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The LncRNA Fendrr Regulates Lung Development via its Triplex Forming Site the Expression of Fibrosis Genes

ABSTRACT: The LncRNA Fendrr Regulates Lung Development via its Triplex Forming Site the Expression of Fibrosis Genes

PROVIDER: PRJNA775610 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16597755_1.fastq.gz	Fastqsanger.gz
	SRR16597755_2.fastq.gz	Fastqsanger.gz
	SRR16597756_1.fastq.gz	Fastqsanger.gz
	SRR16597756_2.fastq.gz	Fastqsanger.gz
	SRR16597757_1.fastq.gz	Fastqsanger.gz

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The LncRNA Fendrr Regulates Lung Development via its Triplex Forming Site the Expression of Fibrosis Genes

Project description:Long non-coding RNAs are a very versatile class of molecules that have important roles in regulating a cells function, including regulating other genes on the transcriptional level. One of these mechanisms is that RNA can directly interact with DNA by recruiting additional components such as proteins to these sites via a RNA:dsDNA triplex formation. We genetically deleted the triplex forming sequence from the lncRNA Fendrr in mice and find that this FendrrBox is partially required for Fendrr function. we We find that the loss of the triplex forming site in developing lungs causes a dysregulation of gene programs, associated with lung fibrosis. Deregulated genes that contain a FendrrBox binding element in their promoter are regulated by Wnt signaling, together with Fendrr, implicating that Fendrr acts in concert with Wnt signaling to regulate lung fibrosis.

2023-04-30 | GSE186703 | GEO

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HIF1α-AS1 is a DNA:DNA:RNA triplex-forming lncRNA interacting with the HUSH complex

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Project description:Exposure to low dose irradiation causes transiently elevated expression of a long ncRNA PARTICLE (Gene PARTICL- 'Promoter of MAT2A-Antisense RadiaTion Induced Circulating LncRNA). PARTICLE affords both a cytosolic scaffold for the tumor suppressor methionine adenosyltransferase (MAT2A) and a nuclear genetic platform for transcriptional repression. In situ hybridisation discloses that PARTICLE-MAT2A associate together following irradiation. Bromouridine tracing and presence in exosomes indicate intercellular transport, and this is supported by ex-vivo data from radiotherapy-treated patients. Surface plasmon resonance indicates that PARTICLE forms a DNA-lncRNA triplex upstream of a MAT2A promoter CpG island. We show that PARTICLE represses MAT2A via methylation and demonstrate that the radiation-induced PARTICLE lncRNA interacts with the transcription repressive complex proteins G9a and SUZ12 (subunit of PRC2). The interplay of PARTICLE with MAT2A, implicates this lncRNA in intercellular communication as well as a recruitment platform for gene silencing machineries through triplex formation in response to irradiation.

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The tissue-specific lncRNA Fendrr is an essential regulator of heart and body wall development in the mouse

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