ArticleGenetics2022
The Caenorhabditis elegans ASPP homolog APE-1 is a junctional protein phosphatase 1 modulator.
Article in Genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- SDS-22 stabilizes GSP-1/-2 PP1 subunits contributing to polarity establishment in C. elegans embryos.EMBO reports · 2025Article
- A Coffin-Siris syndrome-associated mutation modeled in Caenorhabditis elegans affects multiple developmental processes.G3 (Bethesda, Md.) · 2025Article
- ASPPs multimerize protein phosphatase 1.PLoS genetics · 2025Article
- SEM-2/SoxC regulates multiple aspects of C. elegans postembryonic mesoderm development.PLoS genetics · 2025Article
- Dimerization activates the Inversin complex inMolecular biology of the cell · 2024Article
- SEM-2/SoxC regulates multiple aspects ofbioRxiv : the preprint server for biology · 2024Article
- SMOC-1 interacts with both BMP and glypican to regulate BMP signaling in C. elegans.PLoS biology · 2023Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
How serine/threonine phosphatases are spatially and temporally tuned by regulatory subunits is a fundamental question in cell biology. Ankyrin repeat, SH3 domain, proline-rich-region-containing proteins are protein phosphatase 1 catalytic subunit binding partners associated with cardiocutaneous diseases. Ankyrin repeat, SH3 domain, proline-rich-region-containing proteins localize protein phosphatase 1 catalytic subunit to cell-cell junctions, but how ankyrin repeat, SH3 domain, proline-rich-region-containing proteins localize and whether they regulate protein phosphatase 1 catalytic subunit activity in vivo is unclear. Through a Caenorhabditis elegans genetic screen, we find that loss of the ankyrin repeat, SH3 domain, proline-rich-region-containing protein homolog, APE-1, suppresses a pathology called "jowls," providing us with an in vivo assay for APE-1 activity. Using immunoprecipitations and mass spectrometry, we find that APE-1 binds the protein phosphatase 1 catalytic subunit called GSP-2. Through structure-function analysis, we discover that APE-1's N-terminal half directs the APE-1-GSP-2 complex to intercellular junctions. Additionally, we isolated mutations in highly conserved residues of APE-1's ankyrin repeats that suppress jowls yet do not preclude GSP-2 binding, implying APE-1 does more than simply localize GSP-2. Indeed, in vivo reconstitution of APE-1 suggests the ankyrin repeats modulate phosphatase output, a function we find to be conserved among vertebrate homologs.
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