Cytoplasmic RNA decay pathways - Enzymes and mechanisms

Łabno, Anna; Tomecki, Rafał; Dziembowski, Andrzej

doi:10.1016/j.bbamcr.2016.09.023

Cited by 192 publications

(133 citation statements)

References 191 publications

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“…Cap turnover starts when a transcript is subjected to cellular RNA degradation machinery. There are two main mRNA degradation pathways 5′–3′ and 3′–5′, both initiated by poly(A) tail shortening [48]. Although decapping is not the first event in the 5′–3′ mRNA degradation pathway, as it is preceded by deadenylation, it is considered as the first highly irreversible step.…”

Section: Chemically and Enzymatically Labeled Rna Capsmentioning

confidence: 99%

Applications of Phosphate Modification and Labeling to Study (m)RNA Caps

et al. 2017

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The cap is a natural modification present at the 5′ ends of eukaryotic messenger RNA (mRNA), which because of its unique structural features, mediates essential biological functions during the process of gene expression. The core structural feature of the mRNA cap is an N7-methylguanosine moiety linked by a 5′–5′ triphosphate chain to the first transcribed nucleotide. Interestingly, other RNA 5′ end modifications structurally and functionally resembling the m7G cap have been discovered in different RNA types and in different organisms. All these structures contain the ‘inverted’ 5′–5′ oligophosphate bridge, which is necessary for interaction with specific proteins and also serves as a cleavage site for phosphohydrolases regulating RNA turnover. Therefore, cap analogs containing oligophosphate chain modifications or carrying spectroscopic labels attached to phosphate moieties serve as attractive molecular tools for studies on RNA metabolism and modification of natural RNA properties. Here, we review chemical, enzymatic, and chemoenzymatic approaches that enable preparation of modified cap structures and RNAs carrying such structures, with emphasis on phosphate-modified mRNA cap analogs and their potential applications.

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Section: Chemically and Enzymatically Labeled Rna Capsmentioning

confidence: 99%

Applications of Phosphate Modification and Labeling to Study (m)RNA Caps

et al. 2017

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“…Altogether, DDX6 and PAT1B have been proposed to link deadenylation/translational repression with decapping. Finally, the 5'-3' exonuclease XRN1 decays RNAs following decapping by DCP1/2, a step triggered by deadenylation mediated by PAN2/3 and CCR4-NOT or by exosome activity [17].…”

Section: Introductionmentioning

confidence: 99%

GC content shapes mRNA decay and storage in human cells

Courel

Clément

Foretek

et al. 2018

Preprint

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Control of protein expression results from the fine tuning of mRNA synthesis, decay and translation. These processes, which are controlled by a large number of RNA-binding proteins and by localization in RNP granules such as P-bodies, appear often intimately linked although the rules of this interplay are not well understood. In this study, we combined our recent P-body transcriptome with various transcriptomes obtained following silencing of broadly acting mRNA decay and repression factors. This analysis revealed the central role of GC content in mRNA fate, in terms of P-body localization, mRNA translation and mRNA decay. It also rationalized why PBs mRNAs have a strikingly low protein yield. We report too the existence of distinct mRNA decay pathways with preference for AU-rich or GC-rich transcripts. Compared to this impact of the GC content, sequence-specific RBPs and miRNAs appeared to have only modest additional effects on their bulk targets. Altogether, these results lead to an integrated view of post-transcriptional control in human cells where most regulation at the level of translation is dedicated to AU-rich mRNAs, which have a limiting protein yield, whereas regulation at the level of 5' decay applies to GC-rich mRNAs, whose translation is optimal.

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“…Genetic alterations, including chromosome alteration, oncogene activation, miRNA dysregulation, mRNA decay, autophagy and ubiquitin–proteasome system , can affect protein biogenesis and degradation systems, which often results in proteome imbalance. mRNA half‐lives differ significantly between various transcripts in all eukaryotic organisms investigated so far . Interestingly, decay rates for some mRNAs seem to be conserved between different species to some extent .…”

Section: Discussionmentioning

confidence: 99%

DDA1, a novel oncogene, promotes lung cancer progression through regulation of cell cycle

Cheng

Yang

et al. 2017

J Cellular Molecular Medi

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Lung cancer is globally widespread and associated with high morbidity and mortality. DDA1 (DET1 and DDB1 associated 1) was first discovered and registered in the GenBank database by our colleagues. DDA1, an evolutionarily conserved gene, might have significant functions. Recent reports have demonstrated that DDA1 is linked to the ubiquitin–proteasome pathway and facilitates the degradation of target proteins. However, the function of DDA1 in lung cancer was previously unknown. This study aimed to investigate whether DDA1 contributes to tumorigenesis and progression of lung cancer. We found that the expression of DDA1 in normal lung cells and tissue was significantly lower than that in lung cancer and was associated with poor prognosis. DDA1 overexpression promoted proliferation of lung tumour cells and facilitated cell cycle progression in vitro and subcutaneous xenograft tumour progression in vivo. Mechanistically, this was associated with the regulation of S phase and cyclins including cyclin D1/D3/E1. These results indicate that DDA1 promotes lung cancer progression, potentially through promoting cyclins and cell cycle progression. Therefore, DDA1 may be a potential novel target for lung cancer treatment, and a biomarker for tumour prognosis.

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Cytoplasmic RNA decay pathways - Enzymes and mechanisms

Cited by 192 publications

References 191 publications

Applications of Phosphate Modification and Labeling to Study (m)RNA Caps

Applications of Phosphate Modification and Labeling to Study (m)RNA Caps

GC content shapes mRNA decay and storage in human cells

DDA1, a novel oncogene, promotes lung cancer progression through regulation of cell cycle

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