Fig. 4: Expression of the unconventional myosin IC in nuclei of primary cortical neurons decreases with the onset of apoptosis, and concomitant application of the actomyosin inhibitor BDM attenuates this decrease induced by staurosporine treatment.

a Representative confocal images of immunostainings against myosin IC, respective H2B::mCherry signals and merged images with horizontal z-stack projections confirm the expression of myosin IC in the nucleus of cortical neurons with a mostly complementary expression of myosin IC and H2B::mCherry under control conditions. In the early and late phase of apoptosis nuclear myosin IC signal decreased continuously (scales 10 µm). b Representative average z-stack projections of myosin IC signals under untreated control conditions, 2 h and 6 h after staurosporine application and upon additional treatment with the actomyosin inhibitor BDM (scale 20 µm). c Nuclear myosin IC signal intensity significantly decreased upon application of staurosporine for 2 h and 6 h (n = 33/48/33 cells). d, e The concomitant application of the actomyosin inhibitor BDM significantly attenuated the staurosporine-induced decrease in nuclear myosin IC intensity, both after 2 h (n = 48/19 cells) and after 6 h (n = 33/19 cells). Data are represented as boxplots, whiskers MIN to MAX. One-way ANOVA was applied for comparison of differences between control and staurosporine 2 h and 6 h F(2, 123) = 46.73, p < 0.0001 and t-test for comparison of nuclear myosin IC signal intensity upon application of staurosporine only with staurosporine plus BDM after 2 h (p < 0.0001) and 6 h (p < 0.05), respectively.