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Lohmann et al. (2012) identified 6 different heterozygous pathogenic mutations in the THAP1 gene in 6 (1.1%) of 567 patients with dystonia. Five of the mutations (see, e.g., 609520.0008 and 609520.0009) were located in the DNA-binding domain and shown to cause decreased THAP1 activity (20-80% of controls) using a luciferase assay.

The THAP1 gene encodes 2 splice mRNA variants that produce functional proteins. One is a 2.2-kb isoform containing 3 exons, whereas the second is an alternatively spliced 2-kb isoform that lacks exon 2. This second isoform encodes a truncated THAP1 protein without the C terminus of the THAP domain. The 2 isoforms are expressed in many tissues, suggesting that THAP1 has a widespread distribution in humans. In mouse brain tissue, Thap1 shows highest concentration in embryonic whole brain tissue, which declines after birth (summary by Blanchard et al., 2011).

Frederick, N. M., Shah, P. V., Didonna, A., Langley, M. R., Kanthasamy, A. G., Opal, P. Loss of the dystonia gene Thap1 leads to transcriptional deficits that converge on common pathogenic pathways in dystonic syndromes. Hum. Molec. Genet. 28: 1343-1356, 2019. [PubMed: 30590536] [Full Text: https://doi.org/10.1093/hmg/ddy433]

Cayrol et al. (2007) identified THAP1 as a physiologic regulator of human endothelial cell proliferation and cell cycle progression. They found that both THAP1 upregulation via retroviral-mediated gene transfer and THAP1 gene silencing via RNA interference inhibited human endothelial cell proliferation. Microarray analysis revealed that THAP1-mediated growth inhibition was due to coordinated repression of RB1 (614041)/E2F (see 189971) target genes, including RRM1 (180410), a gene required for S-phase DNA synthesis. Chromatin immunoprecipitation assays showed that endogenous THAP1 associated with a consensus THAP1-binding site in the RRM1 promoter in proliferating endothelial cells. Since both overexpression and silencing of THAP1 produced similar phenotypes, Cayrol et al. (2007) concluded that an optimal range of THAP1 expression is essential for endothelial cell proliferation.

In a 33-year-old man with DYT6 (602629), Lohmann et al. (2012) identified a heterozygous 68A-C transversion in the THAP1 gene, resulting in a his23-to-pro (H23P) substitution in the DNA-binding domain. In vitro functional expression studies using a luciferase assay showed that the mutant protein had 20% activity compared to control. The patient had onset of arm dystonia at age 9 years; speech was not affected.

Roussigne, M., Cayrol, C., Clouaire, T., Amalric, F., Girard, J.-P. THAP1 is a nuclear proapoptotic factor that links prostate-apoptosis-response-4 (Par4) to PML nuclear bodies. Oncogene 22: 2432-2442, 2003. [PubMed: 12717420] [Full Text: https://doi.org/10.1038/sj.onc.1206271]

Bessiere, D., Lacroix, C., Campagne, S., Ecochard, V., Guillet, V., Mourey, L., Lopez, F., Czaplicki, J., Demange, P., Milon, A., Girard, J.-P., Gervais, V. Structure-function analysis of the THAP zinc finger of THAP1, a large C2CH DNA-binding module linked to Rb/E2F pathways. J. Biol. Chem. 283: 4352-4363, 2008. [PubMed: 18073205, related citations] [Full Text]

Xiao, J., Zhao, Y., Bastian, R. W., Perlmutter, J. S., Racette, B. A., Tabbal, S. D., Karimi, M., Paniello, R. C., Wszolek, Z. K., Uitti, R. J., Van Gerpen, J. A., Simon, D. K., and 9 others. Novel THAP1 sequence variants in primary dystonia. Neurology 74: 229-238, 2010. [PubMed: 20083799] [Full Text: https://doi.org/10.1212/WNL.0b013e3181ca00ca]

Yellajoshyula et al. (2022) analyzed knockin mice heterozygous for the dystonia-associated Thap1 F81L (609520.0002) mutation and found that F81L was a hypomorphic allele. F81L disrupted Thap1 transcriptional activity, and electron microscopic analysis showed that F81L resulted in hypomyelination in mouse central nervous system. Mechanistically, F81L did not disrupt Thap1 DNA binding at target loci, but it instead impaired the ability of Thap1 to assemble its transcriptional partner Yy1 (600013) to form an active transcriptional complex.

Using the THAP domain of human THAP1 as a prototype, Clouaire et al. (2005) showed that the THAP domain is a zinc-dependent DNA-binding module. Both the isolated THAP domain and full-length THAP1 bound an 11-nucleotide consensus sequence containing a core GGCA motif that was essential for THAP binding. Alanine substitution experiments revealed that the C2CH signature (cys5, cys10, cys54, and his57) and 4 additional conserved residues (pro26, trp36, phe58, and pro78) within the THAP domain were required for DNA binding.

Zakirova et al. (2018) found that Thap1 +/- mice had more differentially expressed genes in striatum and cerebellum than mice heterozygous for a cys54-to-tyr (C54Y) mutation in the zinc-binding motif. RNA sequencing analysis revealed that the dysregulated genes in both genotypes were involved in multiple pathways, including genes related to dystonia. Dysregulation occurred in a genotype- and tissue-dependent manner, causing synaptic plasticity defects in striatum and decreasing neurite outgrowth in striatal neurons. The eIF2-alpha (603907) signaling pathway was among the most dysregulated signaling pathways in striatum and cerebellum of Thap1 +/- mice. Inhibition of eIF2-alpha phosphorylation rescued long-term depression (LTD) in Thap1 +/- mice induced by pharmacologic stimulation of metabotropic glutamate receptors, but not synaptically induced LTD.

Bressman, S. B., Raymond, D., Fuchs, T., Heiman, G. A., Ozelius, L. J., Saunders-Pullman, R. Mutations in THAP1 (DYT6) in early-onset dystonia: a genetic screening study. Lancet Neurol. 8: 441-446, 2009. [PubMed: 19345147, images, related citations] [Full Text]

By searching sequence databases, Clouaire et al. (2005) identified approximately 100 THAP domain-containing proteins in several model organisms. Humans have 12 THAP family members, designated THAP0 (PRKRIR; 607374) to THAP11 (609119). In contrast, mice have only 7 THAP family members: Thap0, Thap1, Thap2 (612531), Thap3 (612532), Thap4 (612533), Thap7 (609518), and Thap11. Zebrafish have 32 THAP family members, the most of any organism examined.

In HeLa cells and human neuroblastoma (SH-SY5Y) cells, Kaiser et al. (2010) demonstrated that the THAP1 protein binds to the promoter of TOR1A (605204) and suppresses promoter activity in a concentration-dependent manner. A THAP-binding site was found in the TOR1A promoter. DYT6 (602629)-associated THAP1 mutations abolished THAP1-mediated repression of TOR1A in these cells, but knockdown of THAP1 in fibroblasts from individuals both with and without a THAP1 mutation showed no change in TOR1A expression. The lack of effect on TOR1A protein levels in fibroblasts and lymphocytes was confirmed by Western blot analysis. The authors suggested that interaction between THAP1 and TOR1A observed in in vitro studies may be specific to nerve cells or brain tissue, or may be subject to developmental regulation. Kaiser et al. (2010) suggested that TOR1A is a target for the transcription factor activity of THAP1, suggesting a molecular link between DYT1 and DYT6.

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By yeast 2-hybrid and in vitro pull-down assays, Roussigne et al. (2003) found that THAP1 interacted with PAR4. Mutation analysis indicated that the death domain of PAR4 was required for the interaction. Roussigne et al. (2003) showed that PML directed recruitment of THAP1 and PAR4 to PML nuclear bodies. Overexpression of THAP1 increased the vulnerability of mouse fibroblasts to serum withdrawal and TNF-alpha (191160)-induced apoptosis. The THAP domain was essential for THAP1 proapoptotic activity.

Cytogenetic location: 8p11.21 Genomic coordinates (GRCh38) : 8:42,836,674-42,843,325 (from NCBI)

The THAP domain is an atypical zinc finger motif characterized by a large C2CH module with up to 53 amino acids between the zinc-coordinating C2 and CH residues. Bessiere et al. (2008) solved the 3-dimensional solution structure of the zinc-containing form of the THAP domain of THAP1 (residues 1 to 81). A distinctive feature of the THAP zinc finger was the presence of a long loop-helix-loop inserted within an antiparallel beta sheet between the C2 and CH residues. Alanine mutagenesis scanning and nuclear magnetic resonance data revealed several residues critical for DNA binding. Lys24 within the first beta strand and arg42 and thr48 within the second loop of the loop-helix-loop motif appeared to be directly involved in DNA binding, with thr48 predicted to contact the GGCA core motif. Except for trp36, mutations of residues located in the helix of the loop-helix-loop motif did not abrogate DNA binding.

In 2 sibs with DYT6 (602629), Xiao et al. (2010) identified a heterozygous 25G-T transversion in exon 1 of the THAP1 gene, resulting in a gly9-to-cys (G9C) substitution in the highly conserved THAP domain. The proband was a 61-year-old woman who developed writing difficulties at age 6 years, followed by cervical and jaw-opening masticatory dystonia as an adult.

Djarmati, A., Schneider, S. A., Lohmann, K., Winkler, S., Pawlack, H., Hagenah, J., Bruggemann, N., Zittel, S., Fuchs, T., Rakovic, A., Schmidt, A., Jabusch, H.-C., Wilcox, R., Kostic, V. S., Siebner, H., Altenmuller, E., Munchau, A., Ozelius, L. J., Klein, C. Mutations in THAP1 (DYT6) and generalised dystonia with prominent spasmodic dysphonia: a genetic screening study. Lancet Neurol. 8: 447-452, 2009. [PubMed: 19345148, related citations] [Full Text]

Yellajoshyula, D., Rogers, A. E., Kim, A. J., Kim, S., Pappas, S. S., Dauer, W. T. A pathogenic DYT-THAP1 dystonia mutation causes hypomyelination and loss of YY1 binding. Hum. Molec. Genet. 31: 1096-1104, 2022. [PubMed: 34686877] [Full Text: https://doi.org/10.1093/hmg/ddab310]

Cytogenetic location: 8p11.21 Genomic coordinates (GRCh38) : 8:42,836,674-42,843,325 (from NCBI)

Frederick et al. (2019) found that Thap1 -/- mice were not viable, but that Thap1 +/- mice did not exhibit spontaneous dystonia due to autoregulation of Thap1 mRNA levels. Mice with Thap1 conditional knockout (cKO) in brain were viable and fertile, but did not show signs of spontaneous dystonia. However, cKO mice exhibited behavioral defects, grip defects, and reduced body weight, size, and clasping. RNA sequencing analysis identified differential gene expression in striatal and cerebellar tissue of Thap1 cKO mice, including dysregulation of genes relevant to dystonic syndromes. Histochemical analysis revealed both neuronal and glial pathology in cKO mice.

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Using CRISPR genome editing, Domingo et al. (2021) introduced multiple dystonia-specific THAP1 mutations to human induced pluripotent stem cells (iPSCs) and differentiated these cells into neural stem cells. Transcriptome profiling revealed that the mutations altered transcription of genes functionally associated with neurodevelopment, lysosomal lipid metabolism, and myelin in the neural stem cells.

Djarmati et al. (2009) identified 2 different heterozygous mutations in the THAP1 gene (609520.0005 and 609520.0006) in 2 (1%) of 160 German patients with dystonia. Both mutation carriers had laryngeal dystonia beginning in childhood that progressed to generalized dystonia. One of the patients had 2 family members with very subtle findings of dystonia.

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By RNA- and chromatin immunoprecipitation-sequencing analyses, Cheng et al. (2022) found that THAP1 mutations targeted only a minority of differentially expressed genes in SH-SY5Y cell lines. Targeting was mainly through indirect pathways, and epigenetic and motif discovery analyses revealed that THAP1 mutations targeted and upregulated expression of SP1 (189906), which in turn dysregulated the genes in SH-SY5Y cell lines.

Cheng, F., Zheng, W., Barbuti, P. A., Bonsi, P., Liu, C., Casadei, N., Ponterio, G., Meringolo, M., Admard, J., Dording, C. M., Yu-Taeger, L., Nguyen, H. P., Grundmann-Hauser, K., Ott, T., Houlden, H., Pisani, A., Kruger, R., Riess, O. DYT6 mutated THAP1 is a cell type dependent regulator of the SP1 family. Brain 145: 3968-3984, 2022. [PubMed: 35015830] [Full Text: https://doi.org/10.1093/brain/awac001]

Houlden, H., Schneider, S. A., Paudel, R., Melchers, A., Schwingenschuh, P., Edwards, M., Hardy, J., Bhatia, K. P. THAP1 mutations (DYT6) are an additional cause of early-onset dystonia. Neurology 74: 846-850, 2010. [PubMed: 20211909] [Full Text: https://doi.org/10.1212/WNL.0b013e3181d5276d]

Houlden et al. (2010) identified 9 different novel mutations in the THAP1 gene in 9 (2.5%) of 362 British patients with dystonia. One individual had a homozygous missense mutation and no family history of dystonia, but functional studies of the mutation were not performed.

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Gross (2019) mapped the THAP1 gene to chromosome 8p11.21 based on an alignment of the THAP1 sequence (GenBank BC021721) with the genomic sequence (GRCh38).

In affected members of 4 Amish-Mennonite families with autosomal dominant torsion dystonia-6 (DYT6; 602629), Fuchs et al. (2009) identified a heterozygous truncating mutation in the THAP1 gene (609520.0001). Fuchs et al. (2009) identified another heterozygous mutation in the THAP1 gene (F81L; 609520.0002) in affected members of a family of German descent with DYT6.

Gross, M. B. Personal Communication. Baltimore, Md. 9/18/2019.

Blanchard, A., Ea, V., Roubertie, A., Martin, M., Coquart, C., Claustres, M., Beroud, C., Collod-Beroud, G. DYT6 dystonia: review of the literature and creation of the UMD locus-specific database (LSDB) for mutations in the THAP1 gene. Hum. Mutat. 32: 1213-1224, 2011. [PubMed: 21793105, related citations] [Full Text]

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Fuchs, T., Gavarini, S., Saunders-Pullman, R., Raymond, D., Ehrlich, M. E., Bressman, S. B., Ozelius, L. J. Mutations in the THAP1 gene are responsible for DYT6 primary torsion dystonia. Nature Genet. 41: 286-288, 2009. [PubMed: 19182804, related citations] [Full Text]

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Cayrol, C., Lacroix, C., Mathe, C., Ecochard, V., Ceribelli, M., Loreau, E., Lazar, V., Dessen, P., Mantovani, R., Aguilar, L., Girard, J.-P. The THAP-zinc finger protein THAP1 regulates endothelial cell proliferation through modulation of pRB/E2F cell-cycle target genes. Blood 109: 584-594, 2007. [PubMed: 17003378] [Full Text: https://doi.org/10.1182/blood-2006-03-012013]

Cheng et al. (2022) found that rats homozygous for Thap1 deletion underwent embryonic lethality. Thap1 +/- rats had decreased Thap1 protein levels in striatum, which caused dysregulation of genes related to dystonic phenotypes. Thap1 +/- rats did not have spontaneous abnormal motor behaviors, but they exhibited behavior abnormalities and dopaminergic dysfunction, likely due to cell type-dependent expression changes of Sp1 and Sp4 (600540).

Kaiser, F. J., Osmanoric, A., Rakovic, A., Erogullari, A., Uflacker, N., Braunholz, D., Lohnau, T., Orolicki, S., Albrecht, M., Gillessen-Kaesbach, G., Klein, C., Lohmann, K. The dystonia gene DYT1 is repressed by the transcription factor THAP1 (DYT6). Ann. Neurol. 68: 554-559, 2010. [PubMed: 20976771, related citations] [Full Text]

In a 68-year-old German man with DYT6 (602629), Djarmati et al. (2009) identified a heterozygous 1-bp deletion (474delA) in exon 3 of the THAP1 gene, resulting in a frameshift and premature termination. He first developed writer's dystonia followed by laryngeal dystonia at age 10 years. He also developed mild to moderate involvement of the limbs and neck. A brother and daughter also carried the mutation had very subtle signs of dystonia on examination. The mutation was not found in 280 unrelated German controls.

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In a 32-year-old woman with DYT6 (602629), Lohmann et al. (2012) identified a heterozygous 70A-G transition in the THAP1 gene, resulting in a lys24-to-glu (K24E) substitution in the DNA-binding domain. In vitro functional expression studies using a luciferase assay showed that the mutant protein had 60% activity compared to control. The patient had onset of neck dystonia at age 8 years, followed by generalized dystonia. Speech was mildly affected.

In affected members of a 2-generation family with DYT6 (602629), Bressman et al. (2009) identified a heterozygous 1-bp deletion (460delC) in the THAP1 gene, resulting in a frameshift and premature termination. The mutation was predicted to leave the DNA-binding domain intact but disrupt the nuclear localization signal. The mutation was not found in 554 control chromosomes.

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Domingo, A., Yadav, R., Shah, S., Hendriks, W. T., Erdin, S., Gao, D., O'Keefe, K., Currall, B., Gusella, J. F., Sharma, N., Ozelius, L. J., Ehrlich, M. E., Talkowski, M. E., Bragg, D. C. Dystonia-specific mutations in THAP1 alter transcription of genes associated with neurodevelopment and myelin. Am. J. Hum. Genet. 108: 2145-2158, 2021. [PubMed: 34672987, images, related citations] [Full Text]

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In affected members of a German family with torsion dystonia-6 (DYT6; 602629), Fuchs et al. (2009) identified a heterozygous 241T-C transition in exon 2 of the THAP1 gene, resulting in a phe81-to-leu (F81L) substitution in a highly conserved and functionally significant AVPTIF motif of the THAP1 protein. The mutation was not found in 514 control chromosomes. In vitro functional expression studies showed that the F81L-mutant protein had reduced binding affinity to target DNA, resulting in loss of DNA binding and transcriptional dysregulation of downstream targets.

Lohmann, K., Uflacker, N., Erogullari, A., Lohnau, T., Winkler, S., Dendorfer, A., Schneider, S. A., Osmanovic, A., Svetel, M., Ferbert, A., Zittel, S., Kuhn, A. A., and 12 others. Identification and functional analysis of novel THAP1 mutations. Europ. J. Hum. Genet. 20: 171-175, 2012. [PubMed: 21847143] [Full Text: https://doi.org/10.1038/ejhg.2011.159]

Xiao et al. (2010) identified 9 different sequence variants in the THAP1 gene in 16 (1.4%) of 1,114 individuals with various forms of dystonia. Six of the variants were predicted to result in missense mutations (see, e.g., 609520.0007). Functional studies were not performed.

Using a cytokine bait in a yeast 2-hybrid screen of a cDNA library prepared from postcapillary high endothelial venules, Roussigne et al. (2003) cloned THAP1. The deduced 213-amino acid protein contains an N-terminal THAP domain, a central proline-rich region, and a bipartite nuclear localization sequence in its C-terminal half. THAP1 colocalized with PAR4 (PAWR; 601936) and PML (102578) within PML nuclear bodies in human endothelial cells.

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In a 35-year-old German man with DYT6 (602629), Djarmati et al. (2009) identified a heterozygous 2-bp deletion (388delTC) in exon 3 of the THAP1 gene, resulting in a frameshift, premature termination, and elimination of the nuclear localization signal. He developed dysphonia at age 9 years, followed by writer's dystonia, further bulbar involvement and jaw-opening dystonia, and generalization affecting the limbs, neck, and trunk. The mutation was not found in 280 unrelated German controls.

In affected members of a 3-generation family with DYT6 (602629), Bressman et al. (2009) identified a heterozygous 266A-G transition in the THAP1 gene, resulting in a lys89-to-arg (K89R) substitution in a conserved region in the DNA-binding domain. The mutation was not found in 554 control chromosomes.

In affected members of 4 Amish-Mennonite families with torsion dystonia 6 (DYT6; 602629), Fuchs et al. (2009) identified a heterozygous 5-bp insertion (134insGGGTT) followed by a 3-bp deletion (137delAAC) in exon 2 of the THAP1 gene. The mutation causes a frameshift at residue 44 and premature termination at residue 73. Haplotype analysis was consistent with a founder effect. The mutation was not identified in 280 Amish-Mennonite control chromosomes.

In a review, Blanchard et al. (2011) noted that 53 different THAP1 mutations had been identified in 56 families with DYT6; there were no apparent genotype/phenotype correlations.

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In 9 (25%) of 36 unrelated families with primary dystonia, Bressman et al. (2009) identified 9 different heterozygous mutations in the THAP1 gene (see, e.g., 609520.0003 and 609250.0004), including 1 family of mixed European ancestry that had the Amish founder mutation (609520.0001). Most of the mutations were in the DNA-binding domain, and 1 was predicted to disrupt the nuclear-localization signal. There were no genotype/phenotype correlations.

The THAP1 gene encodes a THAP domain-containing protein that is considered to be involved in endothelial cell proliferation and proapoptotic processes, and assumed to act as a transcription factor (summary by Kaiser et al., 2010).

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Gross (2019) mapped the THAP1 gene to chromosome 8p11.21 based on an alignment of the THAP1 sequence (GenBank BC021721) with the genomic sequence (GRCh38).

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Gross, M. B. Personal Communication. Baltimore, Md. 9/18/2019.

In a review, Blanchard et al. (2011) noted that 53 different THAP1 mutations had been identified in 56 families with DYT6; there were no apparent genotype/phenotype correlations.

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Clouaire, T., Roussigne, M., Ecochard, V., Mathe, C., Amalric, F., Girard, J.-P. The THAP domain of THAP1 is a large C2CH module with zinc-dependent sequence-specific DNA-binding activity. Proc. Nat. Acad. Sci. 102: 6907-6912, 2005. [PubMed: 15863623, images, related citations] [Full Text]

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Domingo et al. (2021) found that Thap1 +/- mice and knockin mice heterozygous for the Thap1 C54Y mutation displayed subtle motor abnormalities and impaired performance in behavioral assays compared with wildtype. Dysregulation of Thap1 activity impacted formation and/or maintenance of myelin in mutant mouse brain.

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Zakirova, Z., Fanutza, T., Bonet, J., Readhead, B., Zhang, W., Yi, Z., Beauvais, G., Zwaka, T. P., Ozelius, L. J., Blitzer, R. D., Gonzalez-Alegre, P., Ehrlich, M. E. Mutations in THAP1/DYT6 reveal that diverse dystonia genes disrupt similar neuronal pathways and functions. PLoS Genet. 14: e1007169, 2018. Note: Electronic Article. [PubMed: 29364887] [Full Text: https://doi.org/10.1371/journal.pgen.1007169]

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