Transcriptional responses to isobutanol in Saccharomyces cerevisiae wild type and gln3 deletion strains
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Illumina MiSeq
ORGANISM(S): Saccharomyces cerevisiae
SUBMITTER: José Avalos
PROVIDER: E-MTAB-8175 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:To estimate the function of Avin_01720, we performed RNA-seq experiments to compare the transcriptomic profiles of wild type and ΔAvin_01720 strains grown in MB medium without a nitrogen source at 20% oxygen.
2022-04-25 | E-MTAB-10712 | biostudies-arrayexpress
Project description:To identify genes showing oxygen concentration-dependent expression only under nitrogen-fixing conditions, we performed RNA-seq experiments to compare the transcriptomic profiles of wild type cultured in six different conditions where under the MB medium with or without a nitrogen source at 5%, 10%, or 20% oxygen concentrations.
2022-04-25 | E-MTAB-10710 | biostudies-arrayexpress
Project description:A universal feature of the response to stress and nutrient limitation is transcriptional upregulation of genes encoding proteins important for survival. Interestingly, under many of these conditions overall protein synthesis levels are reduced, thereby dampening the stress response at the level of protein expression. For example, during glucose starvation in yeast, translation is rapidly and reversibly repressed, yet transcription of many stress- and glucose-repressed genes is increased. Using ribosome profiling and microscopy, we found that this transcriptionally upregulated gene set consists of two classes: (1) one producing mRNAs that are preferentially translated during glucose limitation and are diffusely localized in the cytoplasm – this class includes many heat shock protein mRNAs; and (2) another producing mRNAs that are poorly translated during glucose limitation, have high rates of translation initiation, and are concentrated in foci that co-localize with P bodies and stress granules – this class is enriched for glucose metabolism mRNAs. Remarkably, the information specifying differential localization and translation of these two classes of mRNAs is encoded in the promoter sequence – promoter responsiveness to heat shock factor (Hsf1) specifies diffuse cytoplasmic localization and preferential translation upon glucose starvation, whereas different promoter elements upstream of genes encoding poorly translated glucose metabolism mRNAs direct these mRNAs to RNA granules under glucose starvation. Thus, promoter sequences and transcription factor binding can influence not only mRNA levels, but also subcellular localization of mRNAs and the efficiency with which they are translated, enabling cells to tailor protein production to environmental conditions. Examination of mRNA translation in S. cerevisiae upon glucose starvation.
2014-07-28 | E-GEOD-56622 | biostudies-arrayexpress
Project description:CHD8, encoding Chromodomain helicase DNA binding protein 8, is a top autism spectrum disorders (ASDs) risk gene. To better understanding the molecular links between CHD8 functions and ASD, we have applied the CRISPR/Cas9 technology to knockout one copy of CHD8 in induced pluripotent stem cells (iPSCs) to mimic the loss of function status that would exist in the developing human embryo prior to neuronal differentiation. Transcriptome profiling (RNA-seq) in neural progenitors and early differentiating neurons revealed that CHD8 hemizygosity (CHD8+/-) affected the expression of several thousands of genes, enriched for functions of neural development, β-catenin/Wnt signaling, extracellular matrix, and skeletal system development. Moreover, CHD8 regulates multiple genes implicated in ASD, schizophrenia and genes associated with brain volume. iPSCs derived from a healthy subject were transduced with CRISPR/Cas9 vectors with single guide RNA sequences to target the N-terminal of CHD8 protein to generate truncated mutation seach of the two target sequences. Two clones, one with a 2-bp (KO1) and the other with a 10-bp (KO2) heterozygous deletion were found.The CHD8+/- iPSC lines were used to generate NPCs and early differentiating neurons for RNA-seq analysis, together with samples prepared from the parental clones, for a total of 8 samples (two biological replicates of wild-type (WT) and CHD8+/- at two neurodevelopmental stages).
2015-11-05 | E-GEOD-71594 | biostudies-arrayexpress
Project description:The oomycete pathogen Phytophthora sojae causes root rot of soybean. During infection, the pathogen is thought to deliver dozens, if not hundreds, of effector proteins into the host to manipulate intracellular systems. Although these pathogen proteins often exhibit similar N-terminal delivery domains, the remaining effector region is rarely homologous to known protein domains, making it difficult to predict its biochemical function during infection. As a complement to studies in the natural host, Saccharomyces cerevisiae has been successfully used as a model system to explore the biochemical function of individual pathogen effectors. The presumption is that many effectors target conserved eukaryotic pathways in the host and consequently the expression of effectors in yeast will confer corresponding phenotypes. Indeed, putative effector functions identified using yeast functional genomic approaches have subsequently been validated in the natural host. Over-expression of the Phytophthora sojae effector Avh172 (PsAvh172) inhibits the growth of Saccharomyces cerevisiae, suggesting that the effector targets a biological pathway conserved with plants. In this study, the transcriptomes of yeast expressing PsAvh172 or an empty vector were compared to examine the global transcriptional response, in hopes of discerning the effectors biochemical target.
2021-01-01 | E-MTAB-4682 | biostudies-arrayexpress
Project description:Oncogene-induced senescence (OIS) and therapy-induced senescence (TIS), while tumor-suppressive, also promote procarcinogenic effects by activating the DNA damage response (DDR), which in turn induces inflammation. This inflammatory response prominently includes an array of cytokines known as the senescence-associated secretory phenotype (SASP). Previous observations link the transcription-associated methyltransferase and oncoprotein MLL1 to the DDR, leading us to investigate the role of MLL1 in SASP expression. Our findings reveal direct MLL1 epigenetic control over proproliferative cell cycle genes: MLL1 inhibition represses expression of proproliferative cell cycle regulators required for DNA replication and DDR activation, thus disabling SASP expression. Strikingly, however, these effects of MLL1 inhibition on SASP gene expression do not impair OIS and, furthermore, abolish the ability of the SASP to enhance cancer cell proliferation. More broadly, MLL1 inhibition also reduces âÂÂSASP-likeâ inflammatory gene expression from cancer cells in vitro and in vivo independently of senescence. Taken together, these data demonstrate that MLL1 inhibition may be a powerful and effective strategy for inducing cancerous growth arrest through the direct epigenetic regulation of proliferation-promoting genes and the avoidance of deleterious OIS- or TIS-related tumor secretomes, which can promote both drug resistance and tumor progression. This study consists of a single replicate of RNA-seq from oncogene-induced senescent (or control) IMR90 cells in a MLL1 knockdown (or WT) background, for a total of four samples
2016-02-23 | E-GEOD-78138 | biostudies-arrayexpress
Project description:In Drosophila, Polycomb Response Elements (PREs) are identified as genomic sequences allowing the maintenance of transcriptional repression in the absence of the initiating signal. Although PREs in Drosophila are well characterized, the existence of mammalian PRE-like elements remains debated. Accumulating evidence supports a model in which CpG islands function to recruit Polycomb-Group complexes (PcG), however, it is not evident which subclasses of CpG islands serve as PREs. Trithorax (Trx), which is required for positive regulation of gene expression in Drosophila, is known to co-bind Drosophila PREs where it is thought to antagonize polycomb-dependent silencing of nearby genes. Here, we demonstrate the existence of Trx-dependent H3K4 dimethylation loci that specifically mark Drosophila PREs and are required for the maintenance of expression of the nearby genes. Similarly, in human cells, we find ~ 3000 MLL1 (human Trx homologue)-dependent H3K4 dimethylation loci, which correlate strongly with CpG island density. In the absence of MLL1 and H3K4 dimethylation at these loci, there is an increase in H3K27 trimethylation levels, suggesting these sites can recruit Polycomb Repressive Complex 2 (PRC2). By inhibiting PRC2-dependent silencing in the absence of MLL1, we establish that a balance exists between MLL1 and PRC2, and their respective capacity to maintain or repress transcription. Thus, by investigating a conserved function between Trx and MLL1, we provide rules for the identification of CpG island subclasses serving as PRE-like sequences within the human genome. To examine changes in histone-modification profiles and gene expression after depletion of Trx in Drosophila S2 cells, and MLL1 in human HCT116 cells. We also treated MLL1-NULL HCT116 cells with GSK126 (5uM) for 4 days and measured changes in gene expression.
2016-07-26 | E-GEOD-81795 | biostudies-arrayexpress
Project description:The KDM6 histone demethylases (UTX/KDM6A and JMJD3/KDM6B) mediate removal of repressive histone H3K27me3 marks to establish transcriptionally permissive chromatin. Loss of UTX in female mice is embryonic lethal. Unexpectedly, male UTX-null mice escape embryonic lethality due to expression of UTY, a paralog lacking H3K27-demethylase activity. This suggests that UTX plays an enzyme-independent role in development, and challenges the need for active H3K27-demethylation in vivo. However, the requirement for active H3K27-demethylation in stem cell-mediated tissue regeneration remains untested. Using an inducible mouse knockout that ablates UTX in satellite cells, we show that active H3K27-demethylation is necessary for muscle regeneration. Indeed, loss of UTX in satellite cells blocks myofiber regeneration in both male and female mice. Furthermore, we demonstrate that UTX mediates muscle regeneration through its H3K27-demethylase activity using a chemical inhibitor, and a demethylase-dead UTX knock-in mouse. Mechanistically, dissection of the muscle regenerative process revealed that UTX is required for expression of the transcription factor Myogenin that drives differentiation of muscle progenitors. Thus, we have identified a critical role for the enzymatic activity of UTX in activating muscle-specific gene expression during myofiber regeneration, revealing for the first time that active H3K27-demethylation has a physiological role in vivo. Satellite cells were sorted based on Cre-dependent expression of TdT reporter gene. Sorted UTXmKO or UTX WT satellite cells were then induced to differentiate for 24 hrs. RNA was then isolated and subjected to RNA-Seq analysis.
2016-03-22 | E-GEOD-69968 | biostudies-arrayexpress
Project description:This experiments follows up ChIPseq experiments and aims to investigate the role of Rad50 on gene expression in drosophila larval stage 3 CNS.
2023-12-01 | E-MTAB-13490 | biostudies-arrayexpress
Project description:Metabolic production of acetyl-CoA has been linked to histone acetylation and gene regulation, however the mechanisms are largely unknown. We show that the metabolic enzyme acetyl-CoA synthetase 2 (ACSS2) is a critical and direct regulator of histone acetylation in neurons and of long-term mammalian memory. We observe increased nuclear ACSS2 in differentiating neurons in vitro. Genome-wide, ACSS2 binding corresponds with increased histone acetylation and gene expression of key neuronal genes. These data indicate that ACSS2 functions as a chromatin-bound co-activator to increase local concentrations of acetyl-CoA and to locally promote histone acetylation for transcription of neuron-specific genes. Remarkably, in vivo attenuation of hippocampal ACSS2 expression in adult mice impairs long-term spatial memory, a cognitive process reliant on histone acetylation. ACSS2 reduction in hippocampus also leads to a defect in upregulation of key neuronal genes involved in memory. These results reveal a unique connection between cellular metabolism and neural plasticity, and establish a link between generation of acetyl-CoA and neuronal chromatin regulation. Global survey of gene expression in CAD cells and differentiated CAD neurons following lentiviral knockdown of ACSS2 or ATP citrate lyase (ACL) (and control = scramble hairpin); survey of hippocampal gene expression changes associated with retrieval of fear memory, after ACSS2-AAV knockdown or in EGFP-AAV control (comparison of 0h vs. 1h post-memory retrieval).
2017-05-01 | E-GEOD-76853 | biostudies-arrayexpress