(A) Revised paradigm, based on data from this study for tubulin
cofactors and Arl2 as a multi-subunit chaperone that cycles to regulate soluble
αβ-tubulin through GTP hydrolysis catalytic cycles, while
providing sites for α and β-tubulin dissociation for biogenesis
and degradation. Through this model, dual GTP hydrolyses in Arl2 and possibly
in αβ-tubulin sequentially induce tubulin dimer dissociation
without release. We suggest that αβ-tubulin is reassembled and
then released. (B) An overall model for how TBC-DEG/TBCC activity
cycles may regulate slowly decaying tubulin by binding along the TBC-DEG
platform, recruiting TBCC, and then dissociating α and β-tubulin
from each other, without dissociation from the TBC-DEG/TBCC platform.
DOI:
http://dx.doi.org/10.7554/eLife.08811.031