Fig. 10. Model for regulation of cell polarity establishment by microtubules and tea1p (see text for additional details). Patterns of polarity establishment are shown for tea1+ cells (A-E) and tea1 mutants (F-J). During steady-state growth in tea1+ cells (A), a growth zone, including polarized cortical actin (red), is at cell tips. tea1p (blue) is targeted to cell tips by association with the plus ends of growing microtubules (green). (B) Representation of a generic state of microtubule depolymerization in conjunction with depolarization of the cortical actin cytoskeleton, which is achieved alternatively by TBZ treatment (which simultaneously affects microtubules), by growth to an extended stationary phase, or by depolymerization of actin with LatB. Under these conditions, some tea1p can remain at cell tips to provide residual cortical landmark cues for polarity re-establishment. During polarity re-establishment (C-E), cells with normal-length microtubules can re-target tea1p back to cell tips (C), whereas cells with short microtubules (e.g. after TBZ treatment, or tea2-1 mutants) target tea1p ectopically to the cell middle (E). This targeting of tea1p helps to set up the new polarity axis. If microtubules are strongly disrupted and thus unable to direct tea1p to the cortex, the residual tea1p-dependent landmarks direct polarity re-establishment back to cell tips (D). In tea1 mutants, microtubules are normal and actin is polarized at cell tips during steady-state growth (F), but the absence of tea1p means that, upon cell depolarization and microtubule depolymerization, cortical landmarks for polarity establishment are not available (G). In addition, because microtubule signalling to the cortex depends on tea1p, tea1 mutants squander the opportunity to retarget the polarity machinery back to cell tips through a microtubule-based mechanism. As a result, polarity is re-established either randomly or following additional unknown cues (H,I,J).