NAA10 p.(N101K) disrupts N-terminal acetyltransferase complex NatA and is associated with developmental delay and hemihypertrophy.


Journal

European journal of human genetics : EJHG
ISSN: 1476-5438
Titre abrégé: Eur J Hum Genet
Pays: England
ID NLM: 9302235

Informations de publication

Date de publication:
02 2021
Historique:
received: 20 11 2019
accepted: 08 09 2020
revised: 31 07 2020
pubmed: 26 9 2020
medline: 19 1 2022
entrez: 25 9 2020
Statut: ppublish

Résumé

Nearly half of all human proteins are acetylated at their N-termini by the NatA N-terminal acetyltransferase complex. NAA10 is evolutionarily conserved as the catalytic subunit of NatA in complex with NAA15, but may also have NatA-independent functions. Several NAA10 variants are associated with genetic disorders. The phenotypic spectrum includes developmental delay, intellectual disability, and cardiac abnormalities. Here, we have identified the previously undescribed NAA10 c.303C>A and c.303C>G p.(N101K) variants in two unrelated girls. These girls have developmental delay, but they both also display hemihypertrophy a feature normally not observed or registered among these cases. Functional studies revealed that NAA10 p.(N101K) is completely impaired in its ability to bind NAA15 and to form an enzymatically active NatA complex. In contrast, the integrity of NAA10 p.(N101K) as a monomeric acetyltransferase is intact. Thus, this NAA10 variant may represent the best example of the impact of NatA mediated N-terminal acetylation, isolated from other potential NAA10-mediated cellular functions and may provide important insights into the phenotypes observed in individuals expressing pathogenic NAA10 variants.

Identifiants

pubmed: 32973342
doi: 10.1038/s41431-020-00728-2
pii: 10.1038/s41431-020-00728-2
pmc: PMC7868364
doi:

Substances chimiques

N-Terminal Acetyltransferase A EC 2.3.1.254
NAA10 protein, human EC 2.3.1.255
N-Terminal Acetyltransferase E EC 2.3.1.258

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

280-288

Références

Arnesen T, Van Damme P, Polevoda B, Helsens K, Evjenth R, Colaert N, et al. Proteomics analyses reveal the evolutionary conservation and divergence of N-terminal acetyltransferases from yeast and humans. Proc Natl Acad Sci USA. 2009;106:8157–62.
pubmed: 19420222
Aksnes H, Ree R, Arnesen T. Co-translational, post-translational, and non-catalytic roles of N-terminal acetyltransferases. Mol Cell. 2019;73:1097–114.
pubmed: 30878283 pmcid: 6962057
Shemorry A, Hwang CS, Varshavsky A. Control of protein quality and stoichiometries by N-terminal acetylation and the N-end rule pathway. Mol Cell. 2013;50:540–51.
pubmed: 23603116 pmcid: 3665649
Holmes WM, Mannakee BK, Gutenkunst RN, Serio TR. Loss of amino-terminal acetylation suppresses a prion phenotype by modulating global protein folding. Nat Commun. 2014;5:4383.
pubmed: 25023910 pmcid: 4140192
Dikiy I, Eliezer D. N-terminal acetylation stabilizes N-terminal helicity in lipid- and micelle-bound alpha-synuclein and increases its affinity for physiological membranes. J Biol Chem. 2014;289:3652–65.
pubmed: 24338013
Scott DC, Monda JK, Bennett EJ, Harper JW, Schulman BA. N-terminal acetylation acts as an avidity enhancer within an interconnected multiprotein complex. Science. 2011;334:674–8.
pubmed: 21940857 pmcid: 3214010
Arnesen T, Anderson D, Baldersheim C, Lanotte M, Varhaug JE, Lillehaug JR. Identification and characterization of the human ARD1-NATH protein acetyltransferase complex. Biochem J. 2005;386(Pt 3):433–43.
pubmed: 15496142 pmcid: 1134861
Arnesen T, Starheim KK, Van Damme P, Evjenth R, Dinh H, Betts MJ, et al. The chaperone-like protein HYPK acts together with NatA in cotranslational N-terminal acetylation and prevention of huntingtin aggregation. Mol Cell Biol. 2010;30:1898–909.
pubmed: 20154145 pmcid: 2849469
Arnesen T, Anderson D, Torsvik J, Halseth HB, Varhaug JE, Lillehaug JR. Cloning and characterization of hNAT5/hSAN: an evolutionarily conserved component of the NatA protein N-α-acetyltransferase complex. Gene. 2006;371:291–5.
pubmed: 16507339
Gautschi M, Just S, Mun A, Ross S, Rucknagel P, Dubaquie Y, et al. The yeast N(alpha)-acetyltransferase NatA is quantitatively anchored to the ribosome and interacts with nascent polypeptides. Mol Cell Biol. 2003;23:7403–14.
pubmed: 14517307 pmcid: 230319
Mullen JR, Kayne PS, Moerschell RP, Tsunasawa S, Gribskov M, Colavito-Shepanski M, et al. Identification and characterization of genes and mutants for an N-terminal acetyltransferase from yeast. EMBO J. 1989;8:2067–75.
pubmed: 2551674 pmcid: 401092
Magin RS, Deng S, Zhang H, Cooperman B, Marmorstein R. Probing the interaction between NatA and the ribosome for co-translational protein acetylation. PLOS One. 2017;12:e0186278.
pubmed: 29016658 pmcid: 5634638
Liszczak G, Goldberg JM, Foyn H, Petersson EJ, Arnesen T, Marmorstein R. Molecular basis for N-terminal acetylation by the heterodimeric NatA complex. Nat Struct Mol Biol. 2013;20:1098–105.
pubmed: 23912279 pmcid: 3766382
Van Damme P, Evjenth R, Foyn H, Demeyer K, De Bock P-J, Lillehaug JR, et al. Proteome-derived peptide libraries allow detailed analysis of the substrate specificities of N(alpha)-acetyltransferases and point to hNaa10p as the post-translational actin N(alpha)-acetyltransferase. Mol Cell Proteom. 2011;10:M110.004580.
Lim J-H, Chun Y-S, Park J-W. Hypoxia-inducible factor-1α obstructs a Wnt signaling pathway by inhibiting the hARD1-mediated activation of β-catenin. Cancer Res. 2008;68:5177–84.
pubmed: 18593917
Qian X, Li X, Cai Q, Zhang C, Yu Q, Jiang Y, et al. Phosphoglycerate kinase 1 phosphorylates Beclin1 to induce autophagy. Mol Cell. 2017;65:917–31.e6.
pubmed: 28238651 pmcid: 5389741
Ree R, Varland S, Arnesen T. Spotlight on protein N-terminal acetylation. Exp Mol Med. 2018;50:90.
Lee C-C, Peng S-H, Shen L, Lee C-F, Du T-H, Kang M-L, et al. The role of N-α-acetyltransferase 10 protein in DNA methylation and genomic imprinting. Mol Cell. 2017;68:89–103.e7.
pubmed: 28943313 pmcid: 6322414
Seo JH, Park J-H, Lee EJ, Vo TTL, Choi H, Kim JY, et al. ARD1-mediated Hsp70 acetylation balances stress-induced protein refolding and degradation. Nat Commun. 2016;7:12882.
pubmed: 27708256 pmcid: 5059642
Ingram AK, Cross GAM, Horn D. Genetic manipulation indicates that ARD1 is an essential Nα-acetyltransferase in Trypanosoma brucei. Mol Biochem Parasit. 2000;111:309–17.
Wang Y, Mijares M, Gall MD, Turan T, Javier A, Bornemann DJ, et al. Drosophila variable nurse cells encodes arrest defective 1 (ARD1), the catalytic subunit of the major N-terminal acetyltransferase complex. Dev Dyn. 2010;239:2813–27.
pubmed: 20882681 pmcid: 3013298
Sönnichsen B, Koski LB, Walsh A, Marschall P, Neumann B, Brehm M, et al. Full-genome RNAi profiling of early embryogenesis in Caenorhabditis elegans. Nature. 2005;434:462–9.
pubmed: 15791247
Ree R, Myklebust LM, Thiel P, Foyn H, Fladmark KE, Arnesen T. The N-terminal acetyltransferase Naa10 is essential for zebrafish development. Biosci Rep. 2015;35:e00249.
pubmed: 26251455 pmcid: 4613686
Kalvik TV, Arnesen T. Protein N-terminal acetyltransferases in cancer. Oncogene. 2013;32:269–76.
pubmed: 22391571
Wu Y, Lyon GJ. NAA10-related syndrome. Exp Mol Med. 2018;50:85.
Saunier C, Støve SI, Popp B, Gérard B, Blenski M, Ahmew N, et al. Expanding the phenotype associated with NAA10-related N-terminal acetylation deficiency. Hum Mutat. 2016;37:755–64.
pubmed: 27094817 pmcid: 5084832
Rope Alan F, Wang K, Evjenth R, Xing J, Johnston Jennifer J, Swensen, Jeffrey J, et al. Using VAAST to identify an X-linked disorder resulting in lethality in male infants due to N-terminal acetyltransferase deficiency. Am J Hum Genet. 2011;89:28–43.
pubmed: 21700266 pmcid: 3135802
Myklebust LM, Van Damme P, Støve SI, Dörfel MJ, Abboud A, Kalvik TV, et al. Biochemical and cellular analysis of Ogden syndrome reveals downstream Nt-acetylation defects. Hum Mol Genet. 2015;24:1956–76.
pubmed: 25489052
Van Damme P, Støve SI, Glomnes N, Gevaert K, Arnesen T. A Saccharomyces cerevisiae model reveals in vivo functional impairment of the ogden syndrome N-terminal acetyltransferase NAA10 Ser37Pro mutant. Mol Cell Proteom. 2014;13:2031–41.
Esmailpour T, Riazifar H, Liu L, Donkervoort S, Huang VH, Madaan S, et al. A splice donor mutation in results in the dysregulation of the retinoic acid signalling pathway and causes Lenz microphthalmia syndrome. J Med Genet. 2014;51:185–96.
pubmed: 24431331 pmcid: 4278941
Popp B, Støve SI, Endele S, Myklebust LM, Hoyer J, Sticht H, et al. De novo missense mutations in the NAA10 gene cause severe non-syndromic developmental delay in males and females. Eur J Hum Genet. 2015;23:602–9.
pubmed: 25099252
Casey JP, Støve SI, McGorrian C, Galvin J, Blenski M, Dunne A, et al. NAA10 mutation causing a novel intellectual disability syndrome with Long QT due to N-terminal acetyltransferase impairment. Sci Rep. 2015;5:16022.
pubmed: 26522270 pmcid: 4629191
Ree R, Geithus AS, Tørring PM, Sørensen KP, Damkjær M, Lynch SA, et al. A novel NAA10 p.(R83H) variant with impaired acetyltransferase activity identified in two boys with ID and microcephaly. BMC Med Genet. 2019;20:101.
pubmed: 31174490 pmcid: 6554967
McTiernan N, Støve SI, Aukrust I, Mårli MT, Myklebust LM, Houge G, et al. NAA10 dysfunction with normal NatA-complex activity in a girl with non-syndromic ID and a de novo NAA10 p.(V111G) variant – a case report. BMC Med Genet. 2018;19:47.
pubmed: 29558889 pmcid: 5859388
Støve SI, Blenski M, Stray-Pedersen A, Wierenga KJ, Jhangiani SN, Akdemir ZC, et al. A novel NAA10 variant with impaired acetyltransferase activity causes developmental delay, intellectual disability, and hypertrophic cardiomyopathy. Eur J Hum Genet. 2018;26:1294–305.
pubmed: 29748569 pmcid: 6117304
Cheng H, Gottlieb L, Marchi E, Kleyner R, Bhardwaj P, Rope AF, et al. Phenotypic and biochemical analysis of an international cohort of individuals with variants in NAA10 and NAA15. Hum Mol Genet. 2019;28:2900–19.
pubmed: 31127942 pmcid: 6736318
Drazic A, Arnesen T. [14C]-acetyl-coenzyme A-based in vitro N-terminal acetylation assay. In: Schilling O, editor. Protein terminal profiling: methods and protocols. New York, NY: Springer New York; 2017. p. 1–8.
Sievers F, Wilm A, Dineen D, Gibson TJ, Karplus K, Li W, et al. Fast, scalable generation of high-quality protein multiple sequence alignments using Clustal Omega. Mol Syst Biol. 2011;7:539.
pubmed: 21988835 pmcid: 3261699
Robert X, Gouet P. Deciphering key features in protein structures with the new ENDscript server. Nucleic Acids Res. 2014;42(W1):W320–W4.
pubmed: 24753421 pmcid: 4086106
Gottlieb L, Marmorstein R. Structure of human NatA and its regulation by the huntingtin interacting protein HYPK. Structure. 2018;26:925–35.e8.
pubmed: 29754825 pmcid: 6031454
Schrödinger, LLC The PyMOL Molecular Graphics System, Version 2.3. 2019.
Langmead B, Salzberg SL. Fast gapped-read alignment with Bowtie 2. Nat Methods. 2012;9:357–9.
pubmed: 22388286 pmcid: 3322381
McKenna A, Hanna M, Banks E, Sivachenko A, Cibulskis K, Kernytsky A, et al. The genome analysis toolkit: a MapReduce framework for analyzing next-generation DNA sequencing data. Genome Res. 2010;20:1297–303.
pubmed: 20644199 pmcid: 2928508
Li H, Handsaker B, Wysoker A, Fennell T, Ruan J, Homer N, et al. The sequence Alignment/Map format and SAMtools. Bioinformatics. 2009;25:2078–9.
pubmed: 19505943 pmcid: 2723002
Cingolani P, Platts A, Wang LL, Coon M, Nguyen T, Wang L, et al. A program for annotating and predicting the effects of single nucleotide polymorphisms, SnpEff: SNPs in the genome of Drosophila melanogaster strain w1118; iso-2; iso-3. Fly. 2012;6:80–92.
pubmed: 22728672 pmcid: 3679285
Flicek P, Amode MR, Barrell D, Beal K, Billis K, Brent S, et al. Ensembl 2014. Nucleic Acids Res. 2014;42(D1):D749–D55.
pubmed: 24316576
Sherry ST, Ward MH, Kholodov M, Baker J, Phan L, Smigielski EM, et al. dbSNP: the NCBI database of genetic variation. Nucleic Acids Res. 2001;29:308–11.
pubmed: 11125122 pmcid: 29783
Auton A, Abecasis GR, Altshuler DM, Durbin RM, Abecasis GR, Bentley DR, et al. A global reference for human genetic variation. Nature. 2015;526:68–74.
pubmed: 26432245
Exome Variant Server. NHLBI GO Exome Sequencing Project (ESP) (Seattle, WA) [ http://evs.gs.washington.edu/EVS/ ].
Lek M, Karczewski KJ, Minikel EV, Samocha KE, Banks E, Fennell T, et al. Analysis of protein-coding genetic variation in 60,706 humans. Nature. 2016;536:285–91.
pubmed: 27535533 pmcid: 5018207
Wang K, Li M, Hakonarson H. ANNOVAR: functional annotation of genetic variants from high-throughput sequencing data. Nucleic Acids Res. 2010;38:e164.
pubmed: 20601685 pmcid: 20601685
Online Mendelian Inheritance in Man, OMIM. McKusick–Nathans Institute of Genetic Medicine, Johns Hopkins University (Baltimore, MD) [ https://omim.org/ ].
Landrum MJ, Lee JM, Benson M, Brown GR, Chao C, Chitipiralla S, et al. ClinVar: improving access to variant interpretations and supporting evidence. Nucleic Acids Res. 2018;46:D1062–d7.
pubmed: 29165669
Firth HV, Richards SM, Bevan AP, Clayton S, Corpas M, Rajan D, et al. DECIPHER: database of chromosomal imbalance and phenotype in humans using Ensembl resources. Am J Hum Genet. 2009;84:524–33.
pubmed: 19344873 pmcid: 2667985
Fokkema IF, Taschner PE, Schaafsma GC, Celli J, Laros JF, den Dunnen JT. LOVD v.2.0: the next generation in gene variant databases. Hum Mutat. 2011;32:557–63.
pubmed: 21520333
Petrovski S, Wang Q, Heinzen EL, Allen AS, Goldstein DB. Genic intolerance to functional variation and the interpretation of personal genomes. PLoS Genet. 2013;9:e1003709.
pubmed: 23990802 pmcid: 3749936
Liu X, Wu C, Li C, Boerwinkle E. dbNSFP v3.0: A one-stop database of functional predictions and annotations for human nonsynonymous and splice-site SNVs. Hum Mutat. 2016;37:235–41.
pubmed: 26555599 pmcid: 4752381
Vetting MWS, de Carvalho LP, Yu M, Hegde SS, Magnet S, Roderick SL, et al. Structure and functions of the GNAT superfamily of acetyltransferases. Arch Biochem Biophys. 2005;433:212–26.
pubmed: 15581578
Richards S, Aziz N, Bale S, Bick D, Das S, Gastier-Foster J, et al. Standards and guidelines for the interpretation of sequence variants: a joint consensus recommendation of the American College of Medical Genetics and Genomics and the Association for Molecular Pathology. Genet Med. 2015;17:405–24.
pubmed: 25741868 pmcid: 4544753
Linster E, Stephan I, Bienvenut WV, Maple-Grødem J, Myklebust LM, Huber M, et al. Downregulation of N-terminal acetylation triggers ABA-mediated drought responses in Arabidopsis. Nat Commun. 2015;6:7640.
pubmed: 26184543 pmcid: 4530475
Magin RS, March ZM, Marmorstein R. The N-terminal acetyltransferase Naa10/ARD1 does not acetylate lysine residues. J Biol Chem. 2016;291:5270–7.
pubmed: 26755727 pmcid: 4777859

Auteurs

Nina McTiernan (N)

Department of Biomedicine, University of Bergen, N-5020, Bergen, Norway.

Harinder Gill (H)

Department of Medical Genetics, Children's and Women's Health Centre of British Columbia, Vancouver, BC, V6H 3N1, Canada.

Carlos E Prada (CE)

Division of Human Genetics, Cincinnati Children's Hospital Medical Center, 45229, Cincinnati, OH, USA.
Department of Pediatrics, University of Cincinnati College of Medicine, 45229, Cincinnati, OH, USA.
Centro de Medicina Genomica y Metabolismo, Fundacion Cardiovascular de Colombia, Floridablanca, Colombia.

Harry Pachajoa (H)

Centro de Investigaciones en Anomalías Congénitas y Enfermedades Raras Universidad Icesi, Cali, Colombia.
Fundación Clínica Valle del Lili, Cali, Colombia.

Juliana Lores (J)

Centro de Investigaciones en Anomalías Congénitas y Enfermedades Raras Universidad Icesi, Cali, Colombia.
Fundación Clínica Valle del Lili, Cali, Colombia.

Thomas Arnesen (T)

Department of Biomedicine, University of Bergen, N-5020, Bergen, Norway. Thomas.Arnesen@uib.no.
Department of Biological Sciences, University of Bergen, N-5020, Bergen, Norway. Thomas.Arnesen@uib.no.
Department of Surgery, Haukeland University Hospital, N-5021, Bergen, Norway. Thomas.Arnesen@uib.no.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH