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MicroRNAs Located in the Hox Gene Clusters Are Implicated in Huntington's Disease Pathogenesis

Hoss, Andrew G., Kartha, Vinay K., Dong, Xianjun, Latourelle, Jeanne C., Dumitriu, Alexandra, Hadzi, Tiffany C., MacDonald, Marcy E., Gusella, James F., Akbarian, Schahram, Chen, Jiang-Fan, Weng, Zhiping, Myers, Richard H.·2014·PLoS Genetics
DOI 10.1371/journal.pgen.1004188PMC PMC3937267
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Figure 1 Differentially expressed miRNAs in Huntington's disease. miR-10b-5p, miR-1247-5p, miR-196a-5p, miR-196b-5p, and miR-615-3p were identified as differentially expressed in Huntington's disease prefrontal cortex compared to non-neurological disease controls by Illumina miRNA-sequencing. Normalized expression values quantified from DESeq analysis are shown on the y-axis. miR-196a-5p, miR-196b-5p and miR-615-3p were essentially not expressed in control samples, while the mean HD expression was 27.49, 11.01 and 6.66 respectively. miR-1247-5p was expressed at moderate levels in both control (mean = 49.44) and HD brain (mean = 102.01). miR-10b-5p was expressed in control (mean = 915.81) and highly expressed in HD brain (mean = 26,020.05). For miRNA, *p<0.05 and ***p<0.001, as determined by DESeq, followed by the Benjamini-Hochberg multiple comparison correction. (HD = Huntington's disease).
Figure 1 Differentially expressed miRNAs in Huntington's disease. miR-10b-5p, miR-1247-5p, miR-196a-5p, miR-196b-5p, and miR-615-3p were identified as differentially expressed in Huntington's disease prefrontal cortex compared to non-neurological disease controls by Illumina miRNA-sequencing. Normalized expression values quantified from DESeq analysis are shown on the y-axis. miR-196a-5p, miR-196b-5p and miR-615-3p were essentially not expressed in control samples, while the mean HD expression was 27.49, 11.01 and 6.66 respectively. miR-1247-5p was expressed at moderate levels in both control (mean = 49.44) and HD brain (mean = 102.01). miR-10b-5p was expressed in control (mean = 915.81) and highly expressed in HD brain (mean = 26,020.05). For miRNA, *p<0.05 and ***p<0.001, as determined by DESeq, followed by the Benjamini-Hochberg multiple comparison correction. (HD = Huntington's disease).CC BY · PubMed Central
Figure 2 miR-10b-5p expression in control, Parkinson's disease and Huntington's disease prefrontal cortex. Up-regulation of miR-10b-5p was confirmed in HD by performing RT-qPCR, comparing nineteen Huntington's disease prefrontal cortex samples to eighteen non-neurological disease control samples (***p<0.001) or fourteen Parkinson's disease samples (***p<0.001). ΔΔCT values of miR-10b-5p in PD and HD as compared to controls are shown on the y-axis. The absence of up-regulation in PD frontal cortex suggests that up-regulation of miR-10b-5p may be HD specific. (CT = cycle threshold; RT-qPCR = reverse transcription quantitative PCR; PD = Parkinson's disease; HD = Huntington's disease).
Figure 2 miR-10b-5p expression in control, Parkinson's disease and Huntington's disease prefrontal cortex. Up-regulation of miR-10b-5p was confirmed in HD by performing RT-qPCR, comparing nineteen Huntington's disease prefrontal cortex samples to eighteen non-neurological disease control samples (***p<0.001) or fourteen Parkinson's disease samples (***p<0.001). ΔΔCT values of miR-10b-5p in PD and HD as compared to controls are shown on the y-axis. The absence of up-regulation in PD frontal cortex suggests that up-regulation of miR-10b-5p may be HD specific. (CT = cycle threshold; RT-qPCR = reverse transcription quantitative PCR; PD = Parkinson's disease; HD = Huntington's disease).CC BY · PubMed Central
Figure 3 miR-10b-5p overexpressing PC12 Q73 cells exhibit reduced cytotoxicity. PC12 cells expressing huntingtin exon 1 with a polyglutamine expansion spanning 73 repeats were transfected with miR-10b-5p or cel-miR-67-3p as a negative control. On day 3 post-differentiation, a subset of cells were treated with 1 uM MG 132. A MTT assay was used to measure cell viability after four days post differentiation. On the Y-axis, the viability percentage was calculated from the initial cell count. Error bars represent SEM. (****p<0.0001; **p<0.001 *p<0.05).
Figure 3 miR-10b-5p overexpressing PC12 Q73 cells exhibit reduced cytotoxicity. PC12 cells expressing huntingtin exon 1 with a polyglutamine expansion spanning 73 repeats were transfected with miR-10b-5p or cel-miR-67-3p as a negative control. On day 3 post-differentiation, a subset of cells were treated with 1 uM MG 132. A MTT assay was used to measure cell viability after four days post differentiation. On the Y-axis, the viability percentage was calculated from the initial cell count. Error bars represent SEM. (****p<0.0001; **p<0.001 *p<0.05).CC BY · PubMed Central
Figure 4 Differentially expressed miRNAs in HD are located in Hox genes clusters. Schematic representation of Hox clusters. Hox genes are represented as numbered boxes (labeled 1–13), miRNA are represented by triangles and other genes in the regions (functional lncRNA, PRAC) are represented by rectangles. Antisense transcripts and pseudogenes are not pictured. Nineteen genes within Hox cluster regions were found significantly differentially expressed in HD prefrontal cortex using mRNA-sequencing (FDR-adjusted p-value<0.05). Four miRNAs, one lncRNA, and fourteen Hox genes were significantly up-regulated in HD (indicated by red), many of which are adjacent to differentially expressed miRNAs. A single Hox gene (HOXD1) was down-regulated in HD (indicated by blue). (HD = Huntington's disease).
Figure 4 Differentially expressed miRNAs in HD are located in Hox genes clusters. Schematic representation of Hox clusters. Hox genes are represented as numbered boxes (labeled 1–13), miRNA are represented by triangles and other genes in the regions (functional lncRNA, PRAC) are represented by rectangles. Antisense transcripts and pseudogenes are not pictured. Nineteen genes within Hox cluster regions were found significantly differentially expressed in HD prefrontal cortex using mRNA-sequencing (FDR-adjusted p-value<0.05). Four miRNAs, one lncRNA, and fourteen Hox genes were significantly up-regulated in HD (indicated by red), many of which are adjacent to differentially expressed miRNAs. A single Hox gene (HOXD1) was down-regulated in HD (indicated by blue). (HD = Huntington's disease).CC BY · PubMed Central

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Research works printed but not linked: 73

  1. 1993, A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes, Cell, 72, 971, 10.1016/0092-8674(93)90585-E · DOI · Paper page
  2. TC Hadzi, 2012, Assessment of cortical and striatal involvement in 523 Huntington disease brains, Neurology, 79, 1708, 10.1212/WNL.0b013e31826e9a5d · DOI · Paper page
  3. JP Vonsattel, 1985, Neuropathological classification of Huntington's disease, Journal of neuropathology and experimental neurology, 44, 559, 10.1097/00005072-198511000-00003 · DOI · Paper page
  4. A Hodges, 2006, Regional and cellular gene expression changes in human Huntington's disease brain, Human molecular genetics, 15, 965, 10.1093/hmg/ddl013 · DOI · Paper page
  5. JH Cha, 2000, Transcriptional dysregulation in Huntington's disease, Trends in neurosciences, 23, 387, 10.1016/S0166-2236(00)01609-X · DOI
  6. JH Cha, 2007, Transcriptional signatures in Huntington's disease, Progress in neurobiology, 83, 228, 10.1016/j.pneurobio.2007.03.004 · DOI
  7. A Lavut, 2012, Sequestration of highly expressed mRNAs in cytoplasmic granules, P-bodies, and stress granules enhances cell viability, PLoS genetics, 8, e1002527, 10.1371/journal.pgen.1002527 · DOI
  8. E Junn, 2012, MicroRNAs in neurodegenerative diseases and their therapeutic potential, Pharmacology & therapeutics, 133, 142, 10.1016/j.pharmthera.2011.10.002 · DOI · Paper page
  9. E Marti, 2010, A myriad of miRNA variants in control and Huntington's disease brain regions detected by massively parallel sequencing, Nucleic acids research, 38, 7219, 10.1093/nar/gkq575 · DOI · Paper page
  10. R Johnson, 2008, A microRNA-based gene dysregulation pathway in Huntington's disease, Neurobiology of disease, 29, 438, 10.1016/j.nbd.2007.11.001 · DOI · Paper page
  11. M Sinha, 2011, Micro RNA -214,-150,-146a and-125b target Huntingtin gene, RNA biology, 8, 1005, 10.4161/rna.8.6.16035 · DOI · Paper page
  12. PH Cheng, 2013, miR-196a Ameliorates Phenotypes of Huntington Disease in Cell, Transgenic Mouse, and Induced Pluripotent Stem Cell Models, American journal of human genetics, 93, 306, 10.1016/j.ajhg.2013.05.025 · DOI · Paper page
  13. ST Lee, 2011, Altered microRNA regulation in Huntington's disease models, Experimental neurology, 227, 172, 10.1016/j.expneurol.2010.10.012 · DOI · Paper page
  14. J Jin, 2012, Interrogation of brain miRNA and mRNA expression profiles reveals a molecular regulatory network that is perturbed by mutant huntingtin, Journal of neurochemistry, 123, 477, 10.1111/j.1471-4159.2012.07925.x · DOI · Paper page
  15. A Sotrel, 1993, Evidence for neuronal degeneration and dendritic plasticity in cortical pyramidal neurons of Huntington's disease: a quantitative Golgi study, Neurology, 43, 2088, 10.1212/WNL.43.10.2088 · DOI · Paper page
  16. M Cudkowicz, 1990, Degeneration of pyramidal projection neurons in Huntington's disease cortex, Annals of neurology, 27, 200, 10.1002/ana.410270217 · DOI
  17. X Gu, 2005, Pathological cell-cell interactions elicited by a neuropathogenic form of mutant Huntingtin contribute to cortical pathogenesis in HD mice, Neuron, 46, 433, 10.1016/j.neuron.2005.03.025 · DOI
  18. HD Rosas, 2005, Regional cortical thinning in preclinical Huntington disease and its relationship to cognition, Neurology, 65, 745, 10.1212/01.wnl.0000174432.87383.87 · DOI
  19. LA Greene, 1976, Establishment of a noradrenergic clonal line of rat adrenal pheochromocytoma cells which respond to nerve growth factor, Proceedings of the National Academy of Sciences of the United States of America, 73, 2424, 10.1073/pnas.73.7.2424 · DOI
  20. H Kita, 2002, Modulation of polyglutamine-induced cell death by genes identified by expression profiling, Human molecular genetics, 11, 2279, 10.1093/hmg/11.19.2279 · DOI
  21. A Wyttenbach, 2001, Polyglutamine expansions cause decreased CRE-mediated transcription and early gene expression changes prior to cell death in an inducible cell model of Huntington's disease, Human molecular genetics, 10, 1829, 10.1093/hmg/10.17.1829 · DOI
  22. S Igarashi, 2003, Inducible PC12 cell model of Huntington's disease shows toxicity and decreased histone acetylation, Neuroreport, 14, 565, 10.1097/00001756-200303240-00007 · DOI
  23. BL Apostol, 2006, Mutant huntingtin alters MAPK signaling pathways in PC12 and striatal cells: ERK1/2 protects against mutant huntingtin-associated toxicity, Human molecular genetics, 15, 273, 10.1093/hmg/ddi443 · DOI
  24. KL Sugars, 2004, Decreased cAMP response element-mediated transcription: an early event in exon 1 and full-length cell models of Huntington's disease that contributes to polyglutamine pathogenesis, The Journal of biological chemistry, 279, 4988, 10.1074/jbc.M310226200 · DOI
  25. X Li, 2010, Inhibiting the ubiquitin-proteasome system leads to preferential accumulation of toxic N-terminal mutant huntingtin fragments, Human molecular genetics, 19, 2445, 10.1093/hmg/ddq127 · DOI
  26. S Anders, 2010, Differential expression analysis for sequence count data, Genome biology, 11, R106, 10.1186/gb-2010-11-10-r106 · DOI · Paper page
  27. DP Bartel, 2009, MicroRNAs: target recognition and regulatory functions, Cell, 136, 215, 10.1016/j.cell.2009.01.002 · DOI · Paper page
  28. H Dweep, 2013, Parallel analysis of mRNA and microRNA microarray profiles to explore functional regulatory patterns in polycystic kidney disease: using PKD/Mhm rat model, PLoS One, 8. 8, e53780, 10.1371/journal.pone.0053780 · DOI
  29. BJ Swalla, 2006, Building divergent body plans with similar genetic pathways, Heredity (Edinb), 97, 235, 10.1038/sj.hdy.6800872 · DOI
  30. S Yekta, 2008, MicroRNAs in the Hox network: an apparent link to posterior prevalence, Nat Rev Genet, 9, 789, 10.1038/nrg2400 · DOI
  31. P Flicek, 2013, Ensembl 2013, Nucleic acids research, 41, D48, 10.1093/nar/gks1236 · DOI
  32. JL Rinn, 2007, Functional demarcation of active and silent chromatin domains in human HOX loci by noncoding RNAs, Cell, 129, 1311, 10.1016/j.cell.2007.05.022 · DOI
  33. Y Miyazaki, 2012, Viral delivery of miR-196a ameliorates the SBMA phenotype via the silencing of CELF2, Nature medicine, 18, 1136, 10.1038/nm.2791 · DOI
  34. PM Gaughwin, 2011, Hsa-miR-34b is a plasma-stable microRNA that is elevated in pre-manifest Huntington's disease, Human molecular genetics, 20, 2225, 10.1093/hmg/ddr111 · DOI · Paper page
  35. M Sinha, 2010, Altered microRNAs in STHdh(Q111)/Hdh(Q111) cells: miR-146a targets TBP, Biochemical and biophysical research communications, 396, 742, 10.1016/j.bbrc.2010.05.007 · DOI
  36. C Soldati, 2013, Dysregulation of REST-regulated coding and non-coding RNAs in a cellular model of Huntington's disease, J Neurochem, 124, 418, 10.1111/jnc.12090 · DOI
  37. JM Woltering, 2008, MiR-10 represses HoxB1a and HoxB3a in zebrafish, PLoS One, 3, e1396, 10.1371/journal.pone.0001396 · DOI
  38. D Tehler, 2011, The miR-10 microRNA precursor family, RNA Biol, 8, 728, 10.4161/rna.8.5.16324 · DOI
  39. NH Foley, 2011, MicroRNAs 10a and 10b are potent inducers of neuroblastoma cell differentiation through targeting of nuclear receptor corepressor 2, Cell death and differentiation, 18, 1089, 10.1038/cdd.2010.172 · DOI
  40. H Huang, 2010, miR-10a contributes to retinoid acid-induced smooth muscle cell differentiation, J Biol Chem, 285, 9383, 10.1074/jbc.M109.095612 · DOI
  41. S Meseguer, 2011, MicroRNAs-10a and -10b contribute to retinoic acid-induced differentiation of neuroblastoma cells and target the alternative splicing regulatory factor SFRS1 (SF2/ASF), J Biol Chem, 286, 4150, 10.1074/jbc.M110.167817 · DOI · Paper page
  42. SL Phua, 2011, Nuclear accumulation of an uncapped RNA produced by Drosha cleavage of a transcript encoding miR-10b and HOXD4, PloS one, 6, e25689, 10.1371/journal.pone.0025689 · DOI
  43. FU Weiss, 2009, Retinoic acid receptor antagonists inhibit miR-10a expression and block metastatic behavior of pancreatic cancer, Gastroenterology, 137, 2136, 10.1053/j.gastro.2009.08.065 · DOI
  44. D Lemons, 2006, Genomic evolution of Hox gene clusters, Science, 313, 1918, 10.1126/science.1132040 · DOI · Paper page
  45. JC Pearson, 2005, Modulating Hox gene functions during animal body patterning, Nature reviews Genetics, 6, 893, 10.1038/nrg1726 · DOI · Paper page
  46. E Wienholds, 2005, MicroRNA expression in zebrafish embryonic development, Science, 309, 310, 10.1126/science.1114519 · DOI · Paper page
  47. R Diez del Corral, 2004, Opposing FGF and retinoid pathways: a signalling switch that controls differentiation and patterning onset in the extending vertebrate body axis, Bioessays, 26, 857, 10.1002/bies.20080 · DOI
  48. T Svingen, 2006, Hox transcription factors and their elusive mammalian gene targets, Heredity (Edinb), 97, 88, 10.1038/sj.hdy.6800847 · DOI
  49. HS Taylor, 1998, HOXA10 is expressed in response to sex steroids at the time of implantation in the human endometrium, J Clin Invest, 101, 1379, 10.1172/JCI1597 · DOI
  50. B Schuettengruber, 2007, Genome regulation by polycomb and trithorax proteins, Cell, 128, 735, 10.1016/j.cell.2007.02.009 · DOI
  51. IS Seong, 2010, Huntingtin facilitates polycomb repressive complex 2, Human molecular genetics, 19, 573, 10.1093/hmg/ddp524 · DOI
  52. S Humbert, 2010, Is Huntington disease a developmental disorder?, EMBO reports, 11, 899, 10.1038/embor.2010.182 · DOI
  53. SC Kirkwood, 2000, Subtle changes among presymptomatic carriers of the Huntington's disease gene, Journal of neurology, neurosurgery, and psychiatry, 69, 773, 10.1136/jnnp.69.6.773 · DOI
  54. RH Myers, 1991, Decreased neuronal and increased oligodendroglial densities in Huntington's disease caudate nucleus, J Neuropathol Exp Neurol, 50, 729, 10.1097/00005072-199111000-00005 · DOI
  55. J Liu, 2005, MicroRNA-dependent localization of targeted mRNAs to mammalian P-bodies, Nature cell biology, 7, 719, 10.1038/ncb1274 · DOI · Paper page
  56. V Balagopal, 2009, Polysomes, P bodies and stress granules: states and fates of eukaryotic mRNAs, Current opinion in cell biology, 21, 403, 10.1016/j.ceb.2009.03.005 · DOI
  57. SN Bhattacharyya, 2006, Relief of microRNA-mediated translational repression in human cells subjected to stress, Cell, 125, 1111, 10.1016/j.cell.2006.04.031 · DOI
  58. N Cougot, 2008, Dendrites of mammalian neurons contain specialized P-body-like structures that respond to neuronal activation, The Journal of neuroscience : the official journal of the Society for Neuroscience, 28, 13793, 10.1523/JNEUROSCI.4155-08.2008 · DOI · Paper page
  59. M Zeitelhofer, 2008, Dynamic interaction between P-bodies and transport ribonucleoprotein particles in dendrites of mature hippocampal neurons, The Journal of neuroscience : the official journal of the Society for Neuroscience, 28, 7555, 10.1523/JNEUROSCI.0104-08.2008 · DOI
  60. JN Savas, 2010, A role for huntington disease protein in dendritic RNA granules, The Journal of biological chemistry, 285, 13142, 10.1074/jbc.M110.114561 · DOI
  61. JN Savas, 2008, Huntington's disease protein contributes to RNA-mediated gene silencing through association with Argonaute and P bodies, Proceedings of the National Academy of Sciences of the United States of America, 105, 10820, 10.1073/pnas.0800658105 · DOI
  62. TJ Kwiatkowski Jr, 2009, Mutations in the FUS/TLS gene on chromosome 16 cause familial amyotrophic lateral sclerosis, Science, 323, 1205, 10.1126/science.1166066 · DOI
  63. B Wolozin, 2012, Regulated protein aggregation: stress granules and neurodegeneration, Molecular neurodegeneration, 7, 56, 10.1186/1750-1326-7-56 · DOI
  64. MP Gantier, 2011, Analysis of microRNA turnover in mammalian cells following Dicer1 ablation, Nucleic acids research, 39, 5692, 10.1093/nar/gkr148 · DOI
  65. PS Mitchell, 2008, Circulating microRNAs as stable blood-based markers for cancer detection, Proceedings of the National Academy of Sciences of the United States of America, 105, 10513, 10.1073/pnas.0804549105 · DOI · Paper page
  66. X Chen, 2008, Characterization of microRNAs in serum: a novel class of biomarkers for diagnosis of cancer and other diseases, Cell research, 18, 997, 10.1038/cr.2008.282 · DOI · Paper page
  67. B Langmead, 2009, Ultrafast and memory-efficient alignment of short DNA sequences to the human genome, Genome Biol, 10, 10.1186/gb-2009-10-3-r25 · DOI · Paper page
  68. AR Quinlan, 2010, BEDTools: a flexible suite of utilities for comparing genomic features, Bioinformatics, 26, 841, 10.1093/bioinformatics/btq033 · DOI · Paper page
  69. KJ Livak, 2001, Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method, Methods, 25, 402, 10.1006/meth.2001.1262 · DOI · Paper page
  70. D Kim, 2013, TopHat2: accurate alignment of transcriptomes in the presence of insertions, deletions and gene fusions, Genome Biol, 14, R36, 10.1186/gb-2013-14-4-r36 · DOI · Paper page
  71. C Trapnell, 2009, TopHat: discovering splice junctions with RNA-Seq, Bioinformatics, 25, 1105, 10.1093/bioinformatics/btp120 · DOI
  72. H Li, 2009, The Sequence Alignment/Map format and SAMtools, Bioinformatics, 25, 2078, 10.1093/bioinformatics/btp352 · DOI · Paper page
  73. A Kasprzyk, 2011, BioMart: driving a paradigm change in biological data management, Database (Oxford) 2011

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Metadata

Authors
Hoss, A. G., Kartha, V. K., Dong, X., Latourelle, J. C., Dumitriu, A., Hadzi, T. C., MacDonald, M. E., Gusella, J. F., Akbarian, S., Chen, J.-F., Weng, Z., & Myers, R. H.
Venue
PLoS Genetics
Publisher
Public Library of Science (PLoS)
Published
2014-02-27
Volume
10
Issue
2
Pages
e1004188
ISSN
1553-7404
DOI
10.1371/journal.pgen.1004188
PMC
PMC3937267
Cited by
111
References
4
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (unspecified)

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Hoss, A. G., Kartha, V. K., Dong, X., Latourelle, J. C., Dumitriu, A., Hadzi, T. C., MacDonald, M. E., Gusella, J. F., Akbarian, S., Chen, J.-F., Weng, Z., & Myers, R. H. (2014). MicroRNAs Located in the Hox Gene Clusters Are Implicated in Huntington's Disease Pathogenesis. PLoS Genetics. https://doi.org/10.1371/journal.pgen.1004188