Saccharomyces cerevisiae
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PROVIDER: PRJNA127777 | ENA |
REPOSITORIES: ENA
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Project description:The yeast Saccharomyces cerevisiae is able to adapt and in situ detoxify lignocellulose derived inhibitors such as furfural and HMF. The length of lag phase for cell growth in response to the inhibitor challenge has been used to measure tolerance of strain performance. Mechanisms of yeast tolerance at the genome level remain unknown. Using systems biology approache, this study investigated comparative transcriptome profiling, metabolic profiling, cell growth response and gene regulatory interactions of yeast strains and selective gene deletion mutations in response to HMF challenges during the lag phase of growth. Three hundred and sixty-five candidate genes were identified and found at least three significant components involving some of these genes that enable yeast adaptation and tolerance to HMF in yeast. First, functional enzyme coding genes such as ARI1, ADH6, ADH7 and OYE3, as well as gene interactions involved in the biotransformation and inhibitor detoxification were direct driving force to reduce HMF damages in cells. Expressions of these genes were regulated by YAP1 and its closely related regulons. Second, a large number of PDR genes, mainly regulated by PDR1 and PDR3, were induced during the lag phase and the PDR gene family-centered functions, including specific and multiple functions involving cellular transport such as TPO1, TPO4, RSB1, PDR5, PDR15, YOR1, and SNQ2, promoted cellular adaptation and survival in order to cope with the inhibitor stress. Third, expressed genes involving degradation of damaged proteins and protein modifications such as SHP1 and SSA4, regulated by RPN4, HSF1 and other co-regulators, were necessary for yeast cells to survive and adapt the HMF stress. A deletion mutation strainΔrpn4 was unable to recover the growth in the presence of HMF. Complex gene interactions and regulatory networks as well as co-regulations exist in yeast adaptation and tolerance to the lignocellulose derived inhibitor HMF. Both induced and repressed genes involving diversified functional categories are accountable for adaptation and energy rebalancing in yeast to survive and adapt the HMF stress during the lag phase of growth. Transcription factor genes YAP1, PDR1, PDR3, RPN4 and HSF1 appeared to play key regulatory rules for global adaptation in the yeast S. cerevisiae.
2010-12-31 | GSE22939 | GEO
Project description:The yeast Saccharomyces cerevisiae is able to adapt and in situ detoxify lignocellulose derived inhibitors such as furfural and HMF. The length of lag phase for cell growth in response to the inhibitor challenge has been used to measure tolerance of strain performance. Mechanisms of yeast tolerance at the genome level remain unknown. Using systems biology approache, this study investigated comparative transcriptome profiling, metabolic profiling, cell growth response and gene regulatory interactions of yeast strains and selective gene deletion mutations in response to HMF challenges during the lag phase of growth. Three hundred and sixty-five candidate genes were identified and found at least three significant components involving some of these genes that enable yeast adaptation and tolerance to HMF in yeast. First, functional enzyme coding genes such as ARI1, ADH6, ADH7 and OYE3, as well as gene interactions involved in the biotransformation and inhibitor detoxification were direct driving force to reduce HMF damages in cells. Expressions of these genes were regulated by YAP1 and its closely related regulons. Second, a large number of PDR genes, mainly regulated by PDR1 and PDR3, were induced during the lag phase and the PDR gene family-centered functions, including specific and multiple functions involving cellular transport such as TPO1, TPO4, RSB1, PDR5, PDR15, YOR1, and SNQ2, promoted cellular adaptation and survival in order to cope with the inhibitor stress. Third, expressed genes involving degradation of damaged proteins and protein modifications such as SHP1 and SSA4, regulated by RPN4, HSF1 and other co-regulators, were necessary for yeast cells to survive and adapt the HMF stress. A deletion mutation strain?rpn4 was unable to recover the growth in the presence of HMF. Complex gene interactions and regulatory networks as well as co-regulations exist in yeast adaptation and tolerance to the lignocellulose derived inhibitor HMF. Both induced and repressed genes involving diversified functional categories are accountable for adaptation and energy rebalancing in yeast to survive and adapt the HMF stress during the lag phase of growth. Transcription factor genes YAP1, PDR1, PDR3, RPN4 and HSF1 appeared to play key regulatory rules for global adaptation in the yeast S. cerevisiae. Cells were incubated on SC medium with HMF(30 mM) 6 h after pre-culture.Cultures grown under the same conditions without the HMF served as control. cells were harvested from 0, 10, 30, 60, 120 min, immediately frozen on dry ice, and then stored at -80 ?. Two replicated experiments were carried out for each condition. Total RNA was isolated by hot phenol method and purified using RNeasy Mini Kit. Genome microarray of S. cerevisiae was fabricated with a version of 70-mer oligo set representing 6,388 genes. A mini-array consisting of quality control genes was designed on the top of the target array. Cy5 labeled RNA at 0 time point was designated as a reference and Cy3 was used to label test samples. An equal amount of at least 30 pmol Cy3 and Cy5 labeling reaction was applied for hybridization. Hybridization was performed based on Hegde et al (2000) with modifications using HS 4800 Hybridization station.
2010-12-31 | E-GEOD-22939 | biostudies-arrayexpress
Project description:Adaptation to hydrogen peroxide in Saccharomyces cerevisiae is profiled with expression arrays. Adaptation describes the process in which a mild dose of toxin (in this case, hydrogen peroxide) is able to protect against a later acute dose. Here, we study two adaptive protocols (0.1 mM H2O2 and 0.1 + 0.4 mM H2O2) and one acute protocol (0.4 mM H2O2) to identify processes uniquely involved in adaptation. Predictions from these studies are validated in expression profiling of deletion mutants of the transcription factors Yap1, Mga2, and Rox1.
2009-04-23 | GSE12602 | GEO
Project description:Stress response pathways allow cells to rapidly sense and respond to deleterious environmental changes, including those caused by pathophysiological disease states. A previous screen for small molecules capable of activating the human heat shock response identified the triterpenoid celastrol as a potent activator of the heat shock transcription factor HSF1. We show here that celastrol likewise activates the homologous Hsf1 of Saccharomyces cerevisiae. Celastrol induced Hsf1 hyperphosphorylation and concurrently activated a synthetic transcriptional reporter as well as endogenous inducible Hsp70 proteins at the same effective concentration seen in mammalian cells. Moreover, celastrol treatment conferred significant resistance to subsequent lethal heat shock. Transcriptional profiling experiments revealed that in addition to Hsf1, celastrol treatment induced the Yap1-dependent oxidant defense regulon. Oxidative stress-responsive genes were likewise induced in mammalian cells, demonstrating that celastrol simultaneously activates two major cellular stress-mediating pathways. As the induction of cellular stress pathways has implications in the treatment of a variety of human diseases including neurodegenerative diosorders, cardiovascular disease and cancer, celastrol thus represents an attractive therapeutic compound. Keywords: single-dose, single time-point gene induction by natural small molecule celastrol compared to heat shock in wild type (BY4741) Saccahromyces cerevisiae
2006-08-26 | GSE5608 | GEO
Project description:In this study, we investigated the transcriptome of Bifidobacterium bifidum PRL2010 during in vitro growth by micro array technology. When B. bifidum PRL2010 was grown in liquid broth, 425 of the 1644 PRL2010 genes represented on the array were expressed in at least one of the three investigated growth phases, i.e., lag-, exponential and stationary phase. These transcriptional analyses identified a core in vitro transcriptome encompassing 150 genes, which resulted expressed in all phases. A proportion of the latter genes were further investigated as potential reference genes by Quantitative Real Time PCR (qRT-PCR) assays. Their expression stability was evaluated under different growth conditions, encompassing cultivation on different carbon sources, exposure to environmental stresses (thermal, acidic and osmotic) and growth phases. Our analyses validated six reference genes suitable for normalizing mRNA expression levels in qRT-PCR experiments applied to bifidobacteria. Transcriptional profiling of B.bifidum PRL2010 at different growth phases (lag phase, early exponential phase, late exponential phase, early stationary phase).
2012-01-05 | E-GEOD-30832 | biostudies-arrayexpress
Project description:Pv11 is an insect cell line established from Polypedilum vanderplanki with ability to survive complete desiccation if they were treated with trehalose. Previous studies showed contribution of HSF1 gene in this adaptation. To determine HSF1 regulatory network in Pv11 cells we prepared RNAseq libraries for wild type Pv11 (WT), HSF1 knoked out (Hsf1-/-), HSf1 resqued (Hsf1-/-; Hsf1-HaloTag/BlaR), and negative control for HSF1 resqued cells (Hsf1-/- HaloTag/BlaR) under normal conditions and under incubation with trehalose for 48 h. Comparison of mRNA profiles showed that HSF1 induced anhydrobiosis-related genes, especially LEA and TRX, but suppressed cellular process-related genes, for example transcription- and translation-related genes.
2021-05-28 | GSE171333 | GEO
Project description:Integrated omics analysis reveals metabolic adaptation of Clostridium thermocellum to lignocellulose-derived growth inhibitors released during the deconstruction of switchgrass
| MSV000080128 | MassIVE
Project description:The vertebrate paralogs Yap1 and Taz are well known Hippo pathway effectors playing a key regulatory process in growth, morphogenesis, cell survival and cancer progression. Upon translocation to the nucleus Yap/Taz interact with Tead proteins and regulate transcription through their conserved C-terminal activation domain. Here we describe yap1b a new teleost paralog of the Yap1/Taz family that evolved specifically in Euteleostei -the largest clade within vertebrates- by duplication and subsequent adaptation of yap1. In contrast, taz paralogs were progressively lost in the Euteleostei lineage. We show that yap1b displays a unique C-terminal transcriptional activation domain that cannot be phosphorylated by kinases of the Src/Yes family. Using DamID-seq, we obtained comparative maps of yap1 and yap1b occupancy in the medaka genome during early embryogenesis; as well as of yap1 and taz in the zebrafish embryo. Our analyses show that both medaka paralogs target a largely overlapping set of genes. To further understand yap1b role, we mutated it by CRISPR-Cas9 in medaka. Yap1b mutants do not display any overt phenotype during embryogenesis or adulthood. However, yap1b mutation strongly enhances the early embryonic malformations described for medaka yap1 mutants. Thus yap1-/- ; yap1b-/- double mutants display more severe body flattening, eye misshaping, and increased apoptosis than yap1-/- single mutants. This negative epistatic interaction indicates overlapping gene functions between yap1 and yap1b. Taken together, our results indicate that, despite its divergent C-terminal transactivation domain, the newly evolved paralog yap1b cooperates with yap1 in regulating cell survival and tissue morphogenesis during early development.
2019-06-01 | GSE120531 | GEO
Project description:The heat shock response is a universal transcriptional response to proteotoxic stress orchestrated by heat shock transcription factor Hsf1 in all eukaryotic cells. Despite over 40 years of intense research, the mechanism of HSF1 activity regulation remains poorly understood at a molecular level. In metazoa Hsf1 trimerizes upon heat shock through a leucin-zipper domain and binds to DNA. How Hsf1 is dislodged from DNA and monomerized remained enigmatic. Here, using purified proteins we demonstrate that unmodified trimeric Hsf1 is dissociated from DNA in vitro by Hsc70 and DnaJB1. Hsc70 binds to multiple sites in Hsf1 with different affinities. Hsf1 trimers are monomerized by successive cycles of entropic pulling, unzipping the triple leucinezipper. Starting this unzipping at several protomers of the Hsf1 trimer results in faster monomerization. This process directly monitors the concentration of Hsc70 and DnaJB1. During heat shock adaptation Hsc70 first binds to a high affinity site in the transactivation domain leading to partial attenuation of the response and subsequently, at higher concentrations, Hsc70 removes Hsf1 from DNA to restore the resting state.
2020-06-22 | PXD017406 | Pride
Project description:Yap1 targets under normal and cobalt surplus growth conditions. Yeast strains (wild-type and yap1 mutant, BY4742 background) were grown until early log-phase and either untreated or exposed to 2mM of CoSO4 for 60 min. Changes in the transcriptome of yap1 mutant cells were then analyzed.
2014-01-01 | E-MEXP-3874 | biostudies-arrayexpress