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A transcriptome analysis study with the focus on the role of long non-coding RNAs in Down syndrome subjects

ABSTRACT: A transcriptome analysis study with the focus on the role of long non-coding RNAs in Down syndrome subjects

PROVIDER: PRJEB45793 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR6089570_1.fastq.gz	Fastqsanger.gz
	ERR6089570_2.fastq.gz	Fastqsanger.gz
	ERR6089580_1.fastq.gz	Fastqsanger.gz
	ERR6089580_2.fastq.gz	Fastqsanger.gz
	ERR6089590_1.fastq.gz	Fastqsanger.gz

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A transcriptome analysis study with the focus on the role of long non-coding RNAs in Down syndrome subjects

Project description:Down syndrome (DS) results from trisomy of chromosome 21 and is the most common genetic cause of intellectual disability (ID). A wide range of comorbidities have been described in DS, such as ID, muscle weakness, hypotonia, congenital heart disease and autoimmune diseases. The pathogenetic mechanisms that are responsible for developing these comorbidities are still far from being understood. It was hypothesized that dosage imbalance on chromosome 21 as a whole disrupts diverse developmental pathways whereas another hypothesis suggests that dosage increase for specific genes on chromosome 21 contributes directly to different aspects of the phenotype in DS. The present study explored mRNAs and lncRNAs expression by using the next generation sequencing analysis (NGS) and the quantitative real-time PCR (qRT-PCR) assay for the confirmation of the NGS results, followed by functional analysis of the results. The enrichment analysis of the results obtained revealed various pathways in which differentially expressed genes are involved. Developmental disorders play a crucial role in the phenotype of people with Down syndrome with particular attention to intellectual developmental disorders.

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Identification of a DNA methylation signature in blood from subjects affected by Down syndrome

Project description:Down syndrome is characterized by a wide spectrum of clinical signs, which include cognitive and endocrine disorders and haematological abnormalities. Although it is well established that the causative defect of Down syndrome is the trisomy of chromosome 21, the molecular bases of Down syndrome phenotype are still largely unknown. We used the Infinium HumanMethylation450 BeadChip to investigate DNA methylation patterns in whole blood from 29 subjects affected by Down syndrome (DS), using their healthy relatives as controls (mothers and unaffected siblings). This family-based model allowed us to monitor possible confounding effects on DNA methylation patterns deriving from genetic and environmental (lifestyle) factors. The identified epigenetic signature of Down syndrome includes differentially methylated regions that, although enriched on chromosome 21, interest most of the other chromosomes and can be functionally linked to the developmental and haematological defects characteristic of the disease. DNA was extracted from whole peripheral blood using the QIAamp 96 DNA Blood Kit (QIAGEN) and quantified by Quant-iT™ PicoGreen (Invitrogen). Sodium bisulphite conversion of 500 ng of each sample was performed using the EZDNA Methylation-Gold Kit according to the manufacturer's recommendation for Illumina Infinium Assay. 4 ul of bisulfite converted DNA were hybridized on Infinium HumanMethylation 450 BeadChip, following manufacturer’s instructions. Arrays were scanned by HiScan SQ scanner (Illumina) and the intensities of the images were extracted using GenomeStudio (2010.3) Methylation module (1.8.5) software. Methylation levels of each CpG is reported as beta value.

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