Figure 1
Figure 1. The persistent NMII-B expression during MK differentiation induces a decreased MK polyploidization. (A) NMII-B (green) as well as NMII-A (red) are present in the contractile ring of LSK cells obtained from A+/A+ WT mice (left) and A+/Ab* heterozygote mice (right). Bars indicate 10 µm. At least 30 dividing MKs were observed with 6 heterozygous and WT mice in 3 independent experiments. (B) No specific accumulation of NMII-A and NMII-B is observed in the contractile ring of CD41+ MKs from A+/A+ WT mice (left). On the contrary, CD41+ MKs derived from A+/Ab* heterozygous mice (right) exhibited a specific localization of NMII-B-GFP (green) in the contractile ring, but without accumulation of NMII-A (red). Bars indicate 10 µm. At least 30 dividing MKs were observed with 6 heterozygotes and 6 WT mice in 3 independent experiments. (C) Persistence of NMII-B expression during MK differentiation decreases the bone marrow MK ploidy level (in vivo) (left). Histograms show the total ploidy, the ploidy level of MKs ≥8N, and the ratio between 2N and 8N to 64N of bone marrow MKs from A+/Ab* heterozygous mice and control WT mice (A+/A+) (right). (D) Persistence of NMII-B expression during MK differentiation decreases the ploidy level of day-3 cultured MKs (in vitro) (top). Histograms show the total ploidy, the ploidy level of MKs ≥8N, and the ratio between 2N and 8N to 64N of cultured MKs derived from bone marrow of A+/Ab* heterozygous mice and control WT mice (A+/A+) (bottom).

The persistent NMII-B expression during MK differentiation induces a decreased MK polyploidization. (A) NMII-B (green) as well as NMII-A (red) are present in the contractile ring of LSK cells obtained from A+/A+ WT mice (left) and A+/Ab* heterozygote mice (right). Bars indicate 10 µm. At least 30 dividing MKs were observed with 6 heterozygous and WT mice in 3 independent experiments. (B) No specific accumulation of NMII-A and NMII-B is observed in the contractile ring of CD41+ MKs from A+/A+ WT mice (left). On the contrary, CD41+ MKs derived from A+/Ab* heterozygous mice (right) exhibited a specific localization of NMII-B-GFP (green) in the contractile ring, but without accumulation of NMII-A (red). Bars indicate 10 µm. At least 30 dividing MKs were observed with 6 heterozygotes and 6 WT mice in 3 independent experiments. (C) Persistence of NMII-B expression during MK differentiation decreases the bone marrow MK ploidy level (in vivo) (left). Histograms show the total ploidy, the ploidy level of MKs ≥8N, and the ratio between 2N and 8N to 64N of bone marrow MKs from A+/Ab* heterozygous mice and control WT mice (A+/A+) (right). (D) Persistence of NMII-B expression during MK differentiation decreases the ploidy level of day-3 cultured MKs (in vitro) (top). Histograms show the total ploidy, the ploidy level of MKs ≥8N, and the ratio between 2N and 8N to 64N of cultured MKs derived from bone marrow of A+/Ab* heterozygous mice and control WT mice (A+/A+) (bottom).

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