Regulation of Microtubule Growth and Catastrophe: Unifying Theory and Experiment

Recent studies have found that microtubule-associated proteins (MAPs) can regulate the dynamical properties of microtubules in unexpected ways. For most MAPs, there is an inverse relationship between their effects on the speed of growth and the frequency of catastrophe, the conversion of a growing microtubule to a shrinking one. Such a negative correlation is predicted by the standard GTP-cap model, which posits that catastrophe is due to loss of a stabilizing cap of GTP-tubulin at the end of a growing microtubule. However, many other MAPs, notably Kinesin-4 and combinations of EB1 with XMAP215, contradict this general rule. In this review, we show that a more nuanced, but still simple, GTP-cap model, can account for the diverse regulatory activities of MAPs.

TrendsThe standard GTP-cap model of microtubule dynamics predicts that faster growing microtubules have a larger stabilizing cap, which results in a lower catastrophe frequency. Recent studies show that for many microtubule-associated proteins (MAPs) this inverse relationship between growth and catastrophe breaks down.MAPs whose effects on microtubule dynamics do not accord with the standard GTP-cap model include XMAP215, kinesin-8, EB1, and kinesin-4.GTP-cap models in which hydrolysis cannot occur in the GTP-tubulin subunits at the end of the protofilaments (i.e., hydrolysis is coupled to polymerization) but does occur stochastically in the lattice (i.e., random hydrolysis) account for the observed effects of MAPs on microtubule dynamics.