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Mutations in tRNA synthetases impair translation and activate the integrated stress response in inherited peripheral neuropathie

ABSTRACT: Mutations in tRNA synthetases impair translation and activate the integrated stress response in inherited peripheral neuropathie

PROVIDER: PRJNA605653 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11050300_1.fastq.gz	Fastqsanger.gz
	SRR11050300_2.fastq.gz	Fastqsanger.gz
	SRR11050400_1.fastq.gz	Fastqsanger.gz
	SRR11050400_2.fastq.gz	Fastqsanger.gz
	SRR11050301_1.fastq.gz	Fastqsanger.gz

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Mutations in tRNA synthetases impair translation and activate the integrated stress response in inherited peripheral neuropathie

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Project description:As compared to Eukaryotes, Bacteria have a reduced tRNA gene set encoding between 30 and 220 tRNAs, which are thought to act in concert for the maintenance of gene translation. Here we show that in some bacteria the tRNA gene set may be partitioned in a housekeeping sub-set that sustains translation, and an inducible one that is generally silent but can be largely induced to provide functionality under particular conditions. In the model cyanobacterium Anabaena sp. PCC 7120, the inducible set forms an operon encoding 23 functional tRNAs. Transcription of these tRNAs is induced by translation stress, i.e. by insults that impair translation, including antibiotics that target the ribosome. The operon is co-regulated with genes encoding proteins like the tRNA ligase RtcB and the stress-specific protein DpsA, probably involved in a response directed to protect the cell and recover translation. Common regulation suggests participation of operonic tRNAs in this response, although mechanistic issues remain to be determined. Similar long tRNA gene operons were found in species across major bacterial phyla and are shown to be distinct in many aspects from other operons that evolved by gene accretion.

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Differential expression of human tRNA genes drives the abundance of tRNA-derived fragments

Project description:The human genome encodes hundreds of tRNA genes but their individual contribution to the tRNA pool is not fully understood. Deep sequencing of tRNA transcripts (tRNA-Seq) can estimate tRNA abundance at single gene resolution, but tRNA structures and post-transcriptional modifications impair these analyses. Here we present a bioinformatics strategy to investigate differential tRNA gene expression and use it to compare tRNA-Seq datasets from cultured human cells and human brain. We find that sequencing caveats affect quantitation of only a subset of human tRNA genes. Unexpectedly, we detect several cases where the differences in tRNA expression among samples do not involve variations at the level of isoacceptor tRNA sets (tRNAs charged with the same amino acid but using different anticodons); but rather among tRNA genes within the same isodecoder set (tRNAs having the same anticodon sequence). Because isodecoder tRNAs are functionally equal in terms of genetic translation, their differential expression may be related to non-canonical tRNA functions. We show that several instances of differential tRNA gene expression result in changes in the abundance of tRNA-derived fragments (tRFs) but not of mature tRNAs. Examples of differentially expressed tRFs include: PIWI-associated RNAs, tRFs present in tissue samples but not in cells cultured in vitro, and somatic tissue-specific tRFs. Our data support that differential expression of tRNA genes regulate non-canonical tRNA functions performed by tRFs.

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| S-EPMC3384309 | biostudies-literature

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