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The super-enhancer derived alncRNA-EC7/Bloodlinc potentiates red blood cell development in trans

ABSTRACT: The super-enhancer derived alncRNA-EC7/Bloodlinc potentiates red blood cell development in trans

PROVIDER: PRJNA380750 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5381860.fastq.gz	Fastqsanger.gz
	SRR5381861.fastq.gz	Fastqsanger.gz
	SRR5381862.fastq.gz	Fastqsanger.gz
	SRR5381853.fastq.gz	Fastqsanger.gz
	SRR5381863.fastq.gz	Fastqsanger.gz

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The super-enhancer derived alncRNA-EC7/Bloodlinc potentiates red blood cell development in trans (RNA-seq)

Project description:Enhancer-derived RNAs are thought to contribute locally to their parent enhancers’ functions. Whether large domains of clustered enhancers (super-enhancers, SEs) also produce cis-acting RNAs, however, remains unclear. Unlike typical enhancers, SEs form large spans of robustly transcribed chromatin, amassing capped and polyadenylated RNAs that are sufficiently abundant to sustain trans functions. Here, we show that one such RNA, alncRNA-EC7/Bloodlinc, is transcribed from a SE of the erythroid membrane transporter SLC4A1/BAND3 but diffuses beyond this site. Bloodlinc localizes to trans-chromosomal loci encoding critical regulators/effectors of terminal erythropoiesis and directly binds chromatin-organizing and transcription factors, including the chromatin attachment factor HNRNPU. Inhibiting Bloodlinc or Hnrnpu compromises the terminal erythropoiesis gene program, blocking red cell production, whereas expressing Bloodlinc ectopically stimulates this program and can promote erythroblast proliferation and enucleation in the absence of differentiation stimuli. Thus, Bloodlinc represents a novel type of trans-acting SE RNA that potentiates red blood cell development.

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The super-enhancer derived alncRNA-EC7/Bloodlinc potentiates red blood cell development in trans (ChIRP-seq)

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The Super-Enhancer-Derived alncRNA-EC7/Bloodlinc Potentiates Red Blood Cell Development in trans.

Project description:Enhancer-derived RNAs are thought to act locally by contributing to their parent enhancer function. Whether large domains of clustered enhancers (super-enhancers) also produce cis-acting RNAs, however, remains unclear. Unlike typical enhancers, super-enhancers form large spans of robustly transcribed chromatin, amassing capped and polyadenylated RNAs that are sufficiently abundant to sustain trans functions. Here, we show that one such RNA, alncRNA-EC7/Bloodlinc, is transcribed from a super-enhancer of the erythroid membrane transporter SLC4A1/BAND3 but diffuses beyond this site. Bloodlinc localizes to trans-chromosomal loci encoding critical regulators and effectors of terminal erythropoiesis and directly binds chromatin-organizing and transcription factors, including the chromatin attachment factor HNRNPU. Inhibiting Bloodlinc or Hnrnpu compromises the terminal erythropoiesis gene program, blocking red cell production, whereas expressing Bloodlinc ectopically stimulates this program and can promote erythroblast proliferation and enucleation in the absence of differentiation stimuli. Thus, Bloodlinc is a trans-acting super-enhancer RNA that potentiates red blood cell development.

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Project description:The super-enhancer derived alncRNA-EC7/Bloodlinc potentiates red blood cell development in trans (RNA-seq)

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Project description:The super-enhancer derived alncRNA-EC7/Bloodlinc potentiates red blood cell development in trans (ChIRP-seq)

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The super-enhancer derived alncRNA-EC7/Bloodlinc potentiates red blood cell development in trans

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