RNA methylation regulates hematopoietic stem and progenitor cell development

2017 ◽  
Vol 44 (10) ◽  
pp. 473-474 ◽  
Author(s):  
Jason Ear ◽  
Shuo Lin
Genes ◽  
2018 ◽  
Vol 9 (2) ◽  
pp. 66 ◽  
Author(s):  
Jenna Richter ◽  
Edouard Stanley ◽  
Elizabeth Ng ◽  
Andrew Elefanty ◽  
David Traver ◽  
...  

2012 ◽  
Vol 109 (43) ◽  
pp. 17579-17584 ◽  
Author(s):  
A. Roy ◽  
G. Cowan ◽  
A. J. Mead ◽  
S. Filippi ◽  
G. Bohn ◽  
...  

2021 ◽  
Vol 5 (3) ◽  
pp. 829-842
Author(s):  
Antonio Maglitto ◽  
Samanta A. Mariani ◽  
Emma de Pater ◽  
Carmen Rodriguez-Seoane ◽  
Chris S. Vink ◽  
...  

Abstract Integrated molecular signals regulate cell fate decisions in the embryonic aortic endothelium to drive hematopoietic stem cell (HSC) generation during development. The G-protein–coupled receptor 56 (Gpr56, also called Adgrg1) is the most highly upregulated receptor gene in cells that take on hematopoietic fate and is expressed by adult bone marrow HSCs. Despite the requirement for Gpr56 in hematopoietic stem/progenitor cell (HS/PC) generation in zebrafish embryos and the highly upregulated expression of GPR56 in treatment-resistant leukemic patients, its function in normal mammalian hematopoiesis remains unclear. Here, we examine the role of Gpr56 in HS/PC development in Gpr56 conditional knockout (cKO) mouse embryos and Gpr knockout (KO) embryonic stem cell (ESC) hematopoietic differentiation cultures. Our results show a bias toward myeloid differentiation of Gpr56 cKO fetal liver HSCs and an increased definitive myeloid progenitor cell frequency in Gpr56KO ESC differentiation cultures. Surprisingly, we find that mouse Gpr97 can rescue Gpr56 morphant zebrafish hematopoietic generation, and that Gpr97 expression is upregulated in mouse Gpr56 deletion models. When both Gpr56 and Gpr97 are deleted in ESCs, no or few hematopoietic PCs (HPCs) are generated upon ESC differentiation. Together, our results reveal novel and redundant functions for these 2 G-protein coupled receptors in normal mammalian hematopoietic cell development and differentiation.


Cell Research ◽  
2017 ◽  
Vol 28 (2) ◽  
pp. 249-252 ◽  
Author(s):  
Junhua Lv ◽  
Yifan Zhang ◽  
Suwei Gao ◽  
Chunxia Zhang ◽  
Yusheng Chen ◽  
...  

2020 ◽  
Author(s):  
A. Maglitto ◽  
S.A. Mariani ◽  
E. de Pater ◽  
C. Rodriguez-Seoane ◽  
C.S. Vink ◽  
...  

AbstractIntegrated molecular signals regulate cell fate during embryonic hematopoietic stem cell (HSC) generation. The G-protein coupled receptor 56 (Gpr56) is the most highly-upregulated receptor gene in cells that take on hematopoietic fate and it is expressed by adult bone marrow HSCs. Although Gpr56 is required for hematopoietic stem/progenitor cell (HS/PC) generation in zebrafish embryos, its function in mammalian hematopoiesis remains unclear. Here we examine the role of Gpr56 in HS/PC development in Gpr56 conditional knockout (cKO) mouse embryos and Gpr knockout (KO) embryonic stem cell (ESC) hematopoietic differentiation cultures. Our results show a myeloid bias of Gpr56 cKO fetal liver HSCs and an increased definitive myeloid progenitor cell frequency in Gpr56KO ESC differentiation cultures. Surprisingly, we find that mouse Gpr97 rescues Gpr56 morphant zebrafish hematopoietic generation, and that Gpr97 expression is upregulated in mouse Gpr56 deletion models. When both Gpr56 and Gpr97 are deleted in ESCs, no/few HS/PCs are generated upon ESC differentiation. Together, our results reveal novel and redundant functions for these two G-protein coupled receptors in normal mammalian hematopoietic cell development and differentiation.


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