(Downloading may take up to 30 seconds.
If the slide opens in your browser, select File -> Save As to save it.)
Click on image to view larger version.



Fig. 2. A model for flux. (A) MT minus-end release from centrosomes could occur either by separation from the {gamma}-tubulin ring complex ({gamma}-TuRC) at or near the centrosome or from the MT-severing activity of centrosome-associated katanin (McNally et al., 1996). (B) A Kin I kinesin is targeted and tethered to an insoluble spindle pole matrix that anchors the spindle pole to the centrosome. Kin I actively drives flux (depicted as blue lines with arrows) by disassembling MT minus-ends. (C) This activity produces a polymer-free gap between the centrosome and the spindle pole that is observed in both live (top panel) and fixed (bottom panel) Drosophila syncytial blastoderm-stage embryos. The top panel shows rhodamine-labeled MTs (red) and GFP-histones (green). Indirect immunofluorescence in the bottom panel shows MTs (red) and KLP10A (green), which localizes within the gap and on centrosomes. (D) Poleward MT flux is driven in the metaphase half-spindle by a spindle-pole-associated Kin I kinesin. kMT length is maintained by the activity of the kinetochore-associated CLASP protein that induces plus-end polymerization.