Figure 7. Model of Doa10-mediated TA protein abundance control increasing targeting fidelity and removing clients of Msp1 dislocase.

TA proteins are post-translationally targeted to the ER by the GET pathway or insert into the OMM by an so far unknown mechanism. In the OMM, TA proteins become subject for Msp1-mediated extraction unless they dimerize or form hetero-oligomers (not shown). The ER-resident E3 ubiquitin ligase Doa10 together with its complex partners targets surplus TA proteins including Msp1-clients from the cytosol for proteasomal degradation in order to improve targeting fidelity and abundance control.