CLASP: a microtubule-based integrator of the hormone-mediated transitions from cell division to elongation

•Auxin causes microtubule entrainment through ROP6-RIC1-mediated severing by katanin.•Actin filament and microtubule positive feedback modulates PIN endocytosis.•CLASP maintains PIN2 protein levels by tethering SNX1 endosomes to microtubules.•CLASP-dependent transfacial microtubule bundles favour cell cycle maintenance.

Plants use robust mechanisms to optimize organ size to prevailing conditions. Modulating the transition from cell division to elongation dramatically affects morphology and size. Although it is well established that auxin, cytokinin and brassinosteroid mediate these transitions, recent works show that the cytoskeleton, which is normally thought to act downstream of these hormones, plays a key role in this regulatory process. In particular, the microtubule-associated protein CLASP has a dual role in meristem maintenance. CLASP modulates levels of the auxin efflux carrier PIN2 by tethering SNX1 endosomes to cortical microtubules, which in turn fine tunes auxin maxima in the root apical meristem. CLASP is also required for transfacial microtubule bundle formation at the sharp cell edges, a feature strongly associated with maintaining the capacity for further cell division.