Transcriptomic analysis of osmotic stress response in yeast xrn1 mutant
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ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae
PROVIDER: GSE151736 | GEO | 2020/11/27
REPOSITORIES: GEO
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Project description:The goal of the project was to study the effects on transcription and mRNA stability of the Xrn1 sudden depletion. We analyzed the effect of Xrn1 depletion caused by protein degradation of an Auxin-degron fusion on the transcription rates, mRNA stabilities and mRNA levels by doing Genomic Run-On (GRO) experiments at 30 min after Auxin addition with a control at 0 min.
2019-02-22 | GSE123326 | GEO
Project description:The goal of the project was to study the transcription rates and mRNA levels, genome-wide, in several mutants in Xrn1 defetive in nuclear import. We used Genomic Run-On (GRO) experiment in wild type and xrn1 mutant strains.
2022-09-30 | GSE158250 | GEO
Project description:To determine the effects of inactivation of both the nosense-mediated mRNA decay pathway and the general 5' to 3' decay pathway on yeast mRNA decay, we compared the expression profiles of the wild-type, xrn1, xrn1 upf1, xrn1 nmd2, and xrn1 upf3 strains.
2011-11-08 | E-MEXP-27 | biostudies-arrayexpress
Project description:Antisense (as)lncRNAs are extensively degraded by the nuclear exosome and the cytoplasmic exoribonuclease Xrn1 in the budding yeast Saccharomyces cerevisiae, lacking RNA interference (RNAi). Whether the ribonuclease III Dicer affects aslncRNAs in close RNAi-capable relatives remains unknown. Using genome-wide RNA profiling, here we show that aslncRNAs are primarily targeted by the exosome and Xrn1 in the RNAi-capable budding yeast Naumovozyma castellii, Dicer only affecting Xrn1-sensitive lncRNAs (XUTs) levels in Xrn1-deficient cells. The dcr1 and xrn1 mutants display synergic growth defects, indicating that Dicer becomes critical in absence of Xrn1. Small RNA sequencing showed that Dicer processes aslncRNAs into small RNAs, with a preference for asXUTs. Consistently, Dicer localizes into the cytoplasm. Finally, we observed an expansion of the exosome-sensitive antisense transcriptome in N. castellii compared to S. cerevisiae, suggesting that the presence of cytoplasmic RNAi has reinforced the nuclear RNA surveillance machinery to temper aslncRNAs expression. Our data provide fundamental insights into aslncRNAs metabolism and open perspectives into the possible evolutionary contribution of RNAi in shaping the aslncRNAs transcriptome.
2019-08-21 | GSE90041 | GEO
Project description:Xrn1 is a cytoplasmic 5’-3’ exoribonuclease responsible for degradation of multiple types of RNA. Data obtained on yeast model described Xrn1 function in degradation of messenger (m)RNA, Rapid transfer (t)RNA Decay (RTD) of hypomodified and unstable tRNA transcripts as well as maturation of 25S ribosomal (r)RNA and small nucleolar (sno)RNAs. Our group discovered previously that deletion of Xrn1 gene results in stabilization of a group of long non-coding RNAs which are often transcribed antisense to protein-coding genes and may regulate their expression on transcriptional level. However much less is known about human (h)Xrn1 function. Data available from human cell lines confirm involvement of hXrn1 in degradation of mRNA, initiator tRNA methionine and some miRNA. The high sequence similarity of Xrn1 between yeast and man suggests that also its function should be well conserved for hXrn1. Therefore, in this experiment using inducible shRNA we want to define hXrn1 targets by analyzing RNAs that are stabilized after Xrn1 silencing with focus on both coding and non-coding transcripts.
2020-01-14 | GSE114605 | GEO
Project description:The main cytoplasmic mRNA decay pathway in yeast uses the 5’-3’ exonuclease Xrn1 (Parker and Song, Nat Struct Mol Biol. 2004 ). This protein shuttles from the cytoplasm to the nucleus, where it has a role as transcription factor (Haimovich et al. Cell 2013). In this work, we find that most of the global phenotypes of an xrn1 mutant are partially complemented by a cytoplasmic version of the paralogous 5’-3’exonuclease Rat1 (cRat1) indicating that this 5’-3’-exonuclease has a similar enzymatic capacity as Xrn1. The lack of a cytoplasmatic 5’-3’-exoribonuclease is the cause of the physiological defects of an xrn1 mutant. The capacity of cRat1 to perform co-translational decay is, however, very limited. The comparison with the strain having a NLS1∆-NLS2∆-Xrn1 version shows that it is slightly deficient in 5’→3’-co-translational decay but much more efficient than cRat1. In both strains, cRat1 and -Xrn1-NLS1&2, the lack of nuclear Xrn1 has a very minor influence on cell growth.
2024-10-23 | GSE193992 | GEO
Project description:Despite the remarkable achievement of immune checkpoint blockade (ICB) therapy, the response rate is relatively low and only a subset of patients can benefit from the treatment. We hypothesize that targeting RNA decay machinery may lead to accumulation of aberrantRNA, triggering interferon (IFN) signaling and sensitizing tumor cells to immunotherapy. With this in mind, we identified an RNA exoribonuclease, XRN1 as a potential target. Silencing of XRN1 suppressed tumor growth in syngeneic immunocompetent mice and potentiated immunotherapy, while silencing of XRN1 alone did not affect tumor growth in immune deficient mice. Mechanistically, XRN1 depletion activated interferon signaling and viral defense pathway; both pathways play determinant roles in regulating immune evasion. In murine tumors engrafted on immmunocompetent mice, XRN1 depletion significantly enhanced immune cell infiltration in solid tumors especially in combinatory with PD-1 blockade. We identified aberrant-RNA sensing signaling proteins (RIG-I/MAVS and PKR) in mediating the expression of IFN genes, as depletion of each of them blunted the elevation of anti-viral/IFN signaling in Xrn1 silenced cells. Analysis of pan-cancer CRISPR screening data indicated that IFN signaling triggered by Xrn1 silencing is a common phenomenon, suggesting that the effect of Xrn1 silencing may be extend to multiple types of cancers.
2023-02-21 | GSE202587 | GEO
Project description:Transcriptomic analysis of osmotic stress response in yeast xrn1 mutant
| PRJNA637065 | ENA
Project description:Despite the remarkable achievement of immune checkpoint blockade (ICB) therapy, the response rate is relatively low and only a subset of patients can benefit from the treatment. We hypothesize that targeting RNA decay machinery may lead to accumulation of aberrantRNA, triggering interferon (IFN) signaling and sensitizing tumor cells to immunotherapy. With this in mind, we identified an RNA exoribonuclease, XRN1 as a potential target. Silencing of XRN1 suppressed tumor growth in syngeneic immunocompetent mice and potentiated immunotherapy, while silencing of XRN1 alone did not affect tumor growth in immune deficient mice. Mechanistically, XRN1 depletion activated interferon signaling and viral defense pathway; both pathways play determinant roles in regulating immune evasion. We identified aberrant-RNA sensing signaling proteins (RIG-I/MAVS and PKR) in mediating the expression of IFN genes, as depletion of each of them blunted the elevation of anti-viral/IFN signaling in Xrn1 silenced cells. Analysis of pan-cancer CRISPR screening data indicated that IFN signaling triggered by Xrn1 silencing is a common phenomenon, suggesting that the effect of Xrn1 silencing may be extend to multiple types of cancers.
2023-02-21 | GSE199744 | GEO
Project description:The rates of mRNA synthesis and degradation determine cellular mRNA levels and can be monitored by comparative Dynamic Transcriptome Analysis (cDTA) that uses non-perturbing metabolic RNA labeling. Here we present cDTA data for 46 yeast strains lacking genes involved in mRNA degradation and metabolism. In these strains, changes in mRNA degradation rates are generally compensated by changes in mRNA synthesis rates, resulting in a buffering of mRNA levels. We show that buffering of mRNA levels requires the RNA exonuclease Xrn1. The buffering is rapidly established when mRNA synthesis is impaired, but is delayed when mRNA degradation is impaired, apparently due to Xrn1-dependent transcription repressor induction. Cluster analysis of the data defines the general mRNA degradation machinery, reveals different substrate preferences for the two mRNA deadenylase complexes Ccr4-Not and Pan2-Pan3, and unveils an interwoven cellular mRNA surveillance network. For this purpose, cDTA was carried out as described in Sun et.al. Genome Res. 2012 (DOI:10.1101/gr.130161.111). S. cerevisiae cultures were grown at 30¡ãC in 50 ml aliquots of YPD medium. S. pombe cultures were grown at 32¡ãC in YES medium. For inhibitor perturbation, BY4741 cells (OD600=0.1) were inoculated from a saturated overnight culture in two 100 ml aliquots of YPD liquid medium, incubated at 30¡ãC and grown to early-log phase (OD600=0.8). Cells were labeled for 6 minutes (sample 0 min). Then cycloheximide was added and cells were labeled for 10 minutes and 60 minutes. Cells were harvested and treated as described in Sun et.al. Genome Res. 2012 (DOI:10.1101/gr.130161.111). 1,10-Phenanthroline was added to the culture to a final concentration of 25 _g/ml as described (Dori-Bachash et al., 2012), and labeled for 6 minutes after 18 minutes treatment. Cells were treated as above. For the anchor-away analysis, S. cerevisiae cells (OD600=0.1) were cultured in two 200 ml aliquots of YPD containing 1_g/ml rapamycin and incubated at 30¡ãC untill OD600 reached 0.8. Due to the instability of rapamycin, we added 1_g/ml rapamycin every two hours. Then a 20 ml sample was taken and labeled with 4sU. The cells were then treated as described in Sun et.al. Genome Res. 2012 (DOI:10.1101/gr.130161.111).
2013-10-18 | E-MTAB-1525 | biostudies-arrayexpress