Fig. 5.
Fig. 5. Abnormal filopodia formation of WAS MKs after adhesion to poly-L-lysine. Cultured cells were pipetted onto poly-L-lysine–coated coverslips. After 30 minutes of adhesion, cells were fixed, permeabilized, and labeled as described in Fig 3. (A and B) Examination of a normal MK with a combination of filters allowing simultaneous visualization of vWF (TRITC), F-actin (FITC), and DNA (Hoechst). The normal MK displays long, thin, and numerous filopodia that contain F-actin, but not vWF, which remains localized in the center of the cell. In contrast, WAS MKs fail to extend long filopodia (C) or extend very short, but less numerous filopodia (D) than do normal MK. Examination of WAS MKs with a combination of filters was not interpretable because of the central localization of F-actin that overlaps with that of vWF and therefore was not shown in this figure.

Abnormal filopodia formation of WAS MKs after adhesion to poly-L-lysine. Cultured cells were pipetted onto poly-L-lysine–coated coverslips. After 30 minutes of adhesion, cells were fixed, permeabilized, and labeled as described in Fig 3. (A and B) Examination of a normal MK with a combination of filters allowing simultaneous visualization of vWF (TRITC), F-actin (FITC), and DNA (Hoechst). The normal MK displays long, thin, and numerous filopodia that contain F-actin, but not vWF, which remains localized in the center of the cell. In contrast, WAS MKs fail to extend long filopodia (C) or extend very short, but less numerous filopodia (D) than do normal MK. Examination of WAS MKs with a combination of filters was not interpretable because of the central localization of F-actin that overlaps with that of vWF and therefore was not shown in this figure.

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