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Human orthorubulavirus 2

ABSTRACT: RNA editing efficiency in the human parainfluenza virus type 2 RNAs

PROVIDER: PRJDB17293 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	DRR524078_1.fastq.gz	Fastqsanger.gz
	DRR524078_2.fastq.gz	Fastqsanger.gz
	DRR524079_1.fastq.gz	Fastqsanger.gz
	DRR524079_2.fastq.gz	Fastqsanger.gz
	DRR524080_1.fastq.gz	Fastqsanger.gz

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Human orthorubulavirus 2

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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.

2014-06-02 | PXD001007 | Pride

Solid-like condensation of MORF8 inhibits RNA editing under heat stress in Arabidopsis

Project description:Heat stress inhibits photosynthesis efficiency, thereby suppressing plant growth and crop yield. However, the mechanism underlying this inhibition is not fully understood. Here, we report that the multiple organellar RNA-editing factor 8 (MORF8) forms condensates with solid-like properties in chloroplast upon heat stress. In vitro data show that the MORF8 condensation is intrinsically heat-dependent and primarily determined by its IDR (intrinsically disordered region). Purification and characterization of MORF8 condensates show that numerous editing factors including PPR proteins and MORFs are partitioned. We provide both genetic and biochemical evidence that MORF8 condensation inhibits chloroplast RNA editing. In agreement, we find that both heat stress and MORF8 condensation lead to reduced editing of RNAs encoding NADH dehydrogenase-like (NDH) complex and impaired NDH activity and photosynthesis efficiency. These findings uncover MORF8 as a putative chloroplastic thermosensor that mediates photosynthesis inhibition by heat and highlight the functional significance of solid material properties of biomolecular condensates.

2025-03-07 | PXD061133 | Pride

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