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Research published in PNAS has shed new light on the mechanism by which hemangioblasts become blood cells.
Hemangioblasts, which give rise to both hematopoietic and endothelial progenitors, have been identified in the embryos of chickens, mice, fish, and humans. It has also become clear that the cells are present in adult organisms.
However, the mechanism by which hemangioblasts differentiate into blood cells and vascular endothelia has remained a mystery in many aspects.
With that in mind, Makoto Kobayashi, PhD, of the University of Tsukuba in Japan, and his colleagues studied hemangioblasts in zebrafish.
The investigators looked for zebrafish mutants with defects in the hemangioblast expression of Gata1, which is not expressed in endothelial progenitors.
This revealed a mutant with downregulation of hematopoietic genes and upregulation of endothelial genes.
The team then identified the gene responsible for this mutant—LSD1. Additional experiments showed that LSD1 silences Etv2, a critical regulator of hemangioblast development.
The investigators said these results indicate that epigenetic silencing of Etv2 by LSD1 may be a significant event required for hemangioblasts to initiate hematopoietic differentiation.
Research published in PNAS has shed new light on the mechanism by which hemangioblasts become blood cells.
Hemangioblasts, which give rise to both hematopoietic and endothelial progenitors, have been identified in the embryos of chickens, mice, fish, and humans. It has also become clear that the cells are present in adult organisms.
However, the mechanism by which hemangioblasts differentiate into blood cells and vascular endothelia has remained a mystery in many aspects.
With that in mind, Makoto Kobayashi, PhD, of the University of Tsukuba in Japan, and his colleagues studied hemangioblasts in zebrafish.
The investigators looked for zebrafish mutants with defects in the hemangioblast expression of Gata1, which is not expressed in endothelial progenitors.
This revealed a mutant with downregulation of hematopoietic genes and upregulation of endothelial genes.
The team then identified the gene responsible for this mutant—LSD1. Additional experiments showed that LSD1 silences Etv2, a critical regulator of hemangioblast development.
The investigators said these results indicate that epigenetic silencing of Etv2 by LSD1 may be a significant event required for hemangioblasts to initiate hematopoietic differentiation.
Research published in PNAS has shed new light on the mechanism by which hemangioblasts become blood cells.
Hemangioblasts, which give rise to both hematopoietic and endothelial progenitors, have been identified in the embryos of chickens, mice, fish, and humans. It has also become clear that the cells are present in adult organisms.
However, the mechanism by which hemangioblasts differentiate into blood cells and vascular endothelia has remained a mystery in many aspects.
With that in mind, Makoto Kobayashi, PhD, of the University of Tsukuba in Japan, and his colleagues studied hemangioblasts in zebrafish.
The investigators looked for zebrafish mutants with defects in the hemangioblast expression of Gata1, which is not expressed in endothelial progenitors.
This revealed a mutant with downregulation of hematopoietic genes and upregulation of endothelial genes.
The team then identified the gene responsible for this mutant—LSD1. Additional experiments showed that LSD1 silences Etv2, a critical regulator of hemangioblast development.
The investigators said these results indicate that epigenetic silencing of Etv2 by LSD1 may be a significant event required for hemangioblasts to initiate hematopoietic differentiation.