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Widespread microRNA degradation elements in target mRNAs can assist the encoded proteins

ABSTRACT: Widespread microRNA degradation elements in target mRNAs can assist the encoded proteins

PROVIDER: PRJNA741532 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14916842.fastq.gz	Fastqsanger.gz
	SRR14916843.fastq.gz	Fastqsanger.gz
	SRR14916844.fastq.gz	Fastqsanger.gz
	SRR14916845.fastq.gz	Fastqsanger.gz
	SRR14916846.fastq.gz	Fastqsanger.gz

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Widespread microRNA degradation elements in target mRNAs can assist the encoded proteins

Project description:Binding of microRNAs (miRNA) to mRNAs normally results in post-transcriptional repression. However, extensive base-pairing between miRNAs and target RNAs can trigger miRNA degradation, a phenomenon called target RNA-directed miRNA degradation (TDMD). Here, we systematically analyzed Argonaute-CLASH (crosslinking, ligation, and sequencing of miRNA-target RNA hybrids) data, and identified numerous candidate TDMD triggers based on their ability to induce non-templated nucleotide addition at the miRNA 3 end. When overexpressed in HEK293T cells, nine highly conserved triggers induce degradation of corresponding miRNAs. Consistent with previous reports, both the TDMD base-pairing and surrounding sequences are important for TDMD. CRISPR knockout of endogenous trigger or ZSWIM8, a ubiquitin ligase essential for TDMD, reduce miRNA degradation. Furthermore, degradation of miR-221 and miR-222 by a trigger in BCL2L11, which encodes an apoptotic protein, enhances apoptosis. Therefore, we uncovered widespread TDMD triggers in target RNAs and demonstrated that they can functionally cooperate with the encoded proteins.

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LARP4 Is an RNA-Binding Protein That Binds Nuclear-Encoded Mitochondrial mRNAs To Promote Mitochondrial Function

Project description:Mitochondria-associated RNA-binding proteins have emerged as key contributors to mitochondrial biogenesis and homeostasis. With few examples known, we set out to identify RBPs that regulate nuclear-encoded mitochondrial mRNAs. Our systematic analysis of RNA targets of 150 RBPs identified RBPs with a preference for binding NEM mRNAs, including LARP4, a La RBP family member. We show that LARP4s targets are particularly enriched in mRNAs that encode respiratory chain complex proteins and mitochondrial ribosome proteins across multiple human cell lines. Through quantitative proteomics, we demonstrate that depletion of LARP4 leads to a significant reduction in RCCP and MRP protein levels. Furthermore, we show that LARP4 depletion reduces mitochondrial function, and that LARP4 re-expression rescues this phenotype. Our findings shed light on a novel function for LARP4 as an RBP that binds to and positively regulates NEM mRNAs to promote mitochondrial respiratory function.

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Rnase L reprograms translation by widespread mRNA turnover escaped by antiviral mRNAs

Project description:Rnase L reprograms translation by widespread mRNA turnover escaped by antiviral mRNAs

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Rnase L reprograms translation by widespread mRNA turnover escaped by antiviral mRNAs

Project description:In response to foreign and endogenous double-stranded RNA (dsRNA), protein kinase R (PKR) and ribonuclease L (RNase L) reprogram translation in mammalian cells. PKR inhibits translation initiation through eIF2 phosphorylation, which triggers stress granule (SG) formation and promotes translation of stress responsive mRNAs. The mechanisms of RNase L-driven translation repression, its contribution to SG assembly, and its regulation of dsRNA stress-induced mRNAs are unknown. We demonstrate that RNase L drives translational shut-off in response to dsRNA by promoting widespread turnover of mRNAs. This alters stress granule assembly and reprograms translation by only allowing for the translation of mRNAs resistant to RNase L degradation, including numerous antiviral mRNAs such as IFN- . Individual cells differentially activate dsRNA responses revealing variation that can affect cellular outcomes. This identifies bulk mRNA degradation and the resistance of antiviral mRNAs as the mechanism by which RNaseL reprograms translation in response to dsRNA.

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Effect of left ventricular assist device support on congestive heart failure patients

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MIR100 host gene-encoded lncRNAs promote cell proliferation by modulating the interaction between HuR and its target mRNAs

Project description:Long non-coding RNAs (lncRNAs) regulate vital biological processes, including cell proliferation, differentiation and development. A subclass of lncRNAs is synthesized from microRNA host genes (MIRHGs) due to pre-miRNA processing, and is categorized as miRNA-host gene lncRNAs (lnc-miRHGs). Presently, it is not clear whether lnc-miRHG perform additional functions. We demonstrate a miRNA-independent role for a nuclear-enriched lnc-miRHG in cell cycle progression. MIR100HG produces spliced and stable lncRNAs (lnc-MIR100HG) that display elevated levels during the G1 phase of the cell cycle. Depletion of lnc-MIR100HG in human cells results in aberrant cell cycle progression with out altering the levels of miRNA encoded within MIR100HG. Notably, lnc-MIR100HG interacts with the HuR/Elav as well as with several of HuR-target mRNAs. Further, lnc-MIR100HG-depleted cells show reduced interaction between HuR and its target mRNAs, indicating that lnc-MIR100HG facilitates interaction between HuR and target mRNAs. Our studies have unearthed novel roles played by miRHG-encoded lncRNAs in regulating RNA binding protein activity, thereby underscoring the importance of determining the function of several hundreds of miRHG lncRNAs that are present in human genome.

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LARP4 Is an RNA-Binding Protein That Binds Nuclear-Encoded Mitochondrial mRNAs To Promote Mitochondrial Function

Project description:LARP4 Is an RNA-Binding Protein That Binds Nuclear-Encoded Mitochondrial mRNAs To Promote Mitochondrial Function

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LARP4 Is an RNA-Binding Protein That Binds Nuclear-Encoded Mitochondrial mRNAs To Promote Mitochondrial Function

Project description:Mitochondrial associated RNA-binding proteins (RBPs) have emerged as key contributors to mitochondrial biogenesis and homeostasis. With few examples described, we set out to identify RBPs that post-transcriptionally regulate nuclear-encoded mitochondrial mRNAs (NEMmRNAs). Our analysis of RNA-target sets of RBPs made available by ENCODE identified several RBPs with a preference for binding NEMmRNAs, of which we selected LARP4, a La RBP family member, for further study. We show that LARP4’s RNA-target set is particularly enriched in mRNAs that encode for respiratory chain complex proteins (RCCPs) and mitochondrial ribosome proteins (MRPs) across multiple human cell lines. CRISPR knockout cells in conjunction with quantitative proteomics show that protein levels of RCCPs and MRPs are significantly reduced upon loss of LARP4. Furthermore, we show that LARP4 depletion reduces mitochondrial function, and this phenotype is ameliorated by LARP4 re-expression. Our findings shed light onto a novel function for LARP4 as an RBP that binds to NEMmRNAs to promote mitochondrial respiratory function.

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