VCF1 is a p97/VCP cofactor promoting recognition of ubiquitylated p97-UFD1-NPL4 substrates.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
19 Mar 2024
Historique:
received: 20 07 2023
accepted: 07 03 2024
medline: 20 3 2024
pubmed: 20 3 2024
entrez: 20 3 2024
Statut: epublish

Résumé

The hexameric AAA+ ATPase p97/VCP functions as an essential mediator of ubiquitin-dependent cellular processes, extracting ubiquitylated proteins from macromolecular complexes or membranes by catalyzing their unfolding. p97 is directed to ubiquitylated client proteins via multiple cofactors, most of which interact with the p97 N-domain. Here, we discover that FAM104A, a protein of unknown function also named VCF1 (VCP/p97 nuclear Cofactor Family member 1), acts as a p97 cofactor in human cells. Detailed structure-function studies reveal that VCF1 directly binds p97 via a conserved α-helical motif that recognizes the p97 N-domain with unusually high affinity, exceeding that of other cofactors. We show that VCF1 engages in joint p97 complex formation with the heterodimeric primary p97 cofactor UFD1-NPL4 and promotes p97-UFD1-NPL4-dependent proteasomal degradation of ubiquitylated substrates in cells. Mechanistically, VCF1 indirectly stimulates UFD1-NPL4 interactions with ubiquitin conjugates via its binding to p97 but has no intrinsic affinity for ubiquitin. Collectively, our findings establish VCF1 as an unconventional p97 cofactor that promotes p97-dependent protein turnover by facilitating p97-UFD1-NPL4 recruitment to ubiquitylated targets.

Identifiants

pubmed: 38503733
doi: 10.1038/s41467-024-46760-4
pii: 10.1038/s41467-024-46760-4
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2459

Subventions

Organisme : Novo Nordisk Fonden (Novo Nordisk Foundation)
ID : NNF14CC0001
Organisme : Novo Nordisk Fonden (Novo Nordisk Foundation)
ID : NNF18OC0030752
Organisme : Lundbeckfonden (Lundbeck Foundation)
ID : R223-2016-281
Organisme : Det Frie Forskningsråd (Danish Council for Independent Research)
ID : 0134-00048B
Organisme : Danmarks Grundforskningsfond (Danish National Research Foundation)
ID : DNRF-115
Organisme : EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)
ID : 812829 (aDDRess)
Organisme : European Molecular Biology Organization (EMBO)
ID : ALTF 1149-2020
Organisme : Deutsche Forschungsgemeinschaft (German Research Foundation)
ID : 424228829
Organisme : EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council)
ID : 715975

Informations de copyright

© 2024. The Author(s).

Références

van den Boom, J. & Meyer, H. VCP/p97-mediated unfolding as a principle in protein homeostasis and signaling. Mol Cell 69, 182–194 (2018).
pubmed: 29153394 doi: 10.1016/j.molcel.2017.10.028
Ye, Y., Tang, W. K., Zhang, T. & Xia, D. A mighty “Protein Extractor” of the cell: structure and function of the p97/CDC48 ATPase. Front. Mol. Biosci. 4, 39 (2017).
pubmed: 28660197 pmcid: 5468458 doi: 10.3389/fmolb.2017.00039
Twomey, E. C. et al. Substrate processing by the Cdc48 ATPase complex is initiated by ubiquitin unfolding. Science 365, eaax1033 (2019).
pubmed: 31249135 pmcid: 6980381 doi: 10.1126/science.aax1033
Bodnar, N. O. & Rapoport, T. A. Molecular mechanism of substrate processing by the Cdc48 ATPase complex. Cell 169, 722–735.e9 (2017).
pubmed: 28475898 pmcid: 5751438 doi: 10.1016/j.cell.2017.04.020
Weith, M. et al. Ubiquitin-independent disassembly by a p97 AAA-ATPase complex drives PP1 holoenzyme formation. Mol. Cell 72, 766–777.e6 (2018).
pubmed: 30344098 doi: 10.1016/j.molcel.2018.09.020
Cooney, I. et al. Structure of the Cdc48 segregase in the act of unfolding an authentic substrate. Science 365, 502–505 (2019).
pubmed: 31249134 pmcid: 7362759 doi: 10.1126/science.aax0486
Pan, M. et al. Mechanistic insight into substrate processing and allosteric inhibition of human p97. Nat. Struct. Mol. Biol. 28, 614–625 (2021).
pubmed: 34262183 doi: 10.1038/s41594-021-00617-2
Pfeffer, G. et al. Multisystem proteinopathy due to VCP mutations: a review of clinical heterogeneity and genetic diagnosis. Genes 13, 963 (2022).
pubmed: 35741724 pmcid: 9222868 doi: 10.3390/genes13060963
Kilgas, S. & Ramadan, K. Inhibitors of the ATPase p97/VCP: from basic research to clinical applications. Cell Chem. Biol. 30, 3–21 (2023).
pubmed: 36640759 doi: 10.1016/j.chembiol.2022.12.007
Buchberger, A., Schindelin, H. & Hanzelmann, P. Control of p97 function by cofactor binding. FEBS Lett. 589, 2578–2589 (2015).
pubmed: 26320413 doi: 10.1016/j.febslet.2015.08.028
Stach, L. & Freemont, P. S. The AAA+ ATPase p97, a cellular multitool. Biochem. J. 474, 2953–2976 (2017).
pubmed: 28819009 doi: 10.1042/BCJ20160783
Hanzelmann, P. & Schindelin, H. The interplay of cofactor interactions and post-translational modifications in the regulation of the AAA+ ATPase p97. Front. Mol. Biosci. 4, 21 (2017).
pubmed: 28451587 pmcid: 5389986 doi: 10.3389/fmolb.2017.00021
Tsuchiya, H. et al. In vivo Ubiquitin linkage-type analysis reveals that the Cdc48-Rad23/Dsk2 Axis Contributes to K48-Linked chain specificity of the proteasome. Mol. Cell 66, 488–502.e7 (2017).
pubmed: 28525741 doi: 10.1016/j.molcel.2017.04.024
Xue, L. et al. Valosin-containing protein (VCP)-adaptor interactions are exceptionally dynamic and subject to differential modulation by a VCP inhibitor. Mol. Cell Proteomics 15, 2970–2986 (2016).
pubmed: 27406709 pmcid: 5013311 doi: 10.1074/mcp.M116.061036
Meyer, H. & van den Boom, J. Targeting of client proteins to the VCP/p97/Cdc48 unfolding machine. Front. Mol. Biosci. 10, 1142989 (2023).
pubmed: 36825201 pmcid: 9941556 doi: 10.3389/fmolb.2023.1142989
Ji, Z. et al. Translocation of polyubiquitinated protein substrates by the hexameric Cdc48 ATPase. Mol. Cell 82, 570–584.e8 (2022).
pubmed: 34951965 doi: 10.1016/j.molcel.2021.11.033
Williams, C., Dong, K. C., Arkinson, C. & Martin, A. The Ufd1 cofactor determines the linkage specificity of polyubiquitin chain engagement by the AAA+ ATPase Cdc48. Mol. Cell 83, 759–769 e7 (2023).
pubmed: 36736315 pmcid: 9992269 doi: 10.1016/j.molcel.2023.01.016
Kochenova, O. V., Mukkavalli, S., Raman, M. & Walter, J. C. Cooperative assembly of p97 complexes involved in replication termination. Nat. Commun. 13, 6591 (2022).
pubmed: 36329031 pmcid: 9633789 doi: 10.1038/s41467-022-34210-y
Fujisawa, R., Polo Rivera, C. & Labib, K. P. M. Multiple UBX proteins reduce the ubiquitin threshold of the mammalian p97-UFD1-NPL4 unfoldase. Elife 11, e76763 (2022).
pubmed: 35920641 pmcid: 9377798 doi: 10.7554/eLife.76763
Huttlin, E. L. et al. Architecture of the human interactome defines protein communities and disease networks. Nature 545, 505–509 (2017).
pubmed: 28514442 pmcid: 5531611 doi: 10.1038/nature22366
Raman, M. et al. Systematic proteomics of the VCP-UBXD adaptor network identifies a role for UBXN10 in regulating ciliogenesis. Nat. Cell Biol. 17, 1356–1369 (2015).
pubmed: 26389662 pmcid: 4610257 doi: 10.1038/ncb3238
Korner, M. et al. The FAM104 proteins VCF1/2 promote the nuclear localization of p97/VCP. Elife 12, e92409 (2023).
Hanzelmann, P. & Schindelin, H. The structural and functional basis of the p97/valosin-containing protein (VCP)-interacting motif (VIM): mutually exclusive binding of cofactors to the N-terminal domain of p97. J. Biol. Chem. 286, 38679–38690 (2011).
pubmed: 21914798 pmcid: 3207442 doi: 10.1074/jbc.M111.274506
Hanzelmann, P., Buchberger, A. & Schindelin, H. Hierarchical binding of cofactors to the AAA ATPase p97. Structure 19, 833–843 (2011).
pubmed: 21645854 doi: 10.1016/j.str.2011.03.018
Beuron, F. et al. Conformational changes in the AAA ATPase p97-p47 adaptor complex. EMBO J. 25, 1967–1976 (2006).
pubmed: 16601695 pmcid: 1456939 doi: 10.1038/sj.emboj.7601055
Conicella, A. E. et al. An intrinsically disordered motif regulates the interaction between the p47 adaptor and the p97 AAA+ ATPase. Proc. Natl. Acad. Sci. USA 117, 26226–26236 (2020).
pubmed: 33028677 pmcid: 7585011 doi: 10.1073/pnas.2013920117
Jumper, J. et al. Highly accurate protein structure prediction with AlphaFold. Nature 596, 583–589 (2021).
pubmed: 34265844 pmcid: 8371605 doi: 10.1038/s41586-021-03819-2
Evans, R. et al. Protein complex prediction with AlphaFold-Multimer. bioRxiv, 2021.10.04.463034 (2022).
Stapf, C., Cartwright, E., Bycroft, M., Hofmann, K. & Buchberger, A. The general definition of the p97/valosin-containing protein (VCP)-interacting motif (VIM) delineates a new family of p97 cofactors. J. Biol. Chem. 286, 38670–38678 (2011).
pubmed: 21896481 pmcid: 3207395 doi: 10.1074/jbc.M111.274472
Isaacson, R. L. et al. Detailed structural insights into the p97-Npl4-Ufd1 interface. J. Biol. Chem. 282, 21361–21369 (2007).
pubmed: 17491009 doi: 10.1074/jbc.M610069200
Lee, H. G., Lemmon, A. A. & Lima, C. D. SUMO enhances unfolding of SUMO-polyubiquitin-modified substrates by the Ufd1/Npl4/Cdc48 complex. Proc. Natl. Acad. Sci. USA 120, e2213703120 (2023).
pubmed: 36574706 doi: 10.1073/pnas.2213703120
Nguyen, T. Q. et al. Structural basis for the interaction between human Npl4 and Npl4-binding motif of human Ufd1. Structure 30, 1530–1537.e3 (2022).
pubmed: 36087575 doi: 10.1016/j.str.2022.08.005
Bekker-Jensen, D. B. et al. An optimized shotgun strategy for the rapid generation of comprehensive human proteomes. Cell Syst. 4, 587–599.e4 (2017).
pubmed: 28601559 pmcid: 5493283 doi: 10.1016/j.cels.2017.05.009
Dantuma, N. P., Lindsten, K., Glas, R., Jellne, M. & Masucci, M. G. Short-lived green fluorescent proteins for quantifying ubiquitin/proteasome-dependent proteolysis in living cells. Nat. Biotechnol. 18, 538–543 (2000).
pubmed: 10802622 doi: 10.1038/75406
Beskow, A. et al. A conserved unfoldase activity for the p97 AAA-ATPase in proteasomal degradation. J. Mol. Biol. 394, 732–746 (2009).
pubmed: 19782090 doi: 10.1016/j.jmb.2009.09.050
Chou, T. F. & Deshaies, R. J. Quantitative cell-based protein degradation assays to identify and classify drugs that target the ubiquitin-proteasome system. J. Biol. Chem. 286, 16546–16554 (2011).
pubmed: 21343295 pmcid: 3089497 doi: 10.1074/jbc.M110.215319
Hart, T. et al. High-resolution CRISPR screens reveal fitness genes and genotype-specific cancer liabilities. Cell 163, 1515–1526 (2015).
pubmed: 26627737 doi: 10.1016/j.cell.2015.11.015
Godderz, D. et al. Cdc48-independent proteasomal degradation coincides with a reduced need for ubiquitylation. Sci. Rep. 5, 7615 (2015).
pubmed: 25556859 pmcid: 5154593 doi: 10.1038/srep07615
Ye, Y., Meyer, H. H. & Rapoport, T. A. Function of the p97-Ufd1-Npl4 complex in retrotranslocation from the ER to the cytosol: dual recognition of nonubiquitinated polypeptide segments and polyubiquitin chains. J. Cell Biol. 162, 71–84 (2003).
pubmed: 12847084 pmcid: 2172719 doi: 10.1083/jcb.200302169
Wang, B. et al. Structure and ubiquitin interactions of the conserved zinc finger domain of Npl4. J. Biol. Chem. 278, 20225–20234 (2003).
pubmed: 12644454 doi: 10.1074/jbc.M300459200
Trusch, F. et al. The N-terminal Region of the Ubiquitin Regulatory X (UBX) Domain-containing Protein 1 (UBXD1) modulates interdomain communication within the valosin-containing protein p97. J. Biol. Chem. 290, 29414–29427 (2015).
pubmed: 26475856 pmcid: 4705944 doi: 10.1074/jbc.M115.680686
Shearer, R. F. et al. K27-linked ubiquitylation promotes p97 substrate processing and is essential for cell proliferation. EMBO J. 41, e110145 (2022).
pubmed: 35349166 pmcid: 9058539 doi: 10.15252/embj.2021110145
Lebofsky, R., Takahashi, T. & Walter, J. C. DNA replication in nucleus-free Xenopus egg extracts. Methods Mol. Biol. 521, 229–252 (2009).
pubmed: 19563110 doi: 10.1007/978-1-60327-815-7_13
Sparks, J. & Walter, J. C. Extracts for analysis of DNA replication in a Nucleus-Free System. Cold Spring Harb Protoc. 2019, 194–206 (2019).
Heubes, S. & Stemmann, O. The AAA-ATPase p97-Ufd1-Npl4 is required for ERAD but not for spindle disassembly in Xenopus egg extracts. J. Cell Sci. 120, 1325–1329 (2007).
pubmed: 17374636 doi: 10.1242/jcs.006924
Poulsen, M., Lukas, C., Lukas, J., Bekker-Jensen, S. & Mailand, N. Human RNF169 is a negative regulator of the ubiquitin-dependent response to DNA double-strand breaks. J. Cell Biol. 197, 189–199 (2012).
pubmed: 22492721 pmcid: 3328375 doi: 10.1083/jcb.201109100
Toledo, L. I. et al. ATR prohibits replication catastrophe by preventing global exhaustion of RPA. Cell 155, 1088–1103 (2013).
pubmed: 24267891 doi: 10.1016/j.cell.2013.10.043
Brunner, A. D. et al. Ultra-high sensitivity mass spectrometry quantifies single-cell proteome changes upon perturbation. Mol. Syst. Biol. 18, e10798 (2022).
pubmed: 35226415 pmcid: 8884154 doi: 10.15252/msb.202110798
Hendriks, I. A. et al. Site-specific characterization of endogenous SUMOylation across species and organs. Nat. Commun. 9, 2456 (2018).
pubmed: 29942033 pmcid: 6018634 doi: 10.1038/s41467-018-04957-4
Cox, J. & Mann, M. MaxQuant enables high peptide identification rates, individualized p.p.b.-range mass accuracies and proteome-wide protein quantification. Nat. Biotechnol. 26, 1367–1372 (2008).
pubmed: 19029910 doi: 10.1038/nbt.1511
Cox, J. et al. Accurate proteome-wide label-free quantification by delayed normalization and maximal peptide ratio extraction, termed MaxLFQ. Mol. Cell Proteom. 13, 2513–2526 (2014).
doi: 10.1074/mcp.M113.031591
Tyanova, S. et al. The Perseus computational platform for comprehensive analysis of (prote)omics data. Nat. Methods 13, 731–740 (2016).
pubmed: 27348712 doi: 10.1038/nmeth.3901
Tusher, V. G., Tibshirani, R. & Chu, G. Significance analysis of microarrays applied to the ionizing radiation response. Proc. Natl. Acad. Sci. USA 98, 5116–5121 (2001).
pubmed: 11309499 pmcid: 33173 doi: 10.1073/pnas.091062498
Chi, H. et al. Comprehensive identification of peptides in tandem mass spectra using an efficient open search engine. Nat. Biotechnol. 36, 1059–1061 (2018).
Iacobucci, C. et al. A cross-linking/mass spectrometry workflow based on MS-cleavable cross-linkers and the MeroX software for studying protein structures and protein-protein interactions. Nat. Protoc. 13, 2864–2889 (2018).
pubmed: 30382245 doi: 10.1038/s41596-018-0068-8
Graham, M., Combe, C., Kolbowski, L. & Rappsilber, J. xiView: a common platform for the downstream analysis of Crosslinking Mass Spectrometry data. bioRxiv, 561829 (2019).
Meng, E. C. et al. UCSF ChimeraX: tools for structure building and analysis. Protein Sci. 32, e4792 (2023).
pubmed: 37774136 pmcid: 10588335 doi: 10.1002/pro.4792
Kroning, A., van den Boom, J., Kracht, M., Kueck, A. F. & Meyer, H. Ubiquitin-directed AAA+ ATPase p97/VCP unfolds stable proteins crosslinked to DNA for proteolysis by SPRTN. J. Biol. Chem. 298, 101976 (2022).
pubmed: 35469923 pmcid: 9127365 doi: 10.1016/j.jbc.2022.101976
Blythe, E. E., Olson, K. C., Chau, V. & Deshaies, R. J. Ubiquitin- and ATP-dependent unfoldase activity of P97/VCP*NPLOC4*UFD1L is enhanced by a mutation that causes multisystem proteinopathy. Proc. Natl. Acad. Sci. USA 114, E4380–E4388 (2017).
pubmed: 28512218 pmcid: 5465906 doi: 10.1073/pnas.1706205114
Vizcaino, J. A. et al. ProteomeXchange provides globally coordinated proteomics data submission and dissemination. Nat. Biotechnol. 32, 223–226 (2014).
pubmed: 24727771 pmcid: 3986813 doi: 10.1038/nbt.2839

Auteurs

Ann Schirin Mirsanaye (AS)

Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, DK-2200, Copenhagen, Denmark.

Saskia Hoffmann (S)

Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, DK-2200, Copenhagen, Denmark.

Melanie Weisser (M)

Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, DK-2200, Copenhagen, Denmark.

Andreas Mund (A)

Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, DK-2200, Copenhagen, Denmark.

Blanca Lopez Mendez (B)

Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, DK-2200, Copenhagen, Denmark.

Dimitris Typas (D)

Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, DK-2200, Copenhagen, Denmark.

Johannes van den Boom (J)

Molecular Biology I, Faculty of Biology, University of Duisburg-Essen, 45117, Essen, Germany.

Bente Benedict (B)

Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, DK-2200, Copenhagen, Denmark.

Ivo A Hendriks (IA)

Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, DK-2200, Copenhagen, Denmark.

Michael Lund Nielsen (ML)

Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, DK-2200, Copenhagen, Denmark.

Hemmo Meyer (H)

Molecular Biology I, Faculty of Biology, University of Duisburg-Essen, 45117, Essen, Germany.

Julien P Duxin (JP)

Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, DK-2200, Copenhagen, Denmark.

Guillermo Montoya (G)

Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, DK-2200, Copenhagen, Denmark.

Niels Mailand (N)

Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, DK-2200, Copenhagen, Denmark. niels.mailand@cpr.ku.dk.
Center for Chromosome Stability, Department of Cellular and Molecular Medicine, University of Copenhagen, DK-2200, Copenhagen, Denmark. niels.mailand@cpr.ku.dk.

Classifications MeSH