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PELOTA and HBS1 suppress co-translational messenger RNA decay in Arabidopsis [mRNA-Seq]

ABSTRACT: PELOTA and HBS1 suppress co-translational messenger RNA decay in Arabidopsis [mRNA-Seq]

PROVIDER: PRJNA1037110 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26744518.fastq.gz	Fastqsanger.gz
	SRR26744519.fastq.gz	Fastqsanger.gz
	SRR26744520.fastq.gz	Fastqsanger.gz
	SRR26744521.fastq.gz	Fastqsanger.gz
	SRR26744522.fastq.gz	Fastqsanger.gz

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PELOTA and HBS1 suppress co-translational messenger RNA decay in Arabidopsis

Project description:PELOTA and HBS1 suppress co-translational messenger RNA decay in Arabidopsis

| PRJNA1037102 | ENA

PELOTA and HBS1 suppress co-translational messenger RNA decay in Arabidopsis [GMUCT]

Project description:Various messenger RNA (mRNA) decay mechanisms play major roles in controlling mRNA quality and quantity in eukaryotic organisms under different conditions. While it is known that the recently discovered co-translational mRNA decay (CTRD), the mechanism that allows mRNAs to be degraded while still being actively translated, is prevalent in yeast, human, and various angiosperms, the regulation of this decay mechanism is less well studied. Moreover, it is still unclear whether this decay mechanism plays any roles in regulation of specific physiological processes in eukaryotes. Here, by re-analyzing the publicly available polysome profiling or ribosome footprinting and degradome sequencing datasets, we discovered that highly translated mRNAs tend to have lower co-translational decay levels. Based on this finding, we then identified Pelota and Hbs1, the translation-related ribosome rescue factors, as suppressors of co-translational mRNA decay in Arabidopsis. Furthermore, we found that Pelota and Hbs1 null mutants have lower germination rates compared to the wild type plants, implying that proper regulation of co-translational mRNA decay is essential for normal developmental processes. In total, our study provides further insights into the regulation of CTRD in Arabidopsis and demonstrates that this decay mechanism does play important roles in Arabidopsis physiological processes.

2023-12-31 | GSE247329 | GEO

PELOTA and HBS1 suppress co-translational messenger RNA decay in Arabidopsis [mRNA-Seq]

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PELOTA and HBS1 suppress co-translational messenger RNA decay in Arabidopsis [GMUCT]

Project description:PELOTA and HBS1 suppress co-translational messenger RNA decay in Arabidopsis [GMUCT]

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PELOTA and HBS1 suppress co-translational messenger RNA decay in Arabidopsis

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

2023-12-31 | GSE247330 | GEO

Genome-wide mapping of uncapped and cleaved transcripts reveals a role for the nuclear messenger RNA cap-binding complex in plant co-translational RNA decay

Project description:RNA turnover is necessary for controlling proper mRNA levels post-transcriptionally. In general, RNA degradation is via exoribonucleases that degrade RNA either from the 5’ end to the 3’ end, such as XRN4, or in the opposite direction by the multi-subunit exosome complex. Here, we use genome-wide mapping of uncapped and cleaved transcripts to reveal the global landscape of co-translational mRNA decay in the Arabidopsis thaliana transcriptome. We found that this process leaves a clear three nucleotide periodicity in open reading frames. This pattern of co-translational degradation is especially evident near the ends of open reading frames, where we observe accumulation of cleavage events focused 16 to 17 nucleotides upstream of the stop codon because of ribosomal pausing during translation termination. Following treatment of Arabidopsis plants with the translation inhibitor cycloheximide, cleavage events accumulate 13 to 14 nucleotides upstream of the start codon where initiating ribosomes have been stalled with these sequences in their P site. Further analysis in xrn4 mutant plants indicates that co-translational RNA decay is XRN4-dependent. Additionally, studies in plants lacking CAP-BINDING PROTEIN80/ABA HYPERSENSITIVE1, the largest subunit of the nuclear mRNA cap-binding complex, reveal a role for this protein in co-translational decay. In total, our results demonstrate the global prevalence and features of co-translational RNA decay in a plant transcriptome.

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4EHP and GIGYF1/2 induce translation-coupled messenger RNA decay

Project description:Although canonical mRNA degradation is generally recognized to be translation dependent, our understanding of the molecular events that coordinate ribosome movement with the decay machinery is still limited. Here, we show that the 4EHP–GIGYF1/2 complex triggers co-translational mRNA decay as a result of altered ribosome activity during elongation. Human cells lacking 4EHP and GIGYF1 and 2 proteins accumulate transcripts known to be degraded in a translation dependent manner or with prominent ribosome pausing. These include mRNAs encoding secretory and membrane-bound proteins or specific tubulin isotypes, among others. 4EHP–GIGYF1/2 fails to reduce target mRNA levels in the absence of ribosome stalling or upon disruption of its interaction with the cap structure, DDX6 and a GYF domain-associated protein. Our studies reveal how a repressor complex linked to neurological disorders minimizes the protein output of a subset of mRNAs.

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Ribosome profiling of early zebrafish embryos -- miRNA-mediated regulation during embryogenesis causes translational repression before mRNA decay

Project description:MicroRNAs regulate gene expression through deadenylation, repression and mRNA decay. However, the contribution of each mechanism in non-steady-state situations remains unclear. We monitored the impact of miR-430 on ribosome occupancy of endogenous mRNAs in wild type and dicer mutants lacking mature miR-430. Our results indicate that miR-430 reduces the number of ribosomes on target mRNAs before causing mRNA decay. Translational repression occurs before complete deadenylation, and disrupting deadenylation using an internal poly(A) tail did not block target repression. Finally, we observe that ribosome density along the length of the target mRNA remains constant, suggesting that translational repression occurs by reducing the initiation rate rather than reducing elongation or causing ribosomal drop-off. In summary, our results show that miR-430 regulates translation initiation before inducing mRNA decay. Time course parallel ribosome profiling and input mRNA quantification in wildtype and MZdicer mutant embryos

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