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Compatibility with Killer explains the Rise of RNAi-deficient Fungi

ABSTRACT: Compatibility with Killer explains the Rise of RNAi-deficient Fungi

PROVIDER: PRJNA146117 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR332049.fastq.gz	Fastqsanger.gz
	SRR332050.fastq.gz	Fastqsanger.gz
	SRR332051.fastq.gz	Fastqsanger.gz
	SRR332052.fastq.gz	Fastqsanger.gz
	SRR332256.fastq.gz	Fastqsanger.gz

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Compatibility with Killer explains the Rise of RNAi-deficient Fungi

Project description:This SuperSeries is composed of the following subset Series: GSE31288: The impact of RNAi on the Saccharomyces cerevisiae transcriptome GSE31290: Small RNAs in S. cerevisiae reconstituted with RNAi Refer to individual Series

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Compatibility with killer explains the rise of RNAi-deficient fungi.

Project description:The RNA interference (RNAi) pathway is found in most eukaryotic lineages but curiously is absent in others, including that of Saccharomyces cerevisiae. We show that reconstituting RNAi in S. cerevisiae causes loss of a beneficial double-stranded RNA virus known as killer virus. Incompatibility between RNAi and killer viruses extends to other fungal species in that RNAi is absent in all species known to possess double-stranded RNA killer viruses, whereas killer viruses are absent in closely related species that retained RNAi. Thus, the advantage imparted by acquiring and retaining killer viruses explains the persistence of RNAi-deficient species during fungal evolution.

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Compatibility with Killer explains the Rise of RNAi-deficient Fungi

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

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Project description:The RNA interference (RNAi) pathway is found in most eukaryotic lineages but curiously is absent in others, including that of Saccharomyces cerevisiae. Here, we show that reconstituting RNAi in S. cerevisiae causes loss of a beneficial dsRNA virus, known as killer virus. Incompatibility between RNAi and killer viruses extends to other fungal species, in that RNAi is absent in all species known to possess dsRNA killer viruses, whereas killer viruses are absent in closely related species that retained RNAi. Thus, the advantage imparted by acquiring and retaining killer viruses explains the persistence of RNAi-deficient species during fungal evolution. Employ high-throughput sequencing of endogenous small RNAs from Saccharomyces cerevisiae wild-type and RNAi-reconstituted strains.

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Project description:The RNA interference (RNAi) pathway is found in most eukaryotic lineages but curiously is absent in others, including that of Saccharomyces cerevisiae. Here, we show that reconstituting RNAi in S. cerevisiae causes loss of a beneficial dsRNA virus, known as killer virus. Incompatibility between RNAi and killer viruses extends to other fungal species, in that RNAi is absent in all species known to possess dsRNA killer viruses, whereas killer viruses are absent in closely related species that retained RNAi. Thus, the advantage imparted by acquiring and retaining killer viruses explains the persistence of RNAi-deficient species during fungal evolution. Examine mRNA abundance of S. cerevisiae wild-type (DPB249), +AGO1 (DPB252), +DCR1 (DPB255) and +AGO1, DCR1 (DPB258).

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Project description:The RNA interference (RNAi) pathway is found in most eukaryotic lineages but curiously is absent in others, including that of Saccharomyces cerevisiae. Here, we show that reconstituting RNAi in S. cerevisiae causes loss of a beneficial dsRNA virus, known as killer virus. Incompatibility between RNAi and killer viruses extends to other fungal species, in that RNAi is absent in all species known to possess dsRNA killer viruses, whereas killer viruses are absent in closely related species that retained RNAi. Thus, the advantage imparted by acquiring and retaining killer viruses explains the persistence of RNAi-deficient species during fungal evolution.

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