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Gene expression analysis of yeast strains with a nonsense mutation in the eRF3-coding gene highlights possible mechanisms of adaptation

ABSTRACT: Gene expression analysis of yeast strains with a nonsense mutation in the eRF3-coding gene highlights possible mechanisms of adaptation

PROVIDER: PRJNA1113596 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29088380_1.fastq.gz	Fastqsanger.gz
	SRR29088380_2.fastq.gz	Fastqsanger.gz
	SRR29088381_1.fastq.gz	Fastqsanger.gz
	SRR29088381_2.fastq.gz	Fastqsanger.gz
	SRR29088382_1.fastq.gz	Fastqsanger.gz

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Gene expression analysis of yeast strains with a nonsense mutation in the eRF3-coding gene highlights possible mechanisms of adaptation

Project description:In yeast Saccharomyces cerevisiae, there are two translation termination factors, eRF1 (SUP45) and eRF3 (SUP35), which are essential for viability. Previous studies have revealed that presence of nonsense mutations in these genes leads to amplification of mutant alleles (sup35-n and sup45-n) which appears to be necessary for viability of such cells. However, the mechanism of this phenomenon remained unclear. In this study, we used RNA-Seq to reveal the complete set of gene expression changes that occur during cellular adaptation to the introduction of the sup35-218 nonsense allele. Our analysis demonstrated significant changes in the transcription of genes that control the cell cycle: decrease in the expression of genes of the anaphase promoting complex APC/C (APC9, CDC23), their activator CDC20 and an increase in the expression of FKH1 transcription factor, main cell cycle kinase CDC28 and cyclins that induce DNA biosynthesis. We propose a model according to which yeast adaptation to nonsense mutations in the translation termination factor genes occurs as a result of a delayed cell cycle progression beyond the G2-M stage, which leads to an extension of the S and G2 phases and an increase in the number of copies of the mutant sup35-n allele.

2024-05-23 | GSE267888 | GEO

Gene Amplification as a Mechanism of Yeast Adaptation to Nonsense Mutations in Release Factor Genes.

Project description:Protein synthesis (translation) is one of the fundamental processes occurring in the cells of living organisms. Translation can be divided into three key steps: initiation, elongation, and termination. In the yeast Saccharomyces cerevisiae, there are two translation termination factors, eRF1 and eRF3. These factors are encoded by the SUP45 and SUP35 genes, which are essential; deletion of any of them leads to the death of yeast cells. However, viable strains with nonsense mutations in both the SUP35 and SUP45 genes were previously obtained in several groups. The survival of such mutants clearly involves feedback control of premature stop codon readthrough; however, the exact molecular basis of such feedback control remain unclear. To investigate the genetic factors supporting the viability of these SUP35 and SUP45 nonsense mutants, we performed whole-genome sequencing of strains carrying mutant sup35-n and sup45-n alleles; while no common SNPs or indels were found in these genomes, we discovered a systematic increase in the copy number of the plasmids carrying mutant sup35-n and sup45-n alleles. We used the qPCR method which confirmed the differences in the relative number of SUP35 and SUP45 gene copies between strains carrying wild-type or mutant alleles of SUP35 and SUP45 genes. Moreover, we compare the number of copies of the SUP35 and SUP45 genes in strains carrying different nonsense mutant variants of these genes as a single chromosomal copy. qPCR results indicate that the number of mutant gene copies is increased compared to the wild-type control. In case of several sup45-n alleles, this was due to a disomy of the entire chromosome II, while for the sup35-218 mutation we observed a local duplication of a segment of chromosome IV containing the SUP35 gene. Taken together, our results indicate that gene amplification is a common mechanism of adaptation to nonsense mutations in release factor genes in yeast.

| S-EPMC8701342 | biostudies-literature

Nonsense-mediated decay in Plasmodium falciparum

Project description:We have HA-tagged two nonsense-mediated decay proteins, UPF1 and UPF2, in the malaria parasite Plasmodium falciparum. We then performed co-immunoprecipitation experiments to determine the protein-protein interactions of these nonsense-mediated decay components.

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Transcription profiling of yeast to analyse mRNAs regulated by the nonsense-mediated and 5 to 3 mRNA Decay Pathways

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Project description:The propensity for Saccharomyces cerevisiae yeast to ferment sugars into ethanol and CO2 has long been useful in the production of a wide range of food and drink. In the production of alcoholic beverages, the yeast strain selected for fermentation is crucial because not all strains are equally proficient in tolerating fermentation stresses. One potential mechanism by which domesticated yeast may have adapted to fermentation stresses is through changes in the expression of stress response genes. MED15 is a general transcriptional regulator and RNA Pol II Mediator complex subunit which modulates the expression of many metabolic and stress response genes. In this study, we explore the role of MED15 in alcoholic fermentation. In addition, we ask whether MED15 alleles from wine, sake or palm wine yeast improve fermentation activity and grape juice fermentation stress responses. And last, we investigate to what extent any differences in activity are due to allelic differences in the lengths of three polyglutamine tracts in MED15. We find that strains lacking MED15 are deficient in fermentation and fermentation stress responses and that MED15 alleles from alcoholic beverage yeast strains can improve both the fermentation capacity and the response to ethanol stresses when transplanted into a standard laboratory strain. Finally, we find that polyglutamine tract length in the Med15 protein is one determinant in the efficiency of the alcoholic fermentation process. These data lead to a working model in which polyglutamine tract length and other types of variability within transcriptional hubs like the Mediator subunit, Med15, may contribute to a reservoir of transcriptional profiles that may provide a fitness benefit in the face of environmental fluctuations.

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Nonsense suppression as a mechanism of genetic complemtation in the opportunistic pathogen Mycobacterium marinum

Project description:Here, we report the discovery of a novel mechanism of genetic complementation in M. marinum. We found that nonsense suppression was causing genetic complementation. Nonsense suppression was linked to alterations in cell permeability and exposure to the aminoglycoside antibiotic, hygromycin.

2019-06-08 | GSE83103 | GEO

Nonsense Mutations in the Yeast SUP35 Gene Affect the [PSI+] Prion Propagation.

Project description:The essential SUP35 gene encodes yeast translation termination factor eRF3. Previously, we isolated nonsense mutations sup35-n and proposed that the viability of such mutants can be explained by readthrough of the premature stop codon. Such mutations, as well as the prion [PSI+], can appear in natural yeast populations, and their combinations may have different effects on the cells. Here, we analyze the effects of the compatibility of sup35-n mutations with the [PSI+] prion in haploid and diploid cells. We demonstrated that sup35-n mutations are incompatible with the [PSI+] prion, leading to lethality of sup35-n [PSI+] haploid cells. In diploid cells the compatibility of [PSI+] with sup35-n depends on how the corresponding diploid was obtained. Nonsense mutations sup35-21, sup35-74, and sup35-218 are compatible with the [PSI+] prion in diploid strains, but affect [PSI+] properties and lead to the formation of new prion variant. The only mutation that could replace the SUP35 wild-type allele in both haploid and diploid [PSI+] strains, sup35-240, led to the prion loss. Possibly, short Sup351-55 protein, produced from the sup35-240 allele, is included in Sup35 aggregates and destabilize them. Alternatively, single molecules of Sup351-55 can stick to aggregate ends, and thus interrupt the fibril growth. Thus, we can conclude that sup35-240 mutation prevents [PSI+] propagation and can be considered as a new pnm mutation.

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Ultraconserved elements are associated with control of splicing regulators by alt splicing and nonsense mediated decay

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