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Uncharged tRNAGln as an indicator of intracellular amino acid level upregulates UBC expression to maintain its charging level I

ABSTRACT: We profiled the cellular tRNA charging landscape using next-generation sequencing and identified a subset of tRNA that sense nutrients. The charging levels of tRNAGln were exclusively and significantly decreased in response to amino acid starvation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE188855 | GEO | 2022/11/30

REPOSITORIES: GEO

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Uncharged tRNAGln as an indicator of intracellular amino acid level upregulates UBC expression to maintain its charging level VI

Project description:We profiled the cellular tRNA charging landscape using next-generation sequencing and identified a subset of tRNA that sense nutrients. The charging levels of tRNAGln were exclusively and significantly decreased in response to amino acid starvation.

2022-11-30 | GSE188861 | GEO

Uncharged tRNAGln as an indicator of intracellular amino acid level upregulates UBC expression to maintain its charging level V

2022-11-30 | GSE188860 | GEO

Uncharged tRNAGln as an indicator of intracellular amino acid level upregulates UBC expression to maintain its charging level IV

2022-11-30 | GSE188859 | GEO

Uncharged tRNAGln as an indicator of intracellular amino acid level upregulates UBC expression to maintain its charging level III

2022-11-30 | GSE188858 | GEO

Uncharged tRNAGln as an indicator of intracellular amino acid level upregulates UBC expression to maintain its charging level II

2022-11-30 | GSE188857 | GEO

Uncharged tRNAGln as an indicator of intracellular amino acid level upregulates UBC expression to maintain its charging level

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-11-30 | GSE188862 | GEO

Translation in amino acid-poor environments is limited by tRNAGln charging

Project description:An inadequate supply of amino acids leads to accumulation of uncharged tRNAs, which can bind and activate GCN2 kinase to reduce translation. Here, we show that glutamine-specific tRNAs selectively become uncharged when extracellular amino acid availability is compromised. In contrast, all other tRNAs retain charging of their cognate amino acids in a manner that is dependent upon intact lysosomal function. In addition to GCN2 activation and reduced total translation, the reduced charging of tRNAGln in amino acid-deprived cells also leads to specific depletion of proteins containing polyglutamine tracts including core binding factor α1, mediator subunit 12, transcriptional coactivator CBP and TATA-box binding protein. Treating amino acid-deprived cells with exogenous glutamine or glutaminase inhibitors restores tRNAGln charging and the levels of polyglutamine-containing proteins. Together, these results demonstrate that the activation of GCN2 and the translation of polyglutamine-encoding transcripts serve as the key sensors of glutamine availability in mammalian cells.

2020-12-14 | GSE157276 | GEO

Translation in amino acid-poor environments is limited by tRNAGln charging

Project description:Translation in amino acid-poor environments is limited by tRNAGln charging

| PRJNA660742 | ENA

tRNA senses cellular nutrient status and senescence via amino acid acylation

2022-11-30 | GSE157510 | GEO

Growth Optimized Aminoacyl-tRNA Synthetase Levels Prevent Maximal tRNA Charging

Project description:Summary Aminoacyl-tRNA synthetases (aaRSs) serve a dual role in charging tRNAs. Their enzymatic activities both provide protein synthesis flux and reduce uncharged tRNA levels. Although uncharged tRNAs can negatively impact bacterial growth, substantial concentrations of tRNAs remain deacylated even under nutrient-rich conditions. Here we show that tRNA charging in Bacillus subtilis is not maximized due to optimization of aaRS production during rapid growth, which prioritizes demands in protein synthesis over charging levels. The presence of uncharged tRNAs is alleviated by precisely tuned translation kinetics and the stringent response, both insensitive to aaRS overproduction but sharply responsive to underproduction, allowing for just-enough aaRS production atop a “fitness cliff”. Notably, we find that the stringent response mitigates fitness defects at all aaRS underproduction levels even without external starvation. Thus, adherence to minimal, flux-satisfying protein production drives limited tRNA charging and provides a basis for the sensitivity and setpoints of an integrated growth-control network.

2020-07-20 | GSE141389 | GEO

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