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Altered microRNA expression profiles in large offspring syndrome and Beckwith-Wiedemann syndrome

ABSTRACT: Altered microRNA expression profiles in large offspring syndrome and Beckwith-Wiedemann syndrome

PROVIDER: PRJNA480853 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7515490.fastq.gz	Fastqsanger.gz
	SRR7515500.fastq.gz	Fastqsanger.gz
	SRR7515481.fastq.gz	Fastqsanger.gz
	SRR7515491.fastq.gz	Fastqsanger.gz
	SRR7515501.fastq.gz	Fastqsanger.gz

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Altered microRNA expression profiles in large offspring syndrome and Beckwith-Wiedemann syndrome

Project description:Altered microRNA expression profiles in large offspring syndrome and Beckwith-Wiedemann syndrome

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Altered microRNA expression profiles in large offspring syndrome and Beckwith-Wiedemann syndrome

Project description:Altered microRNA expression profiles in large offspring syndrome and Beckwith-Wiedemann syndrome

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Altered microRNA expression profiles in large offspring syndrome and Beckwith-Wiedemann syndrome

Project description:The use of assisted reproductive technologies (ART) can induce a congenital overgrowth condition in humans and ruminants, namely Beckwith-Wiedemann syndrome (BWS) and large offspring syndrome (LOS), respectively. Shared phenotypes and epigenotypes have been found between BWS and LOS. We have observed global misregulation of transcripts in bovine foetuses with LOS. microRNAs (miRNAs) are important post-transcriptional gene expression regulators. We hypothesize that there is miRNA misregulation in LOS and that this misregulation is shared with BWS. In this study, small RNA sequencing was conducted to investigate miRNA expression profiles in bovine and human samples. We detected 407 abundant known miRNAs and predicted 196 putative miRNAs from the bovine sequencing results and identified 505 abundant miRNAs in human tongue. Differentially expressed miRNAs (DE-miRNAs) were identified between control and LOS groups in all tissues analysed as well as between BWS and control human samples. DE-miRNAs were detected from several miRNA clusters including DLK1-DIO3 genomic imprinted cluster in LOS and BWS. DNA hypermethylation was associated with downregulation of miRNAs in the DLK1-DIO3. mRNA targets of the DE-miRNAs were predicted and signalling pathways associated with control of organ size (including the Hippo signalling pathway), cell proliferation, apoptosis, cell survival, cell cycle, and cell adhesion were found to be enriched with these genes. Yes associated protein 1 (YAP1) is the core effector of the Hippo signalling pathway, and increased level of active (non-phosphorylated) YAP1 protein was detected in skeletal muscle of LOS foetuses. Overall, our data provide evidence of miRNA misregulation in LOS and BWS.

2019-07-30 | GSE117015 | GEO

imprinting disorders: Beckwith–Wiedemann, Silver–Russell, and Prader-Willi syndromes in Egyptian patients

Project description:19 patients with syndromic ImpDis were 8 clinically diagnosed with Silver-Russell syndrome (SRS), 7 with Prader-Willi syndrome (PWS), and 4 with Beckwith-Wiedemann syndrome (BWS).array chromosomal microarray (CMA) was performed for 12 patients

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Project description:Multi-omic Investigation of Beckwith-Wiedemann Syndrome Hepatoblasto

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Project description:Multi-omic Investigation of Beckwith-Wiedemann Syndrome Hepatoblasto

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Altered microRNA expression profiles in large offspring syndrome and Beckwith-Wiedemann syndrome.

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Highly variable genomic methylation in the Beckwith-Wiedemann syndrome associated with Multi-Locus Imprinting Disturbances

Project description:The expression of imprinted genes, which depends on their gamete of origin, is regulated by DNA sequences characterized by differential methylation between the maternal and paternal alleles (also known as germline differentially methylated regions or gDMRs). A common molecular defect associated with Beckwith-Wiedemann syndrome (BWS), a condition linked to overgrowth and tumors, is the loss of methylation of the KCNQ1OT1-TSS gDMR located on chromosome 11p15.5 (also known as IC2 LoM). Approximately one-third of BWS patients with IC2 LoM exhibit multi-locus imprinting disturbances (MLID). While maternal-effect variants in proteins of the oocyte subcortical maternal complex (SCMC) have been linked to MLID, the underlying mechanisms and health impacts of this epigenetic disturbance remain unclear.

2025-09-30 | GSE297935 | GEO

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