Genome-wide DNA Methylation and RNAseq Analyses Identify Aberrant Signalling Pathways in Focal Cortical Dysplasia (FCD) Type II
Focal cortical dysplasia (FCD) is one of the most common pathologies associated with drug-resistant epilepsy (DRE). The pharmacological targets remain obscured, as the molecular mechanisms underlying FCD are unclear. Implications of epigenetically modulated aberrant gene expression in disease progre...
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| Veröffentlicht in: | Scientific reports 2018-12, Vol.8 (1), p.17976-12, Article 17976 |
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| creator | Dixit, Aparna Banerjee Sharma, Devina Tripathi, Manjari Srivastava, Arpna Paul, Debasmita Prakash, Deepak Sarkar, Chitra Kumar, Krishan Banerjee, Jyotirmoy Chandra, P. Sarat |
| description | Focal cortical dysplasia (FCD) is one of the most common pathologies associated with drug-resistant epilepsy (DRE). The pharmacological targets remain obscured, as the molecular mechanisms underlying FCD are unclear. Implications of epigenetically modulated aberrant gene expression in disease progression are reported in various DRE pathologies except FCD. Here we performed genome-wide CpG-DNA methylation profiling by methylated DNA immunoprecipitation (MeDIP) microarray and RNA sequencing (RNAseq) on cortical tissues resected from FCD type II patients. A total of 19088 sites showed altered DNA methylation in all the CpG islands. Of these, 5725 sites were present in the promoter regions, of which 176 genes showed an inverse correlation between methylation and gene expression. Many of these 176 genes were found to belong to a cohesive network of physically interacting proteins linked to several cellular functions. Pathway analysis revealed significant enrichment of receptor tyrosine kinases (RTK), EGFR, PDGFRA, NTRK3, and mTOR signalling pathways. This is the first study that investigates the epigenetic signature associated with FCD type II pathology. The candidate genes and pathways identified in this study may play a crucial role in the regulation of the pathogenic mechanisms of epileptogenesis associated with FCD type II pathologies. |
| doi_str_mv | 10.1038/s41598-018-35892-5 |
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Sarat</creator><creatorcontrib>Dixit, Aparna Banerjee ; Sharma, Devina ; Tripathi, Manjari ; Srivastava, Arpna ; Paul, Debasmita ; Prakash, Deepak ; Sarkar, Chitra ; Kumar, Krishan ; Banerjee, Jyotirmoy ; Chandra, P. Sarat</creatorcontrib><description>Focal cortical dysplasia (FCD) is one of the most common pathologies associated with drug-resistant epilepsy (DRE). The pharmacological targets remain obscured, as the molecular mechanisms underlying FCD are unclear. Implications of epigenetically modulated aberrant gene expression in disease progression are reported in various DRE pathologies except FCD. Here we performed genome-wide CpG-DNA methylation profiling by methylated DNA immunoprecipitation (MeDIP) microarray and RNA sequencing (RNAseq) on cortical tissues resected from FCD type II patients. A total of 19088 sites showed altered DNA methylation in all the CpG islands. Of these, 5725 sites were present in the promoter regions, of which 176 genes showed an inverse correlation between methylation and gene expression. Many of these 176 genes were found to belong to a cohesive network of physically interacting proteins linked to several cellular functions. Pathway analysis revealed significant enrichment of receptor tyrosine kinases (RTK), EGFR, PDGFRA, NTRK3, and mTOR signalling pathways. This is the first study that investigates the epigenetic signature associated with FCD type II pathology. The candidate genes and pathways identified in this study may play a crucial role in the regulation of the pathogenic mechanisms of epileptogenesis associated with FCD type II pathologies.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-018-35892-5</identifier><identifier>PMID: 30568293</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/51 ; 38 ; 38/39 ; 38/61 ; 38/91 ; 45/22 ; 45/90 ; 631/1647/2017 ; 631/337/176/1988 ; 631/378/340 ; Cortex ; CpG islands ; Deoxyribonucleic acid ; Disease Susceptibility ; DNA ; DNA fingerprinting ; DNA Methylation ; DNA microarrays ; DNA sequencing ; Drug resistance ; Dysplasia ; Epidermal growth factor receptors ; Epigenesis, Genetic ; Epilepsy ; Epilepsy - genetics ; Epilepsy - metabolism ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation ; Genome-Wide Association Study - methods ; Genomes ; Humanities and Social Sciences ; Humans ; Immunoprecipitation ; Malformations of Cortical Development, Group I - genetics ; Malformations of Cortical Development, Group I - metabolism ; Molecular modelling ; multidisciplinary ; Promoter Regions, Genetic ; Ribonucleic acid ; RNA ; Science ; Science (multidisciplinary) ; Signal Transduction ; TOR protein ; Tyrosine</subject><ispartof>Scientific reports, 2018-12, Vol.8 (1), p.17976-12, Article 17976</ispartof><rights>The Author(s) 2018</rights><rights>2018. 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Sarat</creatorcontrib><title>Genome-wide DNA Methylation and RNAseq Analyses Identify Aberrant Signalling Pathways in Focal Cortical Dysplasia (FCD) Type II</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Focal cortical dysplasia (FCD) is one of the most common pathologies associated with drug-resistant epilepsy (DRE). The pharmacological targets remain obscured, as the molecular mechanisms underlying FCD are unclear. Implications of epigenetically modulated aberrant gene expression in disease progression are reported in various DRE pathologies except FCD. Here we performed genome-wide CpG-DNA methylation profiling by methylated DNA immunoprecipitation (MeDIP) microarray and RNA sequencing (RNAseq) on cortical tissues resected from FCD type II patients. A total of 19088 sites showed altered DNA methylation in all the CpG islands. Of these, 5725 sites were present in the promoter regions, of which 176 genes showed an inverse correlation between methylation and gene expression. Many of these 176 genes were found to belong to a cohesive network of physically interacting proteins linked to several cellular functions. Pathway analysis revealed significant enrichment of receptor tyrosine kinases (RTK), EGFR, PDGFRA, NTRK3, and mTOR signalling pathways. This is the first study that investigates the epigenetic signature associated with FCD type II pathology. The candidate genes and pathways identified in this study may play a crucial role in the regulation of the pathogenic mechanisms of epileptogenesis associated with FCD type II pathologies.</description><subject>13/51</subject><subject>38</subject><subject>38/39</subject><subject>38/61</subject><subject>38/91</subject><subject>45/22</subject><subject>45/90</subject><subject>631/1647/2017</subject><subject>631/337/176/1988</subject><subject>631/378/340</subject><subject>Cortex</subject><subject>CpG islands</subject><subject>Deoxyribonucleic acid</subject><subject>Disease Susceptibility</subject><subject>DNA</subject><subject>DNA fingerprinting</subject><subject>DNA Methylation</subject><subject>DNA microarrays</subject><subject>DNA sequencing</subject><subject>Drug resistance</subject><subject>Dysplasia</subject><subject>Epidermal growth factor receptors</subject><subject>Epigenesis, Genetic</subject><subject>Epilepsy</subject><subject>Epilepsy - genetics</subject><subject>Epilepsy - metabolism</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation</subject><subject>Genome-Wide Association Study - methods</subject><subject>Genomes</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Immunoprecipitation</subject><subject>Malformations of Cortical Development, Group I - genetics</subject><subject>Malformations of Cortical Development, Group I - metabolism</subject><subject>Molecular modelling</subject><subject>multidisciplinary</subject><subject>Promoter Regions, Genetic</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Signal Transduction</subject><subject>TOR protein</subject><subject>Tyrosine</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kUFv1DAQhS0EolXpH-CALHEph4Bjx4l9QYp22bJSKQjK2Zp1nF1XXntrZ6ly4q_jdEspHPDFlt6bN575EHpZkrclYeJdqkouRUFKUTAuJC34E3RMScULyih9-uh9hE5Tuib5cCqrUj5HR4zwWlDJjtHPc-PD1hS3tjN4ftniT2bYjA4GGzwG3-Gvl20yN7j14MZkEl52xg-2H3G7MjGCH_A3u86is36Nv8CwuYUxYevxImhweBbiYKfHfEw7B8kCPlvM5m_w1bgzeLl8gZ714JI5vb9P0PfFh6vZx-Li8_ly1l4UmpflUNSNqQklPelI0_GGAdUNZEV20MgVr2tSr_IatCAGRFVpDg2jmvJGEKmrnrMT9P6Qu9uvtqbTeYgITu2i3UIcVQCr_la83ah1-KFqKiVtpoCz-4AYbvYmDWprkzbOgTdhnxTNOFhuSEm2vv7Heh32Me_oziV4RRmfAunBpWNIKZr-4TMlURNidUCsMmJ1h1hNRa8ej_FQ8htoNrCDIWXJr0380_s_sb8A5jiwcw</recordid><startdate>20181219</startdate><enddate>20181219</enddate><creator>Dixit, Aparna Banerjee</creator><creator>Sharma, Devina</creator><creator>Tripathi, Manjari</creator><creator>Srivastava, Arpna</creator><creator>Paul, Debasmita</creator><creator>Prakash, Deepak</creator><creator>Sarkar, Chitra</creator><creator>Kumar, Krishan</creator><creator>Banerjee, Jyotirmoy</creator><creator>Chandra, P. 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Sarat</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genome-wide DNA Methylation and RNAseq Analyses Identify Aberrant Signalling Pathways in Focal Cortical Dysplasia (FCD) Type II</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2018-12-19</date><risdate>2018</risdate><volume>8</volume><issue>1</issue><spage>17976</spage><epage>12</epage><pages>17976-12</pages><artnum>17976</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Focal cortical dysplasia (FCD) is one of the most common pathologies associated with drug-resistant epilepsy (DRE). The pharmacological targets remain obscured, as the molecular mechanisms underlying FCD are unclear. Implications of epigenetically modulated aberrant gene expression in disease progression are reported in various DRE pathologies except FCD. Here we performed genome-wide CpG-DNA methylation profiling by methylated DNA immunoprecipitation (MeDIP) microarray and RNA sequencing (RNAseq) on cortical tissues resected from FCD type II patients. A total of 19088 sites showed altered DNA methylation in all the CpG islands. Of these, 5725 sites were present in the promoter regions, of which 176 genes showed an inverse correlation between methylation and gene expression. Many of these 176 genes were found to belong to a cohesive network of physically interacting proteins linked to several cellular functions. Pathway analysis revealed significant enrichment of receptor tyrosine kinases (RTK), EGFR, PDGFRA, NTRK3, and mTOR signalling pathways. This is the first study that investigates the epigenetic signature associated with FCD type II pathology. The candidate genes and pathways identified in this study may play a crucial role in the regulation of the pathogenic mechanisms of epileptogenesis associated with FCD type II pathologies.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>30568293</pmid><doi>10.1038/s41598-018-35892-5</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/51 38 38/39 38/61 38/91 45/22 45/90 631/1647/2017 631/337/176/1988 631/378/340 Cortex CpG islands Deoxyribonucleic acid Disease Susceptibility DNA DNA fingerprinting DNA Methylation DNA microarrays DNA sequencing Drug resistance Dysplasia Epidermal growth factor receptors Epigenesis, Genetic Epilepsy Epilepsy - genetics Epilepsy - metabolism Gene expression Gene Expression Profiling Gene Expression Regulation Genome-Wide Association Study - methods Genomes Humanities and Social Sciences Humans Immunoprecipitation Malformations of Cortical Development, Group I - genetics Malformations of Cortical Development, Group I - metabolism Molecular modelling multidisciplinary Promoter Regions, Genetic Ribonucleic acid RNA Science Science (multidisciplinary) Signal Transduction TOR protein Tyrosine |
| title | Genome-wide DNA Methylation and RNAseq Analyses Identify Aberrant Signalling Pathways in Focal Cortical Dysplasia (FCD) Type II |
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