Msn2 controls the yeast metabolic focus
Ontology highlight
ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae
PROVIDER: GSE81890 | GEO | 2016/10/08
SECONDARY ACCESSION(S): PRJNA322860
REPOSITORIES: GEO
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Project description:We did transcription profiling on the effect of rlm1 (MAPK Slt2 transcription factor) deletion, slt2 (MAPK of Cell wall intregity pathway) deletion, bcy1 (Regulatory subunit of the cyclic AMP-dependent protein kinase (PKA)) deletion and msn2/4 (Stress-responsive transcriptional activators) deletion in genes involved in Caspofungin response (2 hours of treatment). In addition, we analyzed the genome-wide expression profile of the wild type strain in response to Aminocandin (2 hours of treatment).
2017-01-31 | GSE80394 | GEO
Project description:Transcriptional profiling of Msn2 regulated genes. Both strains are PKAas (TPK1M164G TPK2M147G TPK3M165G) and msn4-delta. One strain has Msn2 C-terminally tagged with mCherry and the other strain is msn2-delta. In this experiment, both strains were exposed to 3 uM 1-NM-PP1, which leads to Msn2 nuclear localization, for 0, 10, 20 and 40 min. The goal was to determine the genes that show a strong upregulation in the presence of Msn2, but no expression change in the absence of Msn2.
2013-10-12 | E-MTAB-1945 | biostudies-arrayexpress
Project description:The heat shock response is an ancient and ubiquitous program allowing organisms to survive adverse environmental conditions. In S. cerevisiae, three transcription factors, Hsf1, Msn2 and Msn4, are thought to regulate the stress response. While Msn2/4 can be deleted, Hsf1 is essential. By combining the depletion of Hsf1 with the deletion of Msn2 and Msn4, we were able to switch off the central stress response. We show that the transcription factors Hsf1 and Msn2/4 follow different strategies and regimes: Whereas Msn2/4 are responsible for a broad metabolic response, Hsf1 triggers a direct chaperone response to stabilize and repair unfolded proteins. Exposure of cells lacking Msn2/4 and Hsf1 to thermal stress resulted in massive protein aggregation. Comparison with wildtype yeast revealed that among the proteins rescued by the stress response are many essential proteins.
2024-01-31 | PXD024352 | Pride
Project description:Light controls control a vast array of biological processes, including cell and organelle motility, stress responses, organismal development and the entrainment of circadian rhythms, that maintain diurnal cycles of activity in organisms from cyanobacteria to humans. Recent studies indicate that a type of antioxidant and signaling proteins, peroxiredoxins, sustain circadian rhythms independent of characterized circadian pacemakers in organisms from all the three kingdoms of life, suggesting a role for H2O2 production in circadian clocks. Whereas many circadian clocks involve photosensitive pigments such as melanopsin and cryptochromes it is unclear whether peroxiredoxins can respond to light stimuli and how they interact with global signaling networks regulating e.g. clocks and aging, such as cyclic AMP (cAMP)/protein kinase A (PKA). In yeast, that lacks decidated photoreceptors, blue light induces cAMP-PKA-dependent, nuclear accumulation of a transcription factor, Msn2. However, the mechanism by which light represses pathway activity to stimulate Msn2 nuclear translocation is unknown. Here we identify increased H2O2–production via a conserved peroxisomal oxidase as the cause of light-induced Msn2 nuclear concentration. The H2O2 signal is transduced by the catalytic cysteines of the peroxiredoxin Tsa1 that relieve Msn2 from inhibitory PKA phosphorylation causing its nuclear accumulation. We propose that yeast senses light via H2O2 and a peroxiredoxin to inhibit cAMP/PKA activity and our data form a framework for the study of light responses in cells lacking dedicated light receptors and cAMP-controlled biological rhythms in multicellular organisms.
2018-07-03 | PXD001853 | Pride
Project description:The aim of this experiment was to determine, using MNAse-Seq, how nucleosomes get remodeled during an Msn2 activation timecourse genome-wide. Diploid strain EY2807/ASH79 with genotype TPK1M164G TPK2M147G TPK3M165G msn4::TRP1/LEU2 MSN2-mCherry NHP6a-iRFP::kanMX was used. This strain is PKAas, so upon addition of the inhibitor 1-NM-PP1, Msn2 translocates to the nucleus and activates gene expression. In this experiment, the diploid strain was exposed to 3 uM 1-NM-PP1 for 0, 5, 10, 20 and 40 min and nucleosome positions determined using by crosslinking, MNAse treatment, nucleosomal DNA purification and paired-end high-throughput sequencing (Illumina). Results from transcriptional profiling of yeast with or without Msn2 expression were also deposited at ArrayExpress under accession number E-MTAB-1945 ( https://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-1945/ ).
2013-10-12 | E-MTAB-1950 | biostudies-arrayexpress
Project description:Msn2-mediated nucleosome remodeling dynamics
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Project description:Exposure of Saccharomyces cerevisiae to alkaline pH represents a stress condition that generates a compensatory reaction. Here we examine a possible role of the protein kinase-A (PKA) pathway in this response. The phenotypic analysis reveals that mutations that activate the PKA pathway (ira1 ira2, bcy1) tend to cause sensitivity to alkaline pH, whereas its deactivation develops tolerance to this stress. We observe that alkalinization causes a transient decrease in cAMP, the main regulator of the pathway. Alkaline pH causes rapid nuclear localization of the PKA-regulated Msn2 transcription factor which, together with Msn4, mediates a general stress response by binding to STRE sequences in many promoters. Consequently, a synthetic STRE-LacZ reporter shows a rapid induction in response to alkaline stress. An msn2 msn4 mutant is sensitive to alkaline pH, and transcriptomic analysis reveals that after 10 minutes of alkaline stress, the expression of many induced genes (47%) depends, at least in part, on the presence of Msn2 and Msn4. Taken together, these results demonstrate that inhibition of the PKA pathway by alkaline pH represents a substantial part of the adaptive response to this kind of stress and that this response involves Msn2/Msn4-mediated gene remodeling. However, the relevance of attenuation of PKA in high pH tolerance is not restricted to regulation of Msn2 function. Eight samples were analyzed: WT and the MCY5278 mutant strain, lacking both Msn2 and Msn4, in the presence of 20 mM KOH (pH 8) and in the presence of 20 mM KCl (non-induced conditions) for 10 and 30 min of stress. 2 biological replicates were analyzed for each condition, and dye-swapping was carried out for each comparison of samples. We compared the expression profiles of: 1) WT +KOH vs. WT +KCl after 10 min 2) msn2 msn4 mutant +KOH vs. msn2 msn4 +KCl after 10 min 3)WT +KOH vs. WT +KCl after 30 min 4) msn2 msn4 mutant +KOH vs. msn2 msn4 +KCl after 30 min Total number of chips analyzed: 16.
2011-07-15 | E-GEOD-27925 | biostudies-arrayexpress
Project description:The pattern of gene transcription in Saccharomyces cerevisiae is strongly affected by the presence of glucose. An increased activity of protein kinase A (PKA), triggered by a rise in the intracellular concentration of cAMP, can account for many of the effects of glucose on transcription. To investigate the requirement of PKA for glucose control of gene expression, we have analyzed global transcription in strains devoid of PKA activity. In S. cerevisiae three genes, TPK1, TPK2, TPK3, encode catalytic subunits of PKA and the triple mutant tpk1 tpk2 tpk3 is unviable. We have worked, therefore, with two strains, tpk1 tpk2 tpk3 yak1 and tpk1 tpk2 tpk3 msn2 msn4, that bear suppressor mutations,. We have identified different classes of genes that can be induced, or repressed, by glucose in the absence of PKA. Among these genes, some are also controlled by a redundant signalling pathway involving PKA activation, while others do not respond to an increase in cAMP concentration. On the other hand, among genes which do not respond to glucose in the absence of PKA, some show a full response to increased cAMP levels, even in the absence of glucose, while others appear to require the cooperation of different signalling pathways. The goal of the present study was to investigate the occurrence of PKA-independent glucose signalling in S. cerevisiae. To this end, we have used global transcription analysis to study the effects of glucose on yeast strains completely devoid of PKA activity. In S. cerevisiae three genes TPK1, TPK2,and TPK3 encode catalytic subunits of PKA. While strains expressing only one of these genes grow normally, a triple null mutant (tpk1 tpk2 tpk3) is not viable (Toda et al 1987). Identification of different mutations able to suppress the growth defect of the triple mutant (Garrett and Broach 1989, Reinders et al 1998, Smith et al 1998) has allowed to determine what is the crucial function of PKA. As shown in Fig.1, PKA is needed to counteract the negative effect of the protein kinase Yak1 on yeast growth (Hartley et al 1994, Moriya et al 2001). In the presence of PKA the protein kinase Rim15 (Reinders et al 1998) and the transcription factors Msn2 and Msn4 (Görner et al 1998) can be phosphorylated and exported to the cytoplasm, transcription of the YAK1 gene, which is activated by Msn2/Msn4 (Smith et al 1998), is reduced, Yak1 levels remain low and growth is not hindered. In the absence of PKA, Rim15 remains in the nucleus where it can activate Msn2/Msn4 (Cameroni et al 2004) that turn on YAK1 transcription, thus blocking growth. This explains why strains lacking Rim15, Msn2/Msn4 or Yak1 no longer require PKA for growth. In this work we have used two isogenic strains lacking PKA and carrying the suppressor mutations msn2 msn4 or yak1. Two different suppressor mutants were used with the aim to enable a dissection of effects of the lack of PKA and effects of the suppressor mutations themselves.
2011-08-08 | E-GEOD-27541 | biostudies-arrayexpress
Project description:Exposure of Saccharomyces cerevisiae to alkaline pH represents a stress condition that generates a compensatory reaction. Here we examine a possible role of the protein kinase-A (PKA) pathway in this response. The phenotypic analysis reveals that mutations that activate the PKA pathway (ira1 ira2, bcy1) tend to cause sensitivity to alkaline pH, whereas its deactivation develops tolerance to this stress. We observe that alkalinization causes a transient decrease in cAMP, the main regulator of the pathway. Alkaline pH causes rapid nuclear localization of the PKA-regulated Msn2 transcription factor which, together with Msn4, mediates a general stress response by binding to STRE sequences in many promoters. Consequently, a synthetic STRE-LacZ reporter shows a rapid induction in response to alkaline stress. An msn2 msn4 mutant is sensitive to alkaline pH, and transcriptomic analysis reveals that after 10 minutes of alkaline stress, the expression of many induced genes (47%) depends, at least in part, on the presence of Msn2 and Msn4. Taken together, these results demonstrate that inhibition of the PKA pathway by alkaline pH represents a substantial part of the adaptive response to this kind of stress and that this response involves Msn2/Msn4-mediated gene remodeling. However, the relevance of attenuation of PKA in high pH tolerance is not restricted to regulation of Msn2 function.
2011-07-16 | GSE27925 | GEO
Project description:We did transcription profiling on the effect of msn2 msn4 deletion, genes involved in several stress process Keywords: cell wall stress response
2008-09-06 | GSE9934 | GEO