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. 2012 Feb 22;122(3):948–962. doi: 10.1172/JCI60455

Figure 6. Dyrk1a is a prominent megakaryocytic tumor-promoting gene.

Figure 6

(A) Fold change gene expression values of Dyrk1a, Chaf1b, and Hlcs, as assessed by real-time PCR, in CD41-positive cells isolated from spleens of Gata1s/Ts1Rhr/MPL W515L recipient mice, compared with those in Gata1s/MPL W515L CD41-selected spleen cells 4 weeks posttransplantation. Mean ± SD. (B) Representative flow cytometry plots depicting the proportion of CD41+ cells derived from cultures of bone marrow progenitors infected with Dyrk1a, CHAF1B, or HLCS encoding viruses or control vector. Percentages of live cells are indicated. (C) Overexpression of Dyrk1a leads to reduced polyploidization of megakaryocytes. Mean ± SD (n = 3–5 per group). *P < 0.004, **P < 0.0008 compared with control infected. (D) Fold change increase in percentage of CD41+ and CD42+ cells after expression of wild-type or kinase-inactive alleles of Dyrk1a in wild-type or Gata1s bone marrow progenitors. Mean percentages ± SD (n = 2–4 per group). (E) Representative flow cytometry plots of Dyrk1a shRNA and control infected progenitors cells cultured under megakaryocytic conditions. Bone marrow cells were derived from Ts1Rhr and Gata1s/Ts1Rhr mice. Percentages of live cells are indicated. (F) Treatment of double (Gata1s/MPL W515L) and triple (Gata1s/Ts1Rhr/MPL W515L) mutant cells with harmine reveals that trisomic cells are more sensitive to DYRK1A inhibition in vitro. Mean ± SD (n = 3–4 per group).