Fig. 5. Partially myosin IIB-depleted notochordal cells exhibit a cortical actin phenotype. (A) Confocal microscopy of Xenopus notochordal control cells injected with moesin-GFP reveals a dynamic cortical actin network in a basket-like distribution, with 3-5 foci of actin visible per cell. (B) These actin-rich foci (asterisk) visibly move within the cell on a sub-minute timescale. (C) Plotting the relative displacement of foci along the embryonic axis in the mediolateral (M) and anterior-posterior (A) directions, reveals that the rate of displacement of these foci is greater in the mediolateral dimension than in the anterior-posterior dimension for notochordal cells (No) (P<0.02 by Student's t-test), and this polarity is also detectable in pre-notochordal cells (PN) but not in animal cap cells (AC). (D) In contrast to control cells, MHC-B MO-injected cells exhibit dramatic disruption of the cortical actin network. Asterisks (also in E) indicate the NSB. (E) Confocal time-lapse sequence of a morphant cell exhibiting aberrant motility concomitant with cortical actin breakdown. Elapsed time is shown in minutes. (F,G) Mildly morphant notochordal cells (1 µM MO) remain in the notochord with intact cortical actin networks, but exhibit profuse filopodia (F) as compared with control notochordal cells (G), revealing a threshold cell polarity phenotype in response to MHC-B depletion. Scale bars: 50 µm.