ArticleEMBO reports2019
Mitochondrial AAA-ATPase Msp1 detects mislocalized tail-anchored proteins through a dual-recognition mechanism.
Article in EMBO reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 62 citations in OpenAlex.
- Membrane Protein Insertion in Cells: Principles, Pathways, and Quality Control.Chemical reviews · 2026Review
- The AAA-ATPase Yta4 inhibits the interaction between Ppa2 and Atg43 to promote Atg43 phosphorylation and mitophagy.The Journal of biological chemistry · 2026Article
- Linked dimers of the AAA+ ATPase Msp1 reveal energetic demands and mechanistic plasticity for substrate extraction from lipid bilayers.FEBS letters · 2026Article
- Lipid bilayer properties govern substrate engagement and extraction by the AAA+ ATPase Msp1.The Journal of biological chemistry · 2025Article
- Msp1 and Pex19-Pex3 cooperate to achieve correct localization of Pex15 to peroxisomes.The FEBS journal · 2025Article
- Overcoming fluorescence loss in mEOS-based AAA+ unfoldase reporters through covalent linkage.Protein expression and purification · 2025Article
- Mitochondrial protein import stress.Nature cell biology · 2025Review
- ATAD1 Regulates Neuronal Development and Synapse Formation Through Tuning Mitochondrial Function.International journal of molecular sciences · 2024Article
- Thorase deficiency causes both Aβ accumulation and tau hyperphosphorylation in mouse brain.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Mitochondrial-derived compartments remove surplus proteins from the outer mitochondrial membrane.The Journal of cell biology · 2024Article
- The AAA+ protein Msp1 recognizes substrates by a hydrophobic mismatch.bioRxiv : the preprint server for biology · 2024Article
- A Msp1-containing complex removes orphaned proteins in the mitochondrial outer membrane ofLife science alliance · 2023Article
- E4 ubiquitin ligase promotes mitofusin turnover and mitochondrial stress response.Molecular cell · 2023Article
- Genetic Deletion of Thorase Causes Purkinje Cell Loss and Impaired Motor Coordination Behavior.Cells · 2023Article
- The AAA-ATPase Yta4/ATAD1 interacts with the mitochondrial divisome to inhibit mitochondrial fission.PLoS biology · 2023Article
- The Endoplasmic Reticulum and the Fidelity of Nascent Protein Localization.Cold Spring Harbor perspectives in biology · 2023Review
- The subset of peroxisomal tail-anchored proteins do not reach peroxisomes via ER, instead mitochondria can be involved.PloS one · 2023Article
- The AAA-ATPase ATAD1 and its partners promote degradation of desmin intermediate filaments in muscle.EMBO reports · 2022Article
- Article
- AAA + ATPase Thorase inhibits mTOR signaling through the disassembly of the mTOR complex 1.Nature communications · 2022Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The conserved AAA-ATPase Msp1 is embedded in the outer mitochondrial membrane and removes mislocalized tail-anchored (TA) proteins upon dysfunction of the guided entry of tail-anchored (GET) pathway. It remains unclear how Msp1 recognizes its substrates. Here, we extensively characterize Msp1 and its substrates, including the mitochondrially targeted Pex15Δ30, and full-length Pex15, which mislocalizes to mitochondria upon dysfunction of Pex19 but not the GET pathway. Moreover, we identify two new substrates, Frt1 and Ysy6. Our results suggest that mislocalized TA proteins expose hydrophobic surfaces in the cytoplasm and are recognized by Msp1 through conserved hydrophobic residues. Introducing a hydrophobic patch into mitochondrial TA proteins transforms them into Msp1 substrates. In addition, Pex15Δ30 and Frt1 contain basic inter-membrane space (IMS) residues critical for their mitochondrial mistargeting. Remarkably, Msp1 recognizes this feature through the acidic D12 residue in its IMS domain. This dual-recognition mechanism involving interactions at the cytoplasmic and IMS domains of Msp1 and substrates greatly facilitates substrate recognition and is required by Msp1 to safeguard mitochondrial functions.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.