scholarly journals Gene Expression Profiling ofClostridium botulinumunder Heat Shock Stress

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Wan-dong Liang ◽  
Yun-tian Bi ◽  
Hao-yan Wang ◽  
Sheng Dong ◽  
Ke-shen Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heat Shock ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Environmental Changes ◽  
Expression Patterns ◽  
Trna Synthetase ◽  
Ph Change ◽  
Heat Shock Stress ◽  
Shock Stress

During growth,C. botulinumis always exposed to different environmental changes, such as temperature increase, nutrient deprivation, and pH change; however, its corresponding global transcriptional profile is uncharacterized. This study is the first description of the genome-wide gene expression profile ofC. botulinumin response to heat shock stress. Under heat stress (temperature shift from 37°C to 45°C over a period of 15 min), 176C. botulinumATCC 3502 genes were differentially expressed. The response included overexpression of heat shock protein genes (dnaKoperon,groESL,hsp20,andhtpG) and downregulation of aminoacyl-tRNA synthetase genes (valS,queA,tyrR, andgatAB) and ribosomal and cell division protein genes (ftsZandftsH). In parallel, several transcriptional regulators (marR,merR, andompRfamilies) were induced, suggesting their involvement in reshuffling of the gene expression profile. In addition, many ABC transporters (oligopeptide transport system), energy production and conversion related genes (glpAandhupL), cell wall and membrane biogenesis related genes (fabZ,fabF, andfabG), flagella-associated genes (flhA,flhM,flhJ,flhS, andmotAB), and hypothetical genes also showed changed expression patterns, indicating that they may play important roles in survival under high temperatures.

scholarly journals Direct link between metabolic regulation and the heat-shock response through the transcriptional regulator PGC-1α

2015 ◽  
Vol 112 (42) ◽  
pp. E5669-E5678 ◽  
Author(s):  
Neri Minsky ◽  
Robert G. Roeder
Keyword(s):  
Gene Expression ◽  
Stress Response ◽  
Heat Shock ◽  
Metabolic Regulation ◽  
Hormone Receptors ◽  
Transcriptional Networks ◽  
Direct Link ◽  
Heat Shock Stress ◽  
Metabolic Genes ◽  
Shock Stress

In recent years an extensive effort has been made to elucidate the molecular pathways involved in metabolic signaling in health and disease. Here we show, surprisingly, that metabolic regulation and the heat-shock/stress response are directly linked. Peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), a critical transcriptional coactivator of metabolic genes, acts as a direct transcriptional repressor of heat-shock factor 1 (HSF1), a key regulator of the heat-shock/stress response. Our findings reveal that heat-shock protein (HSP) gene expression is suppressed during fasting in mouse liver and in primary hepatocytes dependent on PGC-1α. HSF1 and PGC-1α associate physically and are colocalized on several HSP promoters. These observations are extended to several cancer cell lines in which PGC-1α is shown to repress the ability of HSF1 to activate gene-expression programs necessary for cancer survival. Our study reveals a surprising direct link between two major cellular transcriptional networks, highlighting a previously unrecognized facet of the activity of the central metabolic regulator PGC-1α beyond its well-established ability to boost metabolic genes via its interactions with nuclear hormone receptors and nuclear respiratory factors. Our data point to PGC-1α as a critical repressor of HSF1-mediated transcriptional programs, a finding with possible implications both for our understanding of the full scope of metabolically regulated target genes in vivo and, conceivably, for therapeutics.

scholarly journals Protein Expression Profiles of Chlamydia pneumoniae in Models of Persistence versus Those of Heat Shock Stress Response

2006 ◽  
Vol 74 (7) ◽  
pp. 3853-3863 ◽  
Author(s):  
Sanghamitra Mukhopadhyay ◽  
Richard D. Miller ◽  
Erin D. Sullivan ◽  
Christina Theodoropoulos ◽  
Sarah A. Mathews ◽  
...  
Keyword(s):  
Stress Response ◽  
Heat Shock ◽  
Protein Expression ◽  
Chlamydia Pneumoniae ◽  
Expression Profiles ◽  
Stress Component ◽  
Expression Patterns ◽  
Heat Shock Stress ◽  
Shock Stress

ABSTRACT Chlamydia pneumoniae is an obligate intracellular pathogen that causes both acute and chronic human disease. Several in vitro models of chlamydial persistence have been established to mimic chlamydial persistence in vivo. We determined the expression patterns of 52 C. pneumoniae proteins, representing nine functional subgroups, from the gamma interferon (IFN-γ) treatment (primarily tryptophan limitation) and iron limitation (IL) models of persistence compared to those following heat shock (HS) at 42°C. Protein expression patterns of C. pneumoniae persistence indicates a strong stress component, as evidenced by the upregulation of proteins involved in protein folding, assembly, and modification. However, it is clearly more than just a stress response. In IFN persistence, but not IL or HS, amino acid and/or nucleotide biosynthesis proteins were found to be significantly upregulated. In contrast, proteins involved in the biosynthesis of cofactors, cellular processes, energy metabolism, transcription, and translation showed an increased in expression in only the IL model of persistence. These data represent the most extensive protein expression study of C. pneumoniae comparing the chlamydial heat shock stress response to two models of persistence and identifying the common and unique protein level responses during persistence.

Ischemic but not pharmacological preconditioning elicits a gene expression profile similar to unprotected myocardium

2004 ◽  
Vol 20 (1) ◽  
pp. 117-130 ◽  
Author(s):  
Rafaela da Silva ◽  
Eliana Lucchinetti ◽  
Thomas Pasch ◽  
Marcus C. Schaub ◽  
Michael Zaugg
Keyword(s):  
Gene Expression ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Ischemia Reperfusion ◽  
Expression Patterns ◽  
Principal Component ◽  
Gene Clusters ◽  
Stable Gene ◽  
Transcriptional Responses ◽  
Rat Hearts

Pharmacological (PPC) and ischemic preconditioning (IschPC) provide comparable protection against ischemia in the heart. However, the genomic phenotype may depend on the type of preconditioning. Isolated perfused rat hearts were used to evaluate transcriptional responses to PPC and IschPC in the presence (mediator/effector response) or absence (trigger response) of 40 min of test ischemia using oligonucleotide microarrays. IschPC was induced by 3 cycles of 5 min of ischemia, and PPC by 15 min of 2.1 vol% isoflurane. Unsupervised analysis methods were used to identify gene expression patterns. PPC and IschPC were accompanied by marked alterations in gene expression. PPC and IschPC shared only ∼25% of significantly up- and downregulated genes after triggering. The two types of preconditioning induced a more uniform genomic response after ischemia/reperfusion. Numerous genes separated preconditioned from unprotected ischemic hearts. Three stable gene clusters were identified in the trigger response to preconditioning, while eight stable clusters related to cytoprotection, inflammation, remodeling, and long interspersed nucleotide elements (LINEs) were delineated after prolonged ischemia. A single stable sample cluster emerged from cluster analysis for both IschPC and unprotected myocardium, indicating a close molecular relationship between these two treatments. Principal component analysis revealed differences between PPC vs. IschPC, and trigger vs. mediator/effector responses in transcripts predominantly related to biosynthesis and apoptosis. IschPC and PPC similarly but distinctly reprogram the genetic response to ischemic injury. IschPC elicits a postischemic gene expression profile closer to unprotected myocardium than PPC, which may be therefore more advantageous as therapeutic strategy in cardioprotection.

scholarly journals The Hsp70 chaperone is a major player in stress-induced transposable element activation

2019 ◽  
Vol 116 (36) ◽  
pp. 17943-17950 ◽  
Author(s):  
Ugo Cappucci ◽  
Fabrizia Noro ◽  
Assunta Maria Casale ◽  
Laura Fanti ◽  
Maria Berloco ◽  
...  
Keyword(s):  
Heat Shock ◽  
Germ Cells ◽  
Environmental Changes ◽  
Small Noncoding Rnas ◽  
Heat Shock Stress ◽  
Major Player ◽  
Chaperone Complex ◽  
Consequent Increase ◽  
Posttranscriptional Level ◽  
Shock Stress

Previous studies have shown that heat shock stress may activate transposable elements (TEs) in Drosophila and other organisms. Such an effect depends on the disruption of a chaperone complex that is normally involved in biogenesis of Piwi-interacting RNAs (piRNAs), the largest class of germline-enriched small noncoding RNAs implicated in the epigenetic silencing of TEs. However, a satisfying picture of how chaperones could be involved in repressing TEs in germ cells is still unknown. Here we show that, in Drosophila, heat shock stress increases the expression of TEs at a posttranscriptional level by affecting piRNA biogenesis through the action of the inducible chaperone Hsp70. We found that stress-induced TE activation is triggered by an interaction of Hsp70 with the Hsc70−Hsp90 complex and other factors all involved in piRNA biogenesis in both ovaries and testes. Such interaction induces a displacement of all such factors to the lysosomes, resulting in a functional collapse of piRNA biogenesis. This mechanism has clear evolutionary implications. In the presence of drastic environmental changes, Hsp70 plays a key dual role in increasing both the survival probability of individuals and the genetic variability in their germ cells. The consequent increase of genetic variation in a population potentiates evolutionary plasticity and evolvability.

Gene-expression signatures as prognostic for relapse in stage I testicular germ cell tumors (TGCT).

2016 ◽  
Vol 34 (2_suppl) ◽  
pp. 493-493
Author(s):  
Jeremy Howard Lewin ◽  
Philippe L. Bedard ◽  
Robert James Hamilton ◽  
Peter W. M. Chung ◽  
Malcolm J. Moore ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Profile ◽  
Hierarchical Clustering ◽  
Expression Profile ◽  
Expression Patterns ◽  
Rna Extraction ◽  
Germ Cell Tumors ◽  
Gene Expression Pattern ◽  
Stage I ◽  
Testicular Germ Cell

493 Background: Genomic signatures may compliment pathological features in identifying appropriate patients who may benefit from adjuvant therapy in Stage I (SI) TGCT. This study aimed to identify a gene expression pattern to differentiate between relapsed (R) and non-relapsed (NR) SI TGCT. Methods: Patients with SI non-seminoma (NS) and seminoma (S) were identified from an institutional database from 2000 to 2012. All patients were managed with active surveillance. NR-NS and NR-S patients were defined as having no evidence of relapse after 2 and 3 years of surveillance respectively. Following pathology review, RNA extraction and gene expression analysis was performed on archived paraffin embedded tumor and normal testicular tissue using Illumina Whole Genome DASL Human HT-12 V4 BeadChip. Hierarchical clustering analysis, ANOVA and t-tests were used to evaluate candidate genes and expression patterns that could differentiate NR and R samples. Results: 57 patients (12 R-NS, 15 R-S, 15 NR-NS, 15 NR-S) were identified with median relapse time of 5.6 (2.5-18.1) and 19.3 (4.7-65.3) months in NS and S cohorts respectively. 3 additional normal testis samples were included. Poor prognostic factors were more frequent in R versus NR cases (NS: vascular invasion [5/12 vs 0/15]; S: median size [4cm vs 2.8cm]). Unsupervised hierarchical clustering of 22822 probes randomly separated S from NS, indicating no batch effect. One-way ANOVA revealed 4525 significantly varying probes (p < 0.05) however, no statistically significant gene expression profile differentiated the 4 cohorts. A discriminative gene expression profile between R and NR cases was discovered when combining NS and S samples using 10 (p = 0.03) and 30 (p = 0.03) probe signatures with a 10 fold cross-validation. However, this profile was not observed in the S and NS cohorts individually. Conclusions: A discriminating signature for R and NR was identified for SI testis tumors, but not separately for NS and S. Biological relevance of these signatures is to be determined. Further studies are required to corroborate this profile in NS and S. If validated, these expression patterns could help identify patients beyond standard pathological risk algorithms for optimal management.

scholarly journals Survival protection mechanisms and genetic variability induction after stress: two sides of the same Hsp70 coin

2018 ◽  
Author(s):  
Ugo Cappucci ◽  
Fabrizia Noro ◽  
Assunta Maria Casale ◽  
Laura Fanti ◽  
Maria Berloco ◽  
...  
Keyword(s):  
Heat Shock ◽  
Genetic Variability ◽  
Environmental Changes ◽  
Decisive Role ◽  
Transcriptional Level ◽  
Heat Shock Stress ◽  
Chaperone Complex ◽  
Chaperone Hsp70 ◽  
Shock Stress

AbstractPrevious studies have shown that heat shock stress may increase transcription levels and, in some cases, also the transposition of certain transposable elements (TEs) in Drosophila and other organisms. Other studies have also demonstrated that heat shock chaperones as Hsp90 and Hop are involved in repressing transposon’s activity in Drosophila melanogaster by their involvement in crucial steps of the biogenesis of Piwi-interacting RNAs (piRNAs), the largest class of germline-enriched small non-coding RNA implicated in the epigenetic silencing of TEs. However, a satisfying picture of how many chaperones and their respective functional roles could be involved in repressing transposons in germ cell is still unknown. Here we show that in Drosophila heat shock activates transposon′s expression at post-transcriptional level by disrupting a repressive chaperone complex by a decisive role of the stress-inducible chaperone Hsp70. We found that stress-induced transposons activation is triggered by an interaction of Hsp70 with the Hsc70-Hsp90 complex and other factors all involved in piRNA biogenesis in both ovaries and testes. Such interaction induces a displacement of all such factors to the lysosomes resulting in a functional collapse of piRNA biogenesis. In support of a significant role of Hsp70 in transposon activation after stress, we found that the expression under normal conditions of Hsp70 in transgenic flies increases the amount of transposon transcripts and displaces the components of chaperon machinery outside the nuage as observed after heat shock. So that, our results demonstrate that heat shock stress is capable to increase the expression of transposons at post-transcriptional level by affecting piRNA biogenesis through the action of the inducible chaperone Hsp70. We think that such mechanism proposes relevant evolutionary implications. In presence of drastic environmental changes, Hsp70 plays a key dual role in increasing both the survival probability of individuals and the genetic variability in their germ cells. This in turn should be translated into an increase of genetic variability inside the populations thus potentiating their evolutionary plasticity and evolvability.

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