how could snps contribute to gene regulation?

By contrast, the rs1518367 eQTL is associated with reduced transcript levels for SF3B1 only in fetal cortex. Use the Previous and Next buttons to navigate the slides or the slide controller buttons at the end to navigate through each slide. by chromatin immunoprecipitation); and (c) identify the Polycomb subunits that differentiate those sites that enhance or repress transcription within the developing cortex. This work was funded by a University of Auckland FRDF Grant (Confirming spatial connections to unravel how SNPs affect phenotype; 3714499) and a MBIE Catalyst grant (The New Zealand-Australia LifeCourse Collaboration on Genes, Environment, Nutrition and Obesity (GENO); UOAX1611) to JOS. Overall, our findings highlight potential regulatory mechanisms and pathways important for the etiology of ASD in early brain development and adulthood. M.V. How could SNPs contribute to gene regulation? 2022 Sep 16;13:942643. doi: 10.3389/fneur.2022.942643. Genes that have been curated as being involved in ASD (AutDB31; http://autism.mindspec.org/autdb/Welcome.do, assessed on 16/11/2020). SNPs may change the encoded amino acids (nonsynonymous) or can be silent (synonymous) or simply occur in the noncoding regions. Our findings highlight potential mechanisms through which ASD-associated variants potentially contribute to ASD development (fetal) and onset/maintenance (adult). Benefits and limitations of genome-wide association studies. Adv. For example, identical samples were not used in the ChromHMM, eQTL and Hi-C analyses of the fetal and adult cortical tissues. Nucleic Acids Res. ASD-associated SNPs (p<5108, n=454) were downloaded from the GWAS Catalog (Supplementary Tables 1 and 2). Neuropsychol. We functionally annotated the ASD-associated eQTLs to understand the potential regulatory mechanisms of the regions they tagged (Supplementary Table 5). Firstly, SNPs can mark regulatory regions that affect distant genes (i.e. By contrast, incorporating data on spatial chromatin organization (i.e. Article Blondel, V. D., Guillaume, J.-L., Lambiotte, R. & Lefebvre, E. Fast unfolding of communities in large networks. Neurosignals 18, 98112 (2010). [Structural variation in the human genome contributes to variation of traits]. Article Hum. The author declares no competing interests. Nineteen eGenes are regulated by Polycomb-repressed eQTL SNPs, and seven eGenesby trans-acting eQTL SNPs in fetal cortex (Fig. Lettre, G. One step closer to linking GWAS SNPs with the right genes. Removal of all HLA genes from the analysis, identified enrichments for genes involved in fatty acid metabolism and processes related to the endoplasmic-reticulum-associated protein degradation (ERAD) pathway within fetal cortex. Moreover, this approach is not tissue or disease specific and is capable of identifying previously unknown tissue-specific contributions to ASD etiology and its interactions with multimorbid conditions. J. Immunol. Hughes, H. K., Mills Ko, E., Rose, D. & Ashwood, P. immune dysfunction and autoimmunity as pathological mechanisms in autism spectrum disorders. In the meantime, to ensure continued support, we are displaying the site without styles Interestingly, most of the genes within immune-related pathways in fetal cortex are associated with Polycomb-repressed ASD-eQTLs. Musunuru, K. et al. Enrichment within active regulatory elements and histone modification marks was identified using the Roadmap Epigenomics Project 15-state ChromHMM models28,78 for adult dorsolateral prefrontal cortex (E073_15_coreMarks_hg38lift_mnemonics.bed.gz) and fetal brain (E081_15_coreMarks_hg38lift_mnemonics.bed.gz) (downloaded from https://egg2.wustl.edu/roadmap/data/byFileType/chromhmmSegmentations/ChmmModels/coreMarks/jointModel/final/, 22/11/2020) (Supplementary Table 1). PPI data was retrieved from STRING33 (version 11.0; 24/09/2020). dorsolateral prefrontal cortex cells) cortex-specific Hi-C libraries. *Gene transcript levels are associated with the same eQTL in both the fetal and adult cortical tissues. Bootstrapping analysis (n=10,000 iterations) was performed to test if observed overlaps were non-random. identified a form of ASD resulting from a failure of the brain to properly import amino acidsa critical substrate in gene expression56. Desai, D. & Pethe, P. Polycomb repressive complex 1: Regulators of neurogenesis from embryonic to adult stage. Transcript levels for these genes are associated with 65 eQTLs in fetal cortex and 39 eQTLs in adult cortex (Supplementary Table 3). non-coding RNAs); (2) ASD is a spectrum disorder not a single highly characterised phenotype; and (3) like all polygenic disorders, ASD is likely to be a whole of body disorder with important etiological contributions from discrete and distant organs within the body. Impaired amino acid transport at the blood brain barrier is a cause of autism spectrum disorder. This site needs JavaScript to work properly. & Crawford, D. A. The resulting SNP-gene pairs were then used to query adult cortex, or fetal cortex eQTL databases to identify cis- and trans-acting eQTL-eGene interactions (i.e. Genotypes (derived by Array Genotyping) for 219 fetal brain donors20 were downloaded from dbGaP (05/06/2020), processed and prepared in the GTEx format (Supplementary Fig. Brown, C. M., Austin, D. W. & Busija, L. Observable essential fatty acid deficiency markers and autism spectrum disorder. All annotated human genes were chosen as the statistical domain scope. Nat. Transl. Google Scholar. Cell 167, 1481-1494.e18 (2016). The PubMed wordmark and PubMed logo are registered trademarks of the U.S. Department of Health and Human Services (HHS). In this study, we integrated four distinct levels of biological information (GWAS, eQTL, genome organization [Hi-C] and proteinprotein interactions [PPI] networks) to translate genetic variation associated with ASD to the biological pathways that are affectedthrough alterations to the transcription levels of their component proteins in fetal and adult cortical tissues. Google Scholar. (d) 15 and 18 ASD-associated eQTLs affect at least one transcription factor binding sites within the fetal and adult cortical tissues, respectively. By submitting a comment you agree to abide by our Terms and Community Guidelines. Google Scholar. All datasets and software used in the analysis are listed in Supplementary Table 1. & Chen, Y.-T. contributed to the eQTL analysis and commented on the manuscript. Similar changes occur in adult cortex where transcript levels for 15 genes are upregulated in association with a change to the minor allele at the eQTL SNP (Fig. Diagnostic and Statistical Manual of Mental Disorders (DSM-5 (R)) (American Psychiatric Association Publishing, 2013). Briefly, read counts were normalised using the TMM algorithm and genes were selected if they had counts of 0.1 TPM in 20% samples and 6 unnormalized reads in 20% samples. eCollection 2022. Would you like email updates of new search results? By contrast, the rs3129968 minor allele is associated with a reduction in transcript levels for HLA-DRB1, which is expressed at low levels (TPM<1.25) within fetal cortex. These differences can underlie susceptibility to common diseases, human traits, and differential responses to drugs. Sign up for the Nature Briefing: Translational Research newsletter top stories in biotechnology, drug discovery and pharma. 2002;47(11):561-6. doi: 10.1007/s100380200086. Nat. Identification of non-coding silencer elements and their regulation of 3, Supplementary Table 4). Over 11 million proteinprotein interactions (PPIs) were downloaded from STRING database (version 11.0) and combined with cortex-specific expression data (GTEx v8 or Walker et al. rs10791097-SNX19, rs11191419-AS3MT, rs7085104-AS3MT, rs174592-FADS1; Supplementary Table 4). The site is secure. volume11, Articlenumber:15867 (2021) We identified changes within multiple key component pathways of gene expression (i.e. Nat. 1). 2009;29(5):286-91. doi: 10.1080/10799890902911948. BCFtools were used to set variant IDs according to the GTEx variant ID format (e.g. The existence of changes within fetal cortex pathways for endogenous antigens (e.g. N. Engl. Formulate hypotheses Expert Answer 100% (1 rating) Answer : 1 : In an indivisual the protein expression is regulated by higher and lower methods . SNPselector: a web tool for selecting SNPs for genetic association PDF GENETIC ASSOCIATION STUDIES OF COMPLEX DISEASES ByYen - arXiv 3, 1 (2011). & Vasan, R. S. Next-generation genome-wide association studies: Time to focus on phenotype?. Single-Nucleotide Polymorphism - an overview | ScienceDirect Topics However, in noncoding regions, the mechanism of how SNPs contribute to disease susceptibility remains unclear. Cite this article. However, the remaining 15 eQTLs are associated with different eGenes in adult and fetal cortical tissues (Supplementary Table 4). D'Esposito D, Guadagno A, Amoroso CG, Cascone P, Cencetti G, Michelozzi M, Guerrieri E, Ercolano MR. Planta. ASD is widely considered to be a neurodevelopmental disorder resulting from functional changes within the brain. 12, 24782492 (2017). 2b). Transcriptome-wide fetal and adult cortex-specific PPIs (CSPPIs) were constructed by combining the STRING PPI network with cortex-specific expression data from GTEx v8 or fetal brain datasets (Fig. The neurobiology of lipid metabolism in autism spectrum disorders. Wray, N. R., Wijmenga, C., Sullivan, P. F., Yang, J. official website and that any information you provide is encrypted Neurosci. Before Secondly, in our manuscript we focused on cortex-specific eQTL-gene connections. 2023 Apr;11(2):e003164. 1, Supplementary Fig. 16, 551563 (2015). 69, 101468 (2020). For example, rs35828350: (1) upregulates NMB in fetal cortex. 52, 13551363 (2020). aberrant splicing and ASD52,53; upregulation of ribosomal protein genes and a higher ribosomal gene dosage can be linked to ASD risk and severity54,55). These eQTLs were also linked to other psychiatric disorders (e.g. Correspondence to ADS 4). Corley, M. & Kroll, K. L. The roles and regulation of Polycomb complexes in neural development. Nucleic Acids Res. chr1_61170_C_T_b38 where chr1 is chromosome name, 61170 is variant position on the chromosome, C is reference allele, T is alternate allele and b38 is genome build 38). The caveat of this is that the first approach can select the wrong gene and does not account for the effects of . Gene expression is the outcome of numerous processes including transcription, co-transcriptional splicing, mRNA export, and translation. SNPs are located in different regions of genes such as promoters, exons, introns, and 5 and 3 untranslated regions (UTR) and may affect gene expression and regulation. 1, e1500737 (2015). These mechanisms are not limited to impacts on gene regulation and can affect the splicing activity (so called sQTL SNPs 35), or trans-acting factors (e.g. Genotypes (derived by Whole Genome Sequencing) were processed by the Genotype-Tissue Expression (GTEx) project, and filtered genotypes (with minor allele frequency 0.1) for 838 tissue donors were downloaded from dbGaP (https://www.ncbi.nlm.nih.gov/gap/, 01/05/2020). Neuron 83, 518532 (2014). 47, 12281235 (2015). Karczewski, K. J. et al. Within-family IDs were used as sample IDs in the output vcf file (recode vcf-iid bgz). Fetal and adult ASD-associated eQTLs were also associated with schizophrenia, unipolar depression, ADHD, bipolar disorder, anorexia nervosa and obsessivecompulsive disorder (Supplementary Fig. Perez, R. K. et al. PubMed de la Torre-Ubieta, L., Won, H., Stein, J. L. & Geschwind, D. H. Advancing the understanding of autism disease mechanisms through genetics. PubMedGoogle Scholar. Neuron 89, 248268 (2016). 45, 984994 (2013). PubMed Central STRING v11: Proteinprotein association networks with increased coverage, supporting functional discovery in genome-wide experimental datasets. 3). Nat. CrossMap (v0.2.6) was used to convert coordinates of genetic variants from genome build hg19 to hg38, resulting in ~54.8 million genetic variants. Dev. and JavaScript. Briefly, merged fastq files were aligned to the GRCh38 reference genome (Homo_sapiens_assembly38_noALT_noHLA_noDecoy.fasta, gs://gtex-resources) using STAR (v2.5.3a). 2 How could SNPs contribute to gene regulation? Gao Z, Liang Y, Wang Y, Xiao Y, Chen J, Yang X, Shi T. Front Plant Sci. Understanding the impact of SNPs associated with autism - Nature How could SNPs contribute to gene regulation quizlet? To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. 2008, P10008 (2008). Psychiatry 10, 77 (2020). GWAS has been commonly used in identifying SNPs associated with diseases or clinical phenotypes or traits. The proteinprotein interaction (PPIs) network serves as a foundation for cellular signalling circuitry, which mediates cellular responses to environmental and genetic cues. Next, the CoDeS3D algorithm identified the restriction fragments interacting with the SNP-containing restriction fragments. Nature 581, 434443 (2020). SNPs are, of course, already routinely used in human studies to test individual genes or genomic regions for their association with disease phenotypes. Cold Spring Harb. We found 80 and 58 SNPs that mark regulatory regions (i.e. PPI network analyses have been used to discover essential proteins, clusters of proteins with similar, overlapping or combinatorial functions, and associated pathways involved in tissue-specific contributions to ASD etiology17,18. Ann. Stoner, R. et al. Gene Ontology (GO) enrichment and pathways analyses for the eGenes within the ASD-specific CSPPI clusters were performed using the g:GOSt module of the g:Profiler tool81. Cross-Disorder Group of the Psychiatric Genomics Consortium et al. By contrast, the majority of ASD-associated eQTLs, that were identified in the adult cortex, are located within quiescent/low transcribed and weak transcription regions. Science 376, eabf1970 (2022). and commented on the manuscript. Pedapati, E. V. et al. Dysregulation of fatty acid metabolism in early brain development may be a risk factor or marker for early-onset of ASD48. Aberrant Cyclin D1 splicing in cancer: from molecular mechanism to therapeutic modulation. Article How could so-called altruistic behaviors arise through natural selection? In conclusion, we have identified clinically relevant putative functional impacts for ASD-associated genetic variants within fetal and adult cortical tissues. Secondly, common SNPs only account for ~20% to the ASD risk6, suggesting that other genetic (e.g., rare variants, structural variation) and environmental factors also contribute to ASD etiology65,66. Variants that do not have strand information for HumanOmni25-8v1-2_A1 and HumanOmni2-5Exome-8-v1-1-A genotyping chips were excluded (strand files and update_build.sh script were downloaded from https://www.well.ox.ac.uk/~wrayner/strand/, 01/07/2020, Supplementary Table 1). Article JAMA Psychiat. Willsey, A. J. et al. Common genetic variants, acting additively, are a major source of risk for autism. Single nucleotide polymorphism (SNP) is the simplest form of DNA variation among individuals. J.O.S. Finally, our approach focuses on identifying changes in gene regulation that are associated with and may contribute to ASD. Nucleic Acids Res. Finally, beyond changes in the DNA sequence, changes in gene regulation - for example, by sRNAs and epigenetic factors - can play a key role in disease. eQTL datasets for fetal and adult cortex were obtained from Walker et al.20 and GTEx v821, correspondingly. 3). Of 454 ASD-associated SNPs, 344 SNPs were represented in both fetal and adult cortex eQTL databases, and were run through the CoDeS3D pipeline (Fig. Here, we build on prior work to study a large set of anthropometric and biometric traits that could inform health differences by sex. Red stars are a SNPs highly associated with a disease at a p -value of 5 10 8. Most of these fetal ASD-associated eQTLs located within the Polycomb-repressed eQTLs were not identified as eQTLs in the adult cortex (Fig. APOPT1, AS3MT) with the ASD-eQTL. Wang J, Su W, Zhang T, Zhang S, Lei H, Ma F, Shi M, Shi W, Xie X, Di C. Cell Death Dis. MacRae, C. A. *_merged_nodups.txt files) were processed to obtain Hi-C chromatin interaction libraries in the following format: read name, str1, chr1, pos1, frag1 mapq1, str2, chr2, pos2, frag2, mapq2 (str=strand, chr=chromosome, pos=position, frag=restriction site fragment, mapq=mapping quality score, 1 and 2 correspond to read ends in a pair). Adult PPIs form three modules that were enriched in immune pathways and two unknown modules. Nature 518, 317330 (2015). Chromosome conformation elucidates regulatory relationships in developing human brain. Single nucleotide polymorphisms, frequently called SNPs (pronounced "snips"), are the most common type of genetic variation. Front. Introduction. Szklarczyk, D. et al. How do SNPs occur? A Dockerfile (including the CoDeS3D pipeline and downstream analyses), all findings, scripts and reproducibility report are available on github at https://github.com/Genome3d/genetic_regulation_in_ASD. Five genes within this cluster (i.e. Fifthly, we are aware that the tools and datasets used in this study are potentially biased. To identify existing and novel gene associations, we intersected our lists of genes, from fetal and adult cortical tissues, with a curated list of 1237 genes that had been previously implicated in autism development (AutDB31, accessed on 16/11/2020). Integrative analysis of 111 reference human epigenomes. The GTEx Consortium atlas of genetic regulatory effects across human tissues. Cell. ASD-eQTLs within the fetal cortex PPI aminoacyl-tRNA biosynthesis cluster are associated with: (a) increases in transcript levels for five genes (i.e. And by View the full answer ASD, attention-deficit/hyperactivity disorder (ADHD), bipolar disorder, unipolar depression, obsessivecompulsive disorder and schizophrenia), implicating common mechanisms underlying cortical development24. The mutational constraint spectrum quantified from variation in 141,456 humans. the effects of rs7432375 and rs7618871 on PCCB gene transcript levels are not collinear; Supplementary Fig. What are single nucleotide polymorphisms (SNPs)? - MedlinePlus Frontiers | From GWAS to Function: Using Functional Genomics to In our study eQTL data represent composite datasets across critical periods of development (e.g. et al. Collectively these results could indicate the existence of a window of tolerable variation within gene expressionoutside of which there is risk of developing ASD through changes in global gene expression. Won, H. et al. Autism Spectr. Rare genetic susceptibility variants assessment in autism spectrum disorder: Detection rate and practical use. Drug Metab Dispos. The CoDeS3D algorithm then identified the restriction fragments containing the SNPs within fetal (i.e. & Jernigan, T. L. The basics of brain development. In this manuscript we integrated data on cortex-specific spatial chromatin interactions (i.e. Article Until recently, there has been little if any functional follow-up of the actual role a given SNP or gene plays in the trait variation under study ( 22 ). The identified gene sets were enriched for immune pathways, fatty acid metabolism, ribosome biogenesis, aminoacyl-tRNA biosynthesis and the spliceosome in the fetal cortex. Genome Res. Front. An official website of the United States government. McCarthy, S. et al. Only Hi-C libraries that contain >90% alignable unique read pairs, and >50% unique contacts (<40% duplication rate) within the total sequenced read pairs were included in the analysis. 44, 60466054 (2016). As such, the three-dimensional (3D) genome organization, which emerges from the sum of the biophysical interactions within the nucleus, includes tissue-specific spatial interactions between eQTL regions and the genes that they control (hereafter eGenes)12. Bioinformatics 32, 289291 (2016). Husson, T. et al. T.F. MacArthur, J. et al. Neurosci. Golovina, E., Fadason, T., Lints, T.J. et al. von Schimmelmann, M. et al. Eur. cerebellum68) or other organs are important in the pathophysiology of ASD. Our results support a dual role for Polycombas both a repressor and enhancer of transcriptionin the development of ASD risk. 235, 40314045 (2020). Google Scholar. spliceosome and splicing, aminoacyl-tRNA biosynthesis, and ribosome biogenesis) in the fetal cortex. We detail the method, apply it to data from The Cancer Genome Atlas, and provide a tool to explore the findings. Nat. 3). doi: 10.1136/bmjdrc-2022-003164. ISSN 1061-4036 (print). Again transcript levels for 12 genes are reduced. However, studies have shown that Polycomb repressive complexes (PRC) can have a dual role in gene regulation during development45,46. DiStasio, M. M., Nagakura, I., Nadler, M. J. 2022 Sep 23;13:973347. doi: 10.3389/fpls.2022.973347. Usui, N. et al. Question: how could SNP's contribute to gene regulation? - Chegg In the meantime, to ensure continued support, we are displaying the site without styles Most genetic risk for autism resides with common variation. Autism, early psychosis, and social anxiety disorder: Understanding the role of social cognition and its relationship to disability in young adults with disorders characterized by social impairments. Here, we integrated four distinct levels of biological information (GWAS, eQTL, spatial genome organization and proteinprotein interactions) to identify potential regulatory impacts of ASD-associated SNPs (p<5108) on biological pathways within fetal and adult cortical tissues. These simple changes can be of transition or transversion type and they occur throughout the genome at a frequency of about one in 1,000 bp. Ernst, J. Enrichment analyses were performed using R package regioneR79 (permutation test: 1000). Abnormalities in lipid metabolism may affect the proper functioning of the nervous system and, thus can contribute to ASD etiology48,49,50. sharing sensitive information, make sure youre on a federal Res. Previous research has reported shared neurobiological and cellular processes associated with differences in cortical thickness across six psychiatric disorders (i.e. Notably, we found that ASD-eQTL associated changes in transcript levels occurred in adult cortex immune pathways that were associated with processing of exogenous antigen. Nature 516, 349354 (2014). Physiol. Here, we integrated ASD-associated GWAS SNPs with cortex-specific 3D genome structure and eQTL information to identify genes that are spatially regulated in fetal (1421 postconceptional weeks) and adult (2170years of age) cortical tissues. Pepper, K. L. et al. Thank you for visiting nature.com. Google Scholar. Functional annotation of ASD-associated eQTLs revealed that they are involved in diverse regulatory processes. Vannucchi, G., Perugi, G. & Masi, G. Bipolar disorder and ASD. The GTEx eQTL discovery (https://github.com/broadinstitute/gtex-pipeline/tree/master/qtl) pipeline was further used to calculate normalized gene expression and covariates. Understanding the mechanisms underlying the effects of SNPs that . Google Scholar. J Hum Genet. Systematic localization of common disease-associate variation in regulatorty DNA. Autism 3, 9 (2012). Furthermore, we constructed fetal and adult cortex-specific proteinprotein interaction networks and identified that ASD-associated regulatory SNPs impact on immune pathways, fatty acid metabolism, ribosome biogenesis, aminoacyl-tRNA biosynthesis and spliceosome in the fetal cortex. Adult and fetal cortex-specific PPIs (CSPPI) were generated. how could SNP's contribute to gene regulation? Accessibility 20, 327348 (2010). Mottron, L. & Bzdok, D. Autism spectrum heterogeneity: Fact or artifact?. One of main contributions of SNPs in clinical research is genome-wide association study (GWAS). Enhancer elements are functional segments of DNA located in noncoding regions that play an important role in regulating gene expression. Applications of computational tools to predict functional SNPs effects in human ErbB genes. Chang, X. The pipeline included BWA (v0.7.15) alignment of paired-end reads onto the hg38 reference genome, merging paired-end read alignments and removing chimeric, unmapped and duplicated reads. 2d). Increasing role of maternal immune activation in neurodevelopmental disorders. You are using a browser version with limited support for CSS. The Kyoto Encyclopedia of Genes and Genomes (KEGG) database34 was used to query the most impacted biological pathways. Knuesel, I. et al. Of the 80 fetal and 58 adult eQTLs, 30 were observed in both fetal and adult cortical tissues (Fig. Raw Hi-C data were downloaded from dbGaP (accession: phs001190.v1.p1) and GEO (https://www.ncbi.nlm.nih.gov/geo/, accession: GSE87112) and analyzed using Juicer (v1.5)75 (https://github.com/aidenlab/juicer) pipeline to generate Hi-C libraries. Kanehisa, M. & Goto, S. KEGG: Kyoto encyclopedia of genes and genomes. American Psychiatric Association. Behav. Gazal, S. et al. E.G. a, CWAS identify epigenomic features that are genetically associated with a trait. ISSN 2045-2322 (online). Genotype data quality control was performed using PLINK (v2.0). Nat. Van Rooij, D. et al. Recall that the DNA sequence is formed from a chain of . Fifteen of these shared eQTLs control the same eGenes in fetal and adult cortex (e.g. Using proteinprotein interaction (PPI) networks to explore interactions between proteins encoded by known disease-associated genes is a powerful approach to study the etiology of complex diseases, including psychiatric disorders17,18. Virtual histology of cortical thickness and shared neurobiology in 6 psychiatric disorders. Cell Rep. 17, 20422059 (2016). Hi-C chromatin interactions represent all captured pairs of interacting restriction fragments in the genome. Gentile, C. et al. Cortical and subcortical brain morphometry differences between patients with autism spectrum disorder and healthy individuals across the lifespan: Results from the ENIGMA ASD Working Group. For a specific TF-gene pair, detailed information could be observed in the rSNP report page using a link from the SNP in the 'element-gene-related SNPs . Grove, J. et al. Finucane, H. K. et al. 47, D1005D1012 (2019). 2023 Jan 28;257(3):47. doi: 10.1007/s00425-023-04073-8. We contend that our approach represents a valuable strategy to identify potential ASD candidate genes.

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