Genome-wide screen of fission yeast mutants for sensitivity to 6-azauracil, an inhibitor of transcriptional elongation

Yeast ◽  
2015 ◽  
Vol 32 (10) ◽  
pp. 643-655 ◽  
Author(s):  
Huan Zhou ◽  
Qi Liu ◽  
Tianfang Shi ◽  
Yao Yu ◽  
Hong Lu
Keyword(s):  
Fission Yeast ◽  
Transcriptional Elongation ◽  
Genome Wide ◽  
Yeast Mutants

scholarly journals Genome-wide Screening of Genes Associated with Momilactone B Sensitivity in the Fission Yeast

2021 ◽  
Author(s):  
Keisuke Tomita ◽  
Yoko Yashiroda ◽  
Yasuhiro Matsuo ◽  
Jeff S Piotrowski ◽  
Sheena C Li ◽  
...  
Keyword(s):  
Fission Yeast ◽  
Mode Of Action ◽  
Mammalian Cells ◽  
Biological Activities ◽  
Genetic Determinants ◽  
Cellular Mechanisms ◽  
Plant Chemical Defense ◽  
Genome Wide ◽  
Plant Chemical ◽  
Yeast Mutants

Abstract Momilactone B is a natural product with dual biological activities, including antimicrobial and allelopathic properties, and play a major role in plant chemical defense against competitive plants and pathogens. The pharmacological effects of momilactone B on mammalian cells have also been reported. However, little is known about the molecular and cellular mechanisms underlying its broad bioactivity. In this study, the genetic determinants of momilactone B sensitivity in yeast were explored to gain insight into its mode of action. We screened fission yeast mutants resistant to momilactone B from a pooled culture containing genome-wide gene-overexpressing strains in a drug-hypersensitive genetic background. Overexpression of pmd1, bfr1, pap1, arp9, or SPAC9E9.06c conferred resistance to momilactone B. In addition, a drug-hypersensitive, barcoded deletion library was newly constructed and the genes that imparted altered sensitivity to momilactone B upon deletion were identified. Gene Ontology and fission yeast phenotype ontology enrichment analyses predicted the biological pathways related to the mode of action of momilactone B. The validation of predictions revealed that momilactone B induced abnormal phenotypes such as multiseptated cells and disrupted organization of the microtubule structure. This is the first investigation of the mechanism underlying the antifungal activity of momilactone B against yeast. The results and datasets obtained in this study narrow the possible targets of momilactone B and facilitate further studies regarding its mode of action.

scholarly journals Genome-wide Screens for Sensitivity to Ionizing Radiation Identify the Fission Yeast Nonhomologous End Joining Factor Xrc4

2014 ◽  
Vol 4 (7) ◽  
pp. 1297-1306 ◽  
Author(s):  
Jun Li ◽  
Yang Yu ◽  
Fang Suo ◽  
Ling-Ling Sun ◽  
Dan Zhao ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Fission Yeast ◽  
Nonhomologous End Joining ◽  
End Joining ◽  
Genome Wide

scholarly journals Functional Comparison of the Tup11 and Tup12 Transcriptional Corepressors in Fission Yeast

2005 ◽  
Vol 25 (2) ◽  
pp. 716-727 ◽  
Author(s):  
Fredrik Fagerström-Billai ◽  
Anthony P. H. Wright
Keyword(s):  
Gene Expression ◽  
Gene Duplication ◽  
Fission Yeast ◽  
Budding Yeast ◽  
Functional Difference ◽  
Evolutionary Mechanism ◽  
Genome Wide ◽  
Number Of Genes ◽  
Transcriptional Corepressors ◽  
Genome Wide Gene Expression

ABSTRACT Gene duplication is considered an important evolutionary mechanism. Unlike many characterized species, the fission yeast Schizosaccharomyces pombe contains two paralogous genes, tup11 + and tup12 + , that encode transcriptional corepressors similar to the well-characterized budding yeast Tup1 protein. Previous reports have suggested that Tup11 and Tup12 proteins play redundant roles. Consistently, we show that the two Tup proteins can interact together when expressed at normal levels and that each can independently interact with the Ssn6 protein, as seen for Tup1 in budding yeast. However, tup11 − and tup12 − mutants have different phenotypes on media containing KCl and CaCl2. Consistent with the functional difference between tup11 − and tup12 − mutants, we identified a number of genes in genome-wide gene expression experiments that are differentially affected by mutations in the tup11 + and tup12 + genes. Many of these genes are differentially derepressed in tup11 − mutants and are over-represented in genes that have previously been shown to respond to a range of different stress conditions. Genes specifically derepressed in tup12 − mutants require the Ssn6 protein for their repression. As for Tup12, Ssn6 is also required for efficient adaptation to KCl- and CaCl2-mediated stress. We conclude that Tup11 and Tup12 are at least partly functionally diverged and suggest that the Tup12 and Ssn6 proteins have adopted a specific role in regulation of the stress response.

scholarly journals Genome-wide screen for cell growth regulators in fission yeast

2017 ◽  
Vol 130 (12) ◽  
pp. 2049-2055 ◽  
Author(s):  
Louise Weston ◽  
Jessica Greenwood ◽  
Paul Nurse
Keyword(s):  
Cell Growth ◽  
Fission Yeast ◽  
Growth Regulators ◽  
Genome Wide

scholarly journals Target of rapamycin signaling mediates vacuolar fission caused by endoplasmic reticulum stress in Saccharomyces cerevisiae

2015 ◽  
Vol 26 (25) ◽  
pp. 4618-4630 ◽  
Author(s):  
Bobbiejane Stauffer ◽  
Ted Powers
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Intracellular Localization ◽  
Downstream Effectors ◽  
Genome Wide ◽  
Genetic Perturbations ◽  
Response To Stress ◽  
Induced Changes ◽  
Yeast Mutants

The yeast vacuole is equivalent to the mammalian lysosome and, in response to diverse physiological and environmental stimuli, undergoes alterations both in size and number. Here we demonstrate that vacuoles fragment in response to stress within the endoplasmic reticulum (ER) caused by chemical or genetic perturbations. We establish that this response does not involve known signaling pathways linked previously to ER stress but instead requires the rapamycin-sensitive TOR Complex 1 (TORC1), a master regulator of cell growth, together with its downstream effectors, Tap42/Sit4 and Sch9. To identify additional factors required for ER stress–induced vacuolar fragmentation, we conducted a high-throughput, genome-wide visual screen for yeast mutants that are refractory to ER stress–induced changes in vacuolar morphology. We identified several genes shown previously to be required for vacuolar fusion and/or fission, validating the utility of this approach. We also identified a number of new components important for fragmentation, including a set of proteins involved in assembly of the V-ATPase. Remarkably, we find that one of these, Vph2, undergoes a change in intracellular localization in response to ER stress and, moreover, in a manner that requires TORC1 activity. Together these results reveal a new role for TORC1 in the regulation of vacuolar behavior.

scholarly journals Genome-wide localization of pre-RC sites and identification of replication origins in fission yeast

2007 ◽  
Vol 26 (5) ◽  
pp. 1327-1339 ◽  
Author(s):  
Makoto Hayashi ◽  
Yuki Katou ◽  
Takehiko Itoh ◽  
Mitsutoshi Tazumi ◽  
Yoshiki Yamada ◽  
...  
Keyword(s):  
Fission Yeast ◽  
Replication Origins ◽  
Genome Wide

scholarly journals Genome-Wide Screening for Genes Associated with Valproic Acid Sensitivity in Fission Yeast

PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e68738 ◽  
Author(s):  
Lili Zhang ◽  
Ning Ma ◽  
Qingbin Liu ◽  
Yan Ma
Keyword(s):  
Valproic Acid ◽  
Fission Yeast ◽  
Acid Sensitivity ◽  
Genome Wide

scholarly journals RNA polymerase II-independent recruitment of SPT6L at transcription start sites in Arabidopsis

2019 ◽  
Vol 47 (13) ◽  
pp. 6714-6725 ◽  
Author(s):  
Chen Chen ◽  
Jie Shu ◽  
Chenlong Li ◽  
Raj K Thapa ◽  
Vi Nguyen ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Transcription Initiation ◽  
Elongation Factor ◽  
Proper Function ◽  
Gene Body ◽  
Transcription Start ◽  
Transcription Start Sites ◽  
Genome Wide ◽  
Yeast Mutants

Abstract SPT6 is a conserved elongation factor that is associated with phosphorylated RNA polymerase II (RNAPII) during transcription. Recent transcriptome analysis in yeast mutants revealed its potential role in the control of transcription initiation at genic promoters. However, the mechanism by which this is achieved and how this is linked to elongation remains to be elucidated. Here, we present the genome-wide occupancy of Arabidopsis SPT6-like (SPT6L) and demonstrate its conserved role in facilitating RNAPII occupancy across transcribed genes. We also further demonstrate that SPT6L enrichment is unexpectedly shifted, from gene body to transcription start site (TSS), when its association with RNAPII is disrupted. Protein domains, required for proper function and enrichment of SPT6L on chromatin, are subsequently identified. Finally, our results suggest that recruitment of SPT6L at TSS is indispensable for its spreading along the gene body during transcription. These findings provide new insights into the mechanisms underlying SPT6L recruitment in transcription and shed light on the coordination between transcription initiation and elongation.

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