Compatibility with Killer explains the Rise of RNAi-deficient Fungi
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ABSTRACT:
PROVIDER: PRJNA146117 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
2011-08-09 | E-GEOD-31300 | biostudies-arrayexpress
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.
| S-EPMC3790311 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2011-08-10 | GSE31300 | GEO
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.
2011-08-10 | E-GEOD-31290 | biostudies-arrayexpress
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).
2011-08-10 | E-GEOD-31288 | biostudies-arrayexpress
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.
2011-08-10 | GSE31290 | GEO
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.
2011-08-10 | GSE31288 | GEO
Project description:We transfected K562 cells with a STARR-seq plasmid library of paired promoter and enhancer sequences to characterize activation and compatibility between promoters and enhancers.
2021-10-25 | GSE184426 | GEO
Project description:Gene expression is in part controlled by cis-regulatory elements (CREs) such as enhancers and repressive elements. Anecdotal evidence has indicated that a CRE and a promoter need to be biochemically compatible for promoter regulation to occur, but this compatibility has remained poorly characterised in mammalian cells. By systematic reporter assays of thousands of CRE – promoter pairs from three Mb-sized genomic regions in mouse cells, we found that CREs vary substantially in their promoter compatibility, with more than half showing significant selectivity. This selectivity does not correlate with looping interactions, suggesting that chromatin folding and compatibility are two orthogonal mechanisms of gene regulation.
2021-10-21 | GSE186265 | GEO