We hypothesized that broad-scale expression profiling would provide insight into the regulatory pathways that control gene expression in response to stress, and potentially identify novel heat-responsive genes. HEp2 cells were heated at 37 to 43 C for 60 min to gauge the heat shock response, using as a proxy inducible HSP-70 quantified by western blot analysis. Based on these results, microarray experiments were conducted at 37, 40, 41, 42 and 43C (3 replicates/temperature x 5 groups = 15 U95Aver2 GeneChips). Using linear modeling, we compared the sets of microarrays at 40, 41, 42 and 43C with the 37C baseline temperature and took the union of the genes exhibiting differential gene expression signal to create two sets of heat shock response genes, each set reflecting either increased or decreased RNA abundance. Leveraging human and mouse orthologous alignments, we used the two lists of co-expressed genes to predict transcription factor binding sites in silico, including those for heat shock factor 1 (HSF1) and heat shock factor 2 (HSF2) transcription factors. We discovered HSF1 and HSF2 binding sites in 15 genes not previously associated with the heat shock response. We conclude that microarray experiments coupled with upstream promoter analysis can be used to identify novel genes that respond to heat shock. Additional experiments are required to validate these putative heat shock proteins and facilitate a deeper understanding of the mechanisms involved during the stress response.
Transcriptional profiles of human epithelial cells in response to heat: computational evidence for novel heat shock proteins.
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View SamplesIn the exon array data set, gene level analysis was performed on HepG2 cells exposed to atorvastatin.
RNA-sequencing analysis of HepG2 cells treated with atorvastatin.
Cell line
View SamplesHydrogen peroxide (H2O2) can act as a signaling molecule that influences various aspects of plant growth and development, including stress signaling and cell death. Catalase deficient plants are pioneering systems which accumulate hydrogen peroxide (H2O2) from peroxisomal origin during photorespiratory challenges. Respiratory burst oxidase homologues D and F are known to participate in intracellular oxidative stress response launched in cat2 mutants (Chaouch et al., 2012). We studied the compared the transcriptional response of cat2 rbohD and cat2 rbohF double mutants versus the cat2 background to further adress their role during photorespiratory stress.
The ROS Wheel: Refining ROS Transcriptional Footprints.
Age
View SamplesWe report the profiling of induced mRNA transcripts in two C. elegan replicate populations -- WT (N2) and mutant strain with deficient HLH30. Both strains were fed either OP50 strain of e-coli (normal feed) or S. aureus Overall design: Examination of infected versus uninfected wildtype and mutant lawns of animals
Innate host defense requires TFEB-mediated transcription of cytoprotective and antimicrobial genes.
Subject
View SamplesHydrogen peroxide (H2O2) is a potent signaling molecule influencing various aspects of plant growth and development. Its limited lifetime and specific production sites in the plant cell necessitate the existence of specialized mechanisms that relay H2O2-encoded information. To discover such mechanisms, we focused on peroxisomal H2O2 production triggered by enhanced photorespiration in Arabidopsis mutants lacking catalase activity (cat2-2), and looked for second-site mutations that attenuate the negative effects (Fv'/Fm' decline and lesion formation) of H2O2 build up. A mutation residing in the GRAS family transcriptional regulator SHORT-ROOT (SHR) was found to underlie the increased performance of cat2-2 knock-outs under photorespiratory stress. In contrast to shr, introduction of the scr mutation in cat2-2 background did not improve the photorespiratory performance of plants lacking peroxisomal catalase. The absence of SHR negatively affected the activity of the photorespiratory enzymes glycolate oxidase and catalase, which was accompanied with elevated glycolate content and inability to accumulate glycine under conditions promoting photorespiration. The transcriptome signature of cat2-2 shr-6 double mutants exposed to photorespiratory stress lacked jasmonate-dependent signaling components, otherwise induced in cat2-2. The photorespiratory phenotype of cat2-2 was found to be modulated by exogenous sugars both in the presence and absence of shr. Taken together, these findings highlight a crucial role for SHR in H2O2 signal transduction and stress tolerance.
The ROS Wheel: Refining ROS Transcriptional Footprints.
Age, Specimen part, Treatment, Time
View SamplesSix weeks old Arabidopsis plants were transferred to a low CO2 (100 ppm) environment during 24 hours and compared to control plants kept under ambient CO2 conditions. Limited CO2 availability will cause higher rates of photorespiration and affect the plant redox homeostasis. We studied the transcriptomic impact of exposing plants to a lower CO2 environment to further eliculidate the signaling pathways during photorespiratory stress.
The ROS Wheel: Refining ROS Transcriptional Footprints.
Age, Treatment
View SamplesExcessive levels of reactive oxygen species (ROS) cause cellular stress through damage to all classes of macromolecules and result in cell death. However, ROS can also act as signaling molecules in various biological processes. In plants, ROS signaling has been documented in environmental stress perception, plant development and cell death amongst others. Knowledge on the regulatory events governing ROS signal transduction is however still scratching the surface. To further elucidate the transcriptional response and regulation upon ROS accumulation we supplemented Arabidopsis seedlings with a 10mM hydrogen peroxide (H2O2) solution to trigger oxidative stress.
The ROS Wheel: Refining ROS Transcriptional Footprints.
Age, Specimen part
View SamplesA genetic association between the ANP32A gene and osteoarthritis has been suggested. We compared transcriptome profiles of the articular cartilage and subchondral bone from mice deficient in ANP32A with wild-type mice to get insights into the role of ANP32A in the pathogenesis of ostearthritis.
ANP32A regulates ATM expression and prevents oxidative stress in cartilage, brain, and bone.
Age, Specimen part
View SamplesDietary restriction (DR) extends lifespan in a wide variety of species, yet the underlying mechanisms are not well understood. Here we show that the Caenorhabditis elegans HNF4a-related nuclear hormone receptor NHR-62 is required for metabolic and physiologic responses associated with DR-induced longevity. nhr-62 mediates the longevity of eat-2 mutants, a genetic mimetic of dietary restriction, and blunts the longevity response of DR induced by bacterial food dilution at low nutrient levels. Metabolic changes associated with DR, including decreased Oil Red O staining, decreased triglyceride levels, and increased autophagy are partly reversed by mutation of nhr-62. Additionally, the DR fatty acid profile is altered in nhr-62mutants. Expression profiles reveal that several hundred genes induced by DR depend on the activity of NHR-62, including a putative lipase required for the DR response. This study provides critical evidence of nuclear hormone receptor regulation of the DR longevity response, suggesting hormonal and metabolic control of life span. Overall design: Young adult worms before bearing eggs inside were collected. N2 serves as the control of wild type. 3 biological replicates included in this experiment.
Dietary restriction induced longevity is mediated by nuclear receptor NHR-62 in Caenorhabditis elegans.
Subject
View SamplesSmall RNAs (sRNA) that act by base pairing with trans-encoded mRNAs modulate metabolism in response to a variety of environmental stimuli. Here, we describe an Hfq-binding sRNA (FnrS) whose expression is induced upon a shift from aerobic to anaerobic conditions and which acts to down regulate the levels of a variety of mRNAs encoding metabolic enzymes. Anaerobic induction in minimal medium depends strongly on FNR but is also affected by ArcA and CRP. Whole genome expression analysis showed that the levels of at least 32 mRNAs are down regulated upon FnrS overexpression, 15 of which are predicted to base pair with FnrS by TargetRNA. The sRNA is highly conserved across its entire length in numerous enterobacteria, and mutation analysis revealed that two separate regions of FnrS base pair with different sets of target mRNAs. The majority of the target genes previously reported to be down regulated in an FNR-dependent manner lack recognizable FNR binding sites. We thus suggest that FnrS extends the FNR regulon and increases the efficiency of anaerobic metabolism by repressing the synthesis of enzymes that are not needed under these conditions.
Reprogramming of anaerobic metabolism by the FnrS small RNA.
No sample metadata fields
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