Principal Investigator Frank Solomon
A genetic analysis identified a loss-of-function mutation that protects cells against toxic beta-tubulin. PLP1 defines a new, early step in the tubulin folding. A substantial fraction of the beta-tubulin made in plp1 cells is not competent to form tubulin heterodimers and also is not toxic. Plp1p acts upstream of the GimC/prefoldin complex and the cytoplasmic chaperonin. Indeed, plp1 suppresses both the microtubule phenotypes and the tubulin downregulation caused by pac10 deletion. We believe that Plp1p facilitates the transfer of nascent beta-tubulin polypeptides to the protein folding apparatus, and that it is specific for beta-tubulin relative to alpha-tubulin.