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Figure 2


Fig. 2. Myo52 movement upon actin filaments is driven by its own motor activity drives. (a,b) Myo52-cGFP localisation (middle panels, red labelling in bottom panels) is abolished in mutant cells (arrows) that lack (a) the fission yeast tropomyosin or (b) profillin, but not in simultaneously observed TRITC-lectin-labelled wild-type cells (upper panels, green labelling in bottom panels). (c) Myo52 links with medial-ring-associated actin filaments in for3{Delta} cells, lacking the normal interphase filament distribution. (d) Velocity distributions of Myo52 foci (green) and GFP-Crn1 labelled actin patches (red) are significantly different. (e,f) ATP depletion using 10 nM FCCP abolishes (f) Myo52 but not (e) actin-patch movement. (g) Point mutations introduced to residues within the Myo52 protein that were predicted to disrupt the motor function of the protein. Growth curves indicate that none of the mutant proteins were able to complement the myo52{Delta} allele. (h) Compared with wild-type Myo52 movements of these rigour mutants had a reduced velocity (Y509G and G689A) or were abolished completely (F490A and G689V).





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