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ABSTRACT: Study of RNA editing in Leptomonas pyrrhocoris mitochondrion

PROVIDER: PRJNA392757 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5796660_1.fastq.gz	Fastqsanger.gz
	SRR5796660_2.fastq.gz	Fastqsanger.gz
	SRR5796661_1.fastq.gz	Fastqsanger.gz
	SRR5796661_2.fastq.gz	Fastqsanger.gz
	SRR5796658_1.fastq.gz	Fastqsanger.gz

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Genome-wide identification and functional analysis of Apobec-1 mediated C-to-U RNA editing in mouse small intestine and liver

Project description:Background: RNA editing encompasses a post-transcriptional process in which the genomically templated sequence is enzymatically altered and introduces a modified base into the edited transcript. Mammalian C-to-U RNA editing represents a distinct subtype of base modification, whose prototype is intestinal apolipoproteinB (apoB) mRNA, mediated by the catalytic deaminase Apobec-1. However, the genome-wide identification, tissue-specificity and functional implications of Apobec-1 mediated C-to-U RNA editing remains incomplete. Results: Deep sequencing, data filtering and Sanger-sequence validation of intestinal and hepatic RNA from wild-type and Apobec-1 deficient mice revealed 56 novel editing sites in 54 intestinal mRNAs and 22 novel sites in 17 liver mRNAs (74-81% Sanger sequenced validated), all within 3’ untranslated regions. Eleven of 17 liver RNAs shared editing sites with intestinal RNAs, while 6 sites were unique to liver. Changes in RNA editing led to corresponding changes in intestinal mRNA and protein levels in 11 genes. RNA editing in vivo following tissue-specific Apobec-1 adenoviral or transgenic Apobec-1 overexpression revealed that a subset of targets identified in wild-type mice were restored in Apobec-1 deficient mouse intestine and liver following Apobec-1 rescue. We found distinctive polysome profiles for several RNA editing targets and demonstrated novel exonic editing sites in nuclear preparations from intestine (but not hepatic) apoB RNA. RNA editing was validated using cell-free extracts from wild-type but not Apobec-1 deficient mice, demonstrating that Apobec-1 is required. Conclusions: These studies define selective, tissue-specific targets of Apobec-1 dependent RNA editing and show the functional consequences of editing are both transcript- and tissue-specific.

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