PDZ-directed substrate recruitment is the primary determinant of specific 4E-BP1 dephosphorylation by PP1-Neurabin
Phosphoprotein phosphatase 1 (PP1) relies on association with PP1-interacting proteins (PIPs) to generate substrate-specific PIP/PP1 holoenzymes, but the lack of well-defined substrates has hindered elucidation of the mechanisms involved. We previously demonstrated that the Phactr1 PIP confers sequence specificity on the Phactr1/PP1 holoenzyme by remodelling the PP1 hydrophobic substrate groove. Phactr1 defines a group of 'RVxF-ΦΦ-R-W' PIPs that all interact with PP1 in a similar fashion. Here, we use a PP1-PIP fusion approach to address sequence specificity and identify substrates of the RVxF-ΦΦ-R-W family PIPs. We show that the four Phactr proteins confer identical sequence specificities on their holoenzymes. We identify the 4E-BP and p70 S6K translational regulators as substrates for the Neurabin/Spinophilin PIPs, implicated in neuronal plasticity, pointing to a role for their holoenzymes in mTORC1-dependent translational control. Biochemical and structural experiments show that in contrast to the Phactrs, substrate recruitment and catalytic efficiency of the PP1-Neurabin and PP1-Spinophilin fusions is primarily determined by substrate interaction with the PDZ domain adjoining their RVxF-ΦΦ-R-W motifs, rather than by recognition of the remodelled PP1 hydrophobic groove. Thus, even PIPs that interact with PP1 in a similar manner use different mechanisms to ensure substrate selectivity.
Authors
- Stéphane Mouilleron (ORCID: https://orcid.org/0000-0001-7977-6298)
- Dhira Joshi (ORCID: https://orcid.org/0000-0001-8660-2528)
- Richard Treisman (ORCID: https://orcid.org/0000-0002-9658-0067)
- Roman O Fedoryshchak (ORCID: https://orcid.org/0000-0003-1865-8372)
- Karim El-Bouri (ORCID: https://orcid.org/0000-0002-4542-0856)
Institutions
- The Francis Crick Institute (GB)
Publication Details
- Journal
- eLife
- Published
- 2024-11-20
- DOI
- https://doi.org/10.7554/elife.103403
- Primary Topic
- Mitochondrial Function and Pathology
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Wellcome Trust
- Francis Crick Institute
- Cancer Research UK
- Medical Research Council