Figure 4
Figure 4. Ts1Cje mice, with or without Gata1 mutation, do not develop a myeloproliferative disorder. (A) Disease incidence was monitored in a cohort of Ts1Cje mice, and in Ts1Cje mice that carried a loss of function exon 2 mutation in Gata1 (Gata1Plt13), over a 2-year period (n = 9-13 mice of each genotype). Mice were killed when they exhibited signs of illness, and an autopsy and histologic analysis were performed. Ts1Cje mice had a similar life expectancy to disomic mice (○, □). The presence of the Gata1Plt13 mutation did not significantly alter the survival curve of Ts1Cje mice, nor did it alter the disease spectrum (●, ■). (B) BM sections (original magnification ×100) from 2-year-old Ts1Cje mice. The Gata1Plt13 mutation normally leads to increased numbers of megakaryocytes and bone overgrowth in the BM. Crossing this mutation onto the Ts1Cje background did not alter this phenotype. (C) Spleen sections (original magnification ×100) from aged mice also did not show any signs of myelofibrosis in Ts1Cje mice. The Gata1Plt13 mutation normally leads to increased numbers of megakaryocytes in the spleen, and this frequency was not altered by crossing to the Ts1Cje mice (insets; original magnification ×200).

Ts1Cje mice, with or without Gata1 mutation, do not develop a myeloproliferative disorder. (A) Disease incidence was monitored in a cohort of Ts1Cje mice, and in Ts1Cje mice that carried a loss of function exon 2 mutation in Gata1 (Gata1Plt13), over a 2-year period (n = 9-13 mice of each genotype). Mice were killed when they exhibited signs of illness, and an autopsy and histologic analysis were performed. Ts1Cje mice had a similar life expectancy to disomic mice (○, □). The presence of the Gata1Plt13 mutation did not significantly alter the survival curve of Ts1Cje mice, nor did it alter the disease spectrum (●, ■). (B) BM sections (original magnification ×100) from 2-year-old Ts1Cje mice. The Gata1Plt13 mutation normally leads to increased numbers of megakaryocytes and bone overgrowth in the BM. Crossing this mutation onto the Ts1Cje background did not alter this phenotype. (C) Spleen sections (original magnification ×100) from aged mice also did not show any signs of myelofibrosis in Ts1Cje mice. The Gata1Plt13 mutation normally leads to increased numbers of megakaryocytes in the spleen, and this frequency was not altered by crossing to the Ts1Cje mice (insets; original magnification ×200).

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