scholarly journals Duration of Heat Stress Effect on Invasiveness ofL. monocytogenesStrains

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Ewa Wałecka-Zacharska ◽  
Renata Gmyrek ◽  
Krzysztof Skowron ◽  
Katarzyna Kosek-Paszkowska ◽  
Jacek Bania
Keyword(s):  
Heat Stress ◽  
Stress Response ◽  
Heat Shock ◽  
Optimal Growth ◽  
Growth Conditions ◽  
Stress Effect ◽  
Heat Shock Stress ◽  
Heat Treated ◽  
Strain Dependent ◽  
Invasion Capacity

During food production and food conservation, as well as the passage through the human gastrointestinal (GI) tract,L. monocytogenesis exposed to many adverse conditions which may elicit a stress response. As a result the pathogen may become more resistant to other unpropitious factors and may change its virulence. It has been shown that low and high temperature, salt, low pH, and high pressure affect the invasion capacity ofL. monocytogenes. However, there is a scarcity of data on the duration of the stress effect on bacterial biology, including invasiveness. The aim of this work was to determine the period during whichL. monocytogenesinvasiveness remains altered under optimal conditions following exposure of bacteria to mild heat shock stress. TenL. monocytogenesstrains were exposed to heat shock at 54°C for 20 minutes. Then both heat-treated and nontreated control bacteria were incubated under optimal growth conditions, 37°C, for up to 72 hours and the invasion capacity was tested. Additionally, the expression of virulence and stress response genes was investigated in 2 strains. We found that heat stress exposure significantly decreases the invasiveness of all tested strains. However, during incubation at 37°C the invasion capacity of heat-treated strains recovered to the level of nontreated controls. The observed effect was strain-dependent and lasted from less than 24 hours to 72 hours. The invasiveness of 6 out of the 10 nontreated strains decreased during incubation at 37°C. The expression ofinlABcorrelated with the increase of invasiveness but the decrease of invasiveness did not correlate with changes of the level of these transcripts.Conclusions. The effect of heat stress onL. monocytogenesinvasiveness is strain-dependent and was transient, lasting up to 72 hours.

scholarly journals Effect of Temperatures Used in Food Storage on Duration of Heat Stress Induced Invasiveness of L. monocytogenes

2019 ◽  
Vol 7 (10) ◽  
pp. 467
Author(s):  
Wałecka-Zacharska ◽  
Korkus ◽  
Skowron ◽  
Wietlicka-Piszcz ◽  
Kosek-Paszkowska ◽  
...  
Keyword(s):  
Heat Stress ◽  
Storage Conditions ◽  
Food Storage ◽  
Stress Effect ◽  
Limited Data ◽  
Temperature Dependent ◽  
Heat Treated ◽  
The Impact ◽  
And Oxidative Stress ◽  
Invasion Capacity

The unpropitious conditions of the food processing environmenttrigger in Listeria monocytogenes stress response mechanisms that may affect the pathogen’s virulence. To date, many studies have revealed that acid, osmotic, heat, cold and oxidative stress modify invasiveness of L. monocytogenes. Nonetheless, there is limited data on the duration of the stress effect on bacterial invasiveness. Since most food is stored at low or room temperatures we studied the impact of these temperatures on the duration of heat stress effect on invasiveness of 8 L. monocytogenes strains. Bacteria were heat-treated for 20 min at 54 °C and then incubated at 5 and 20 °C up to 14 days. A decrease in invasiveness over time was observed for bacteria not exposed to heating. It was found that heat shock significantly reduced the invasion capacity of all strains and the effect lasted between 7 and 14 days at both 5 and 20 °C. In conclusion, 20-min heating reduces invasion capacity of all L. monocytogenes strains; however, the stress effect is temporary and lasts between 7 and 14 days in the food storage conditions. The invasiveness of bacteria changes along with the incubation time and is temperature-dependent.

scholarly journals Heat Stress Responses and Thermotolerance in Maize

2021 ◽  
Vol 22 (2) ◽  
pp. 948
Author(s):  
Zhaoxia Li ◽  
Stephen H. Howell
Keyword(s):  
Transcription Factors ◽  
Heat Stress ◽  
Stress Response ◽  
Heat Shock ◽  
Stress Responses ◽  
Rna Splicing ◽  
Optimal Growth ◽  
Heat Stress Response ◽  
Genes Encoding ◽  
Heat Shock Responses

High temperatures causing heat stress disturb cellular homeostasis and impede growth and development in plants. Extensive agricultural losses are attributed to heat stress, often in combination with other stresses. Plants have evolved a variety of responses to heat stress to minimize damage and to protect themselves from further stress. A narrow temperature window separates growth from heat stress, and the range of temperatures conferring optimal growth often overlap with those producing heat stress. Heat stress induces a cytoplasmic heat stress response (HSR) in which heat shock transcription factors (HSFs) activate a constellation of genes encoding heat shock proteins (HSPs). Heat stress also induces the endoplasmic reticulum (ER)-localized unfolded protein response (UPR), which activates transcription factors that upregulate a different family of stress response genes. Heat stress also activates hormone responses and alternative RNA splicing, all of which may contribute to thermotolerance. Heat stress is often studied by subjecting plants to step increases in temperatures; however, more recent studies have demonstrated that heat shock responses occur under simulated field conditions in which temperatures are slowly ramped up to more moderate temperatures. Heat stress responses, assessed at a molecular level, could be used as traits for plant breeders to select for thermotolerance.

scholarly journals Genome-wide identification and analysis of the heat shock transcription factor family in moso bamboo (Phyllostachys edulis)

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Bin Huang ◽  
Zhinuo Huang ◽  
Ruifang Ma ◽  
Jialu Chen ◽  
Zhijun Zhang ◽  
...  
Keyword(s):  
Heat Stress ◽  
Stress Response ◽  
Heat Shock ◽  
Gene Family ◽  
Regulatory Elements ◽  
Moso Bamboo ◽  
Naphthalene Acetic Acid ◽  
Plant Responses ◽  
Heat Stress Response ◽  
Regulatory Pathways

AbstractHeat shock transcription factors (HSFs) are central elements in the regulatory network that controls plant heat stress response. They are involved in multiple transcriptional regulatory pathways and play important roles in heat stress signaling and responses to a variety of other stresses. We identified 41 members of the HSF gene family in moso bamboo, which were distributed non-uniformly across its 19 chromosomes. Phylogenetic analysis showed that the moso bamboo HSF genes could be divided into three major subfamilies; HSFs from the same subfamily shared relatively conserved gene structures and sequences and encoded similar amino acids. All HSF genes contained HSF signature domains. Subcellular localization prediction indicated that about 80% of the HSF proteins were located in the nucleus, consistent with the results of GO enrichment analysis. A large number of stress response–associated cis-regulatory elements were identified in the HSF upstream promoter sequences. Synteny analysis indicated that the HSFs in the moso bamboo genome had greater collinearity with those of rice and maize than with those of Arabidopsis and pepper. Numerous segmental duplicates were found in the moso bamboo HSF gene family. Transcriptome data indicated that the expression of a number of PeHsfs differed in response to exogenous gibberellin (GA) and naphthalene acetic acid (NAA). A number of HSF genes were highly expressed in the panicles and in young shoots, suggesting that they may have functions in reproductive growth and the early development of rapidly-growing shoots. This study provides fundamental information on members of the bamboo HSF gene family and lays a foundation for further study of their biological functions in the regulation of plant responses to adversity.

Identification of cis and trans components of a novel heat shock stress regulatory pathway in Saccharomyces cerevisiae

1993 ◽  
Vol 13 (1) ◽  
pp. 248-256
Author(s):  
N Kobayashi ◽  
K McEntee
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Stress Response ◽  
Heat Shock ◽  
Reporter Gene ◽  
Heat Shock Element ◽  
Cis Acting ◽  
Heat Shock Stress ◽  
Specific Complex ◽  
Cis And Trans ◽  
Shock Stress

The stress-responsive DDR2 gene (previously called DDRA2) of Saccharomyces cerevisiae is transcribed at elevated levels following stress caused by heat shock or DNA damage. Previously, we identified a 51-bp promoter fragment, oligo31/32, which conferred heat shock inducibility on the heterologous CYC1-lacZ reporter gene in S. cerevisiae (N. Kobayashi and K. McEntee, Proc. Natl. Acad. Sci. USA 87:6550-6554, 1990). Using a series of synthetic oligonucleotides, we have identified a pentanucleotide, CCCCT (C4T), as an essential component of this stress response sequence. This element is not a binding site for the well-characterized heat shock transcription factor which recognizes a distinct cis-acting heat shock element in the promoters of many heat shock genes. Here we demonstrate the ability of oligonucleotides containing the C4T sequence to confer heat shock inducibility on the reporter gene and show that the presence of two such elements produces more than additive effects on induction. Gel retardation experiments have been used to demonstrate specific complex formation between C4T-containing fragments and one or more yeast proteins. Formation of these complexes was not competed by fragments containing mutations in the C4T sequence nor by heat shock element-containing competitor DNAs. Fragments containing the C4T element bound to a single 140-kDa polypeptide, distinct from heat shock transcription factors in yeast crude extracts. These experiments identify key cis- and trans-acting components of a novel heat shock stress response pathway in S. cerevisiae.

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 A Hot Water Extract of Sideritis scardica Prolongs Life Span and Enhances Heat Shock Resistance in Caenorhabditis elegans

2020 ◽  
Vol 15 (4) ◽  
pp. 1934578X2091728
Author(s):  
Yoshihiko Nishioka ◽  
Seiya Nishikawa ◽  
Toshiyuki Shibata
Keyword(s):  
Heat Stress ◽  
Caenorhabditis Elegans ◽  
Stress Response ◽  
Heat Shock ◽  
Life Span ◽  
Water Extract ◽  
Hot Water ◽  
Control Group ◽  
C Elegans ◽  
Hot Water Extract

Sideritis scardica is a Lamiaceae plant that is endemic to the alpine zone of the Balkan Peninsula. The tea of S. scardica has been handed down as a “tea of longevity” in the Rhodope region of Bulgaria for an unknown amount of time. In this study, we prepared a hot water extract of S. scardica (SHWE) and examined its effects on both life span and stress response in living tissue using Caenorhabditis elegans and its transgenic mutants. The life span of wild-type N2 worms was prolonged by approximately 15% at the SHWE concentration of 5 µg/mL and approximately 22% at the SHWE concentration of 50 µg/mL, as compared with the control group. The effect of SHWE on the expression of heat shock protein 16.2 (HSP-16.2) under heat stress was investigated using TJ375 worms, a transgenic mutant of C. elegans. In the TJ375 worms pretreated with SHWE, the fluorescence intensity of green fluorescent protein fluorescence, which indicates the expression of HSP-16.2, was significantly increased. In the assay using TJ356 worms, the worms pretreated with SHWE did not show the translocation of DAF-16, a forkhead transcription factor class O homolog, from the cytoplasm to nucleus under heat stress. Additionally, under heat stress, the pretreatment of SHWE improved the survival rate of GR1307 worms, a knockout mutant of daf-16. These results indicate that SHWE enhances HSP-16.2 expression through a stress-response pathway (eg, HSF-1 pathway) other than the DAF-16 pathway, resulting in a prolonged life span of C. elegans under heat stress.

scholarly journals Molecular Basis of the Defective Heat Stress Response in Mycobacterium leprae

2007 ◽  
Vol 189 (24) ◽  
pp. 8818-8827 ◽  
Author(s):  
Diana L. Williams ◽  
Tana L. Pittman ◽  
Mike Deshotel ◽  
Sandra Oby-Robinson ◽  
Issar Smith ◽  
...  
Keyword(s):  
Heat Stress ◽  
Stress Response ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Elevated Temperatures ◽  
Transcriptional Response ◽  
Mycobacterium Leprae ◽  
Heat Stress Response ◽  
Regulatory Circuits ◽  
Shock Response

ABSTRACT Mycobacterium leprae, a major human pathogen, grows poorly at 37°C. The basis for its inability to survive at elevated temperatures was investigated. We determined that M. leprae lacks a protective heat shock response as a result of the lack of transcriptional induction of the alternative sigma factor genes sigE and sigB and the major heat shock operons, HSP70 and HSP60, even though heat shock promoters and regulatory circuits for these genes appear to be intact. M. leprae sigE was found to be capable of complementing the defective heat shock response of mycobacterial sigE knockout mutants only in the presence of a functional mycobacterial sigH, which orchestrates the mycobacterial heat shock response. Since the sigH of M. leprae is a pseudogene, these data support the conclusion that a key aspect of the defective heat shock response in M. leprae is the absence of a functional sigH. In addition, 68% of the genes induced during heat shock in M. tuberculosis were shown to be either absent from the M. leprae genome or were present as pseudogenes. Among these is the hsp/acr2 gene, whose product is essential for M. tuberculosis survival during heat shock. Taken together, these results suggest that the reduced ability of M. leprae to survive at elevated temperatures results from the lack of a functional transcriptional response to heat shock and the absence of a full repertoire of heat stress response genes, including sigH.

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