritic cells (cDCs), inflammatory monocytes, and neutrophils compared to wild-type mice. This result confirmed the bone marrow origin of progenitors for these subsets since c-Myb is essential for their development. Production of L-DCs and resident monocytes was not affected by the c-MybE308G mutation. These subsets may derive from different progenitors than those in bone marrow, and are potentially established in the spleen during embryogenesis. An alternative explanation may be needed for why there was no change in CD8+ cDCs in booreana spleen since these cells are known to derive from common dendritic progenitors in bone marrow. © 2017 Papathanasiou et al. 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 credited.
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20191101
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectArticle
dc.subjectbone marrow biopsy
dc.subjectcell maturation
dc.subjectembryo development
dc.subjectflow cytometry
dc.subjectgene mutation
dc.subjecthematopoietic stem cell
dc.subjectmouse
dc.subjectmutagenesis
dc.subjectmyelopoiesis
dc.subjectnonhuman
dc.subjectphenotype
dc.subjectprevalence
dc.subjectanimal
dc.subjectB lymphocyte
dc.subjectbone marrow cell
dc.subjectC57BL mouse
dc.subjectcell culture
dc.subjectcoculture
dc.subjectcytology
dc.subjectdendritic cell
dc.subjectfemale
dc.subjectgenetics
dc.subjectmetabolism
dc.subjectpoint mutation
dc.subjectspleen
dc.subjectstroma cell
dc.subjectCD8 antigen
dc.subjectprotein c Myb
dc.subjectAnimals
dc.subjectAntigens, CD8
dc.subjectB-Lymphocytes
dc.subjectBone Marrow Cells
dc.subjectCells, Cultured
dc.subjectCoculture Techniques
dc.subjectDendritic Cells
dc.subjectFemale
dc.subjectFlow Cytometry
dc.subjectHematopoietic Stem Cells
dc.subjectMice
dc.subjectMice, Inbred C57BL
dc.subjectMyeloid Cells
dc.subjectMyelopoiesis
dc.subjectPoint Mutation
dc.subjectProto-Oncogene Proteins c-myb
dc.subjectSpleen
dc.subjectStromal Cells
dc.typeArticle
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.1371/journal.pone.0176345
dc.description.sourcetitlePLoS ONE
dc.description.volume12
dc.description.issue4
dc.description.pagee0176345
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