Figure 1.
Figure 1. Generation of the Gata1S310A and Gata13SA knock-in mice. (A) Schematic representation of the mouse Gata1 protein. The N-terminal activation domain, amino acids 1-83, is shaded in gray and the highly conserved zinc fingers and surrounding domains are drawn in black. The serine residues that are phosphorylated in MEL cells are indicated. Serine 310 (diamond) was targeted alone or together with serines 42 and 172 (asterisks). (B) The Gata1S310A and Gata13SA knock-in alleles generated by homologous recombination. Point mutations were introduced that changed the serine to alanine at residue 310 (Gata1S310A) or residues 72, 142, and 310 (Gata13SA) to abolish phosphorylation at these sites. (C,D) Erythropoiesis is preserved in Gata1S310A and Gata13SA mice. Cells at various stages of erythropoiesis were seen in fetal livers at 14.5 dpc (C) and in the bone marrow of adult mice (D) harboring Gata1S310A and Gata13SA mutations. Original magnification ×1000.

Generation of the Gata1S310A and Gata13SA knock-in mice. (A) Schematic representation of the mouse Gata1 protein. The N-terminal activation domain, amino acids 1-83, is shaded in gray and the highly conserved zinc fingers and surrounding domains are drawn in black. The serine residues that are phosphorylated in MEL cells are indicated. Serine 310 (diamond) was targeted alone or together with serines 42 and 172 (asterisks). (B) The Gata1S310A and Gata13SA knock-in alleles generated by homologous recombination. Point mutations were introduced that changed the serine to alanine at residue 310 (Gata1S310A) or residues 72, 142, and 310 (Gata13SA) to abolish phosphorylation at these sites. (C,D) Erythropoiesis is preserved in Gata1S310A and Gata13SA mice. Cells at various stages of erythropoiesis were seen in fetal livers at 14.5 dpc (C) and in the bone marrow of adult mice (D) harboring Gata1S310A and Gata13SA mutations. Original magnification ×1000.

Close Modal

or Create an Account

Close Modal
Close Modal