bFGF signaling and v-Myb cooperate in sustained growth of primitive erythroid progenitors

Bartůněk, Petr; Pajer, Petr; Karafiát,; Blendinger, Gitta; Dvořák, Michal; Zenke, Martin

doi:10.1038/sj.onc.1205103

Cited by 9 publications

(7 citation statements)

References 25 publications

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“…It has been shown that Fgf8a function maintains expression of pax2a (one of the earliest kidney genes) in the midbrain-hindbrain boundary, another area in the embryo where pax2a is expressed (Reifers et al, 1998). Moreover, Fgfs suppress precocious blood differentiation (Bartůnek et al, 2002; Colas et al, 2008; Walmsley et al, 2008; Willey et al, 2006). Perhaps by keeping cells in a kidney program and preventing cells from beginning a blood or endothelial program of development, Fgf8a holds cells in the less differentiated kidney state (like a tail stem cell progenitor).…”

Section: Discussionmentioning

confidence: 99%

Zebrafish Tbx16 regulates intermediate mesoderm cell fate by attenuating Fgf activity

Warga¹,

Mueller²,

Ho³

et al. 2013

Developmental Biology

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Progenitors of the zebrafish pronephros, red blood and trunk endothelium all originate from the ventral mesoderm and often share lineage with one another, suggesting that their initial patterning is linked. Previous studies have shown that spadetail (spt) mutant embryos, defective in tbx16 gene function, fail to produce red blood cells, but retain the normal number of endothelial and pronephric cells. We report here that spt mutants are deficient in all the types of early blood, have fewer endothelial cells as well as far more pronephric cells compared to wildtype. In vivo cell tracing experiments reveal that blood and endothelium originate in spt mutants almost exclusively from the dorsal mesoderm whereas, pronephros and tail originate from both dorsal and ventral mesoderm. Together these findings suggest possible defects in posterior patterning. In accord with this, gene expression analysis show that mesodermal derivatives within the trunk and tail of spt mutants have acquired more posterior identity. Secreted signaling molecules belonging to the Fgf, Wnt and Bmp families have been implicated as patterning factors of the posterior mesoderm. Further investigation demonstrate that Fgf and Wnt signaling are elevated throughout the nonaxial region of the spt gastrula. By manipulating Fgf signaling we show that Fgfs both promote pronephric fate and repress blood and endothelial fate. We conclude that Tbx16 plays an important role in regulating the balance of intermediate mesoderm fates by attenuating Fgf activity.

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Section: Discussionmentioning

confidence: 99%

Zebrafish Tbx16 regulates intermediate mesoderm cell fate by attenuating Fgf activity

Warga¹,

Mueller²,

Ho³

et al. 2013

Developmental Biology

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“…The role of c-Myb in developmental stages preceding the onset of defi nitive hematopoiesis in vertebrates is not well understood. Although mouse embryos with the disrupted c-myb gene did not display any signifi cant abnormalities in the development of primitive hematopoietic cells [14], c-myb oncogenic derivatives have been demonstrated in numerous in vitro studies to regulate development of primitive avian hematopoietic cells including proliferation, differentiation, and commitment [18,39,40;Z. Horejsi,unpublished data].…”

Section: Discussionmentioning

confidence: 99%

Transcription factor c-Myb is involved in the regulation of the epithelial-mesenchymal transition in the avian neural crest

Karafiát

Dvořáková

Krejčí

et al. 2005

Cell. Mol. Life Sci.

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Multipotential neural crest cells (NCCs) originate by an epithelial-mesenchymal transition (EMT) during vertebrate embryogenesis. We show for the first time that the key hematopoietic factor c-Myb is synthesized in early chick embryos including the neural tissue and participates in the regulation of the trunk NCCs. A reduction of endogenous c-Myb protein both in tissue explants in vitro and in embryos in ovo, prevented the formation of migratory NCCs. A moderate over-expression of c-myb in naive intermediate neural plates triggered the EMT and NCC migration probably through cooperation with BMP4 signaling because (i) BMP4 activated c-myb expression, (ii) elevated c-Myb caused accumulation of transcripts of the BMP4 target genes msx1 and slug, and (iii) the reduction of c-Myb prevented the BMP4-induced formation of NCCs. The data show that in chicken embryos, the c-myb gene is expressed prior to the onset of hematopoiesis and participates in the formation and migration of the trunk neural crest.

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“…EPO interacts with its cognate receptor, EPOR, and promotes erythroid progenitor self-renewal, survival, and differentiation, while SCF mediates proliferation of these progenitors. Other important factors that control erythropoiesis include fibroblast growth factor 2 (FGF2) [ 28 ], insulin (INS), insulin-like growth factor 1 (IGF1) [ 29 ], transforming growth factor α (TGF α ) and TGF β family members (TGF β , bone morphogenetic protein 4, BMP4) [ 30 – 34 ], and glucocorticoids (GCs, such as dexamethasone, Dex) [ 35 ]. These factors could either promote erythroid progenitor self-renewal or take part in their differentiation, depending on the cooperating signals.…”

Section: Ontogeny Of Thrombocytes and Erythrocytesmentioning

confidence: 99%

Origins of the Vertebrate Erythro/Megakaryocytic System

Svoboda

Bartůněk

2015

BioMed Research International

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Vertebrate erythrocytes and thrombocytes arise from the common bipotent thrombocytic-erythroid progenitors (TEPs). Even though nonmammalian erythrocytes and thrombocytes are phenotypically very similar to each other, mammalian species have developed some key evolutionary improvements in the process of erythroid and thrombocytic differentiation, such as erythroid enucleation, megakaryocyte endoreduplication, and platelet formation. This brings up a few questions that we try to address in this review. Specifically, we describe the ontology of erythro-thrombopoiesis during adult hematopoiesis with focus on the phylogenetic origin of mammalian erythrocytes and thrombocytes (also termed platelets). Although the evolutionary relationship between mammalian and nonmammalian erythroid cells is clear, the appearance of mammalian megakaryocytes is less so. Here, we discuss recent data indicating that nonmammalian thrombocytes and megakaryocytes are homologs. Finally, we hypothesize that erythroid and thrombocytic differentiation evolved from a single ancestral lineage, which would explain the striking similarities between these cells.

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bFGF signaling and v-Myb cooperate in sustained growth of primitive erythroid progenitors

Cited by 9 publications

References 25 publications

Zebrafish Tbx16 regulates intermediate mesoderm cell fate by attenuating Fgf activity

Zebrafish Tbx16 regulates intermediate mesoderm cell fate by attenuating Fgf activity

Transcription factor c-Myb is involved in the regulation of the epithelial-mesenchymal transition in the avian neural crest

Origins of the Vertebrate Erythro/Megakaryocytic System

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