Drl.3 governs primitive hematopoiesis in zebrafish
- Pimtong, W., Datta, M., Ulrich, A.M., Rhodes, J.
- Scientific Reports 4: 5791 (Journal)
- Registered Authors
- Datta, Madhusmita, Pimtong, Wittaya, Rhodes, Jennifer
- Cell biology, Haematopoiesis
- MeSH Terms
- Antibody Formation
- Cell Differentiation*
- Cell Lineage
- Embryo, Nonmammalian/cytology
- Embryo, Nonmammalian/physiology*
- Gene Expression Regulation, Developmental
- HEK293 Cells
- Hematopoietic Stem Cells/cytology
- Hematopoietic Stem Cells/physiology*
- In Situ Hybridization
- RNA, Messenger/genetics
- Real-Time Polymerase Chain Reaction
- Reverse Transcriptase Polymerase Chain Reaction
- Zebrafish Proteins/genetics
- Zebrafish Proteins/immunology
- Zebrafish Proteins/metabolism*
- 25051985 Full text @ Sci. Rep.
Pimtong, W., Datta, M., Ulrich, A.M., Rhodes, J. (2014) Drl.3 governs primitive hematopoiesis in zebrafish. Scientific Reports. 4:5791.
The molecular program controlling hematopoietic differentiation is not fully understood. Here, we describe a family of zebrafish genes that includes a novel hematopoietic regulator, draculin-like 3 (drl.3). We found that drl.3 is expressed in mesoderm-derived hematopoietic cells and is retained during erythroid maturation. Moreover, drl.3 expression correlated with erythroid development in gata1a- and spi1b-depleted embryos. Loss-of-function analysis indicated that drl.3 plays an essential role in primitive erythropoiesis and, to a lesser extent, myelopoiesis that is independent of effects on vasculature, emergence of primitive and definitive progenitor cells and cell viability. While drl.3 depletion reduced gata1a expression and inhibited erythroid development, enforced expression of gata1a was not sufficient to rescue erythropoiesis, indicating that the regulation of hematopoiesis by drl.3 extends beyond control of gata1a expression. Knockdown of drl.3 increased the proportion of less differentiated, primitive hematopoietic cells without affecting proliferation, establishing drl.3 as an important regulator of primitive hematopoietic cell differentiation.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes