Adaptive evolution under modest thermal stress improves the thermotolerance and ethanol fermentability of Saccharomyces cerevisiae
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ABSTRACT:
PROVIDER: PRJNA755963 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15509627_1.fastq.gz | Fastqsanger.gz | |||
| SRR15509627_2.fastq.gz | Fastqsanger.gz | |||
| SRR15509628_1.fastq.gz | Fastqsanger.gz | |||
| SRR15509628_2.fastq.gz | Fastqsanger.gz | |||
| SRR15509629_1.fastq.gz | Fastqsanger.gz |
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Project description:Thermotolerance development of robust Saccharomyces cerevisiae is necessary to enhance enzyme activity of cellulase, lower cooling costs, and reduce cell harm from the bad-distributed heat transfer in large-scale fermentation. The process-based studies of adaptive evolution have been well documented, but it remains unknown for the underlying molecular mechanism of the improved thermotolerance and the facilitated ethanol fermentability derived from adaptive evolution. Here, a robust thermotolerant S. cerevisiae Z100 was obtained with significantly improved ethanol fermentability under the stress of high temperature (50 oC) after 91 days’ adaptive evolution. RNA sequencing showed that adaptive evolution and its derived thermotolerance contributed to the unique gene transcriptional landscapes of the evolved strain. An interesting phenomenon was that the gene transcriptional signals of carbon metabolism were strengthened not at 50 oC but at 30 oC in S. cerevisiae Z100, and thus suggested that the improved thermotolerance led to the enhanced ethanol fermentability at 30 oC. The deeply repressed gene transcriptional expression indicated ribosome would be another key thermotolerant mechanism for the evolved strain. This study would provide a robust thermotolerant S. cerevisiae for bioethanol production and an important clue for future synthetic biology to thermotolerance engineering of fermentation strains.
2021-08-20 | GSE182342 | GEO
Project description:From preliminary experiments, HSP70 deficient MEF cells display moderate thermotolerance to a severe heatshock of 45.5 degrees after a mild preshock at 43 degrees, even in the absence of hsp70 protein. We would like to determine which genes in these cells are being activated to account for this thermotolerance. Keywords: thermal stress, heat shock response, knockout, cell culture, hsp70
2009-04-09 | GSE11120 | GEO
Project description:Photosystem II (PSII) is the most thermally sensitive component of photosynthesis. Thermal acclimation of this complex activity is likely to be critically important to the ability of photosynthetic organisms to tolerate temperature changes in the environment. We have analysed gene expression using whole-genome microarrays and monitored alterations in physiology during acclimation of PSII to elevated growth temperature in Synechocystis sp. PCC 6803. PSII acclimation is complete within 480 minutes of exposure to elevated temperature and is associated with a highly dynamic transcriptional response. 176 genes were identified and classified into seven distinct response profile groups. Response profiles suggest the existence of an early transient phase and a sustained phase to the acclimation response. The early phase was characterised by induction of general stress response genes, including heat shock proteins, which are likely to influence PSII thermal stability. The sustained phase consisted of acclimation-specific alterations that are involved in other cellular processes. Sustained responses included genes involved in phycobillisome structure and modification, photosynthesis, respiration, lipid metabolism and motility. Approximately 60% of genes with sustained altered expression levels have no known function. The potential role of differentially expressed genes in thermotolerance and acclimation is discussed. We have characterised the acclimation physiology of selected gene ‘knockouts’ to elucidate possible gene function in the response. All mutants show lower PSII rates under normal growth conditions. Basal PSII thermotolerance was affected by mutations in clpB1, cpcC2, hspA, htpG and slr1674. Final PSII thermotolerance was affected by mutations in cpcC2, hik34, hspA and hypA1, suggesting that these gene products play roles in long-term thermal acclimation of PSII. Gene expression levels were compared during a time-course (up to 8 hours) of thermal acclimation (from 25C to 38C) of a wild-type strain grown under continuous illumination and bubbled with CO2 -enriched air. Up to four independent biological replicates were generated and analysed. Each array: replicate matched time-point vs. 0hr control.
2010-04-09 | E-GEOD-21133 | biostudies-arrayexpress
Project description:Photosystem II (PSII) is the most thermally sensitive component of photosynthesis. Thermal acclimation of this complex activity is likely to be critically important to the ability of photosynthetic organisms to tolerate temperature changes in the environment. We have analysed gene expression using whole-genome microarrays and monitored alterations in physiology during acclimation of PSII to elevated growth temperature in Synechocystis sp. PCC 6803. PSII acclimation is complete within 480 minutes of exposure to elevated temperature and is associated with a highly dynamic transcriptional response. 176 genes were identified and classified into seven distinct response profile groups. Response profiles suggest the existence of an early transient phase and a sustained phase to the acclimation response. The early phase was characterised by induction of general stress response genes, including heat shock proteins, which are likely to influence PSII thermal stability. The sustained phase consisted of acclimation-specific alterations that are involved in other cellular processes. Sustained responses included genes involved in phycobillisome structure and modification, photosynthesis, respiration, lipid metabolism and motility. Approximately 60% of genes with sustained altered expression levels have no known function. The potential role of differentially expressed genes in thermotolerance and acclimation is discussed. We have characterised the acclimation physiology of selected gene ‘knockouts’ to elucidate possible gene function in the response. All mutants show lower PSII rates under normal growth conditions. Basal PSII thermotolerance was affected by mutations in clpB1, cpcC2, hspA, htpG and slr1674. Final PSII thermotolerance was affected by mutations in cpcC2, hik34, hspA and hypA1, suggesting that these gene products play roles in long-term thermal acclimation of PSII.
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Project description:Analysis of transcriptome in moss Physcomitrella patens CNGCb null mutant at 25 and 34 degrees C for 30 minutes. Results provide insight into role of CNGCb in acquired thermotolerance induced by non-lethal heat treatment. Typically at dawn of a hot summer day, land plants need precise molecular thermometers to sense harmless increments in the ambient temperature to timely develop a heat-shock response (HSR) and accumulate protective heat shock proteins (Hsps), in anticipation of upcoming harmful temperatures at mid-day. Here, we found that the CNGCb gene from Physcomitrella patens and its Arabidopsis ortholog CNGC2, encode for a component of cyclic nucleotide gated Ca2+ channels acting as the primary thermosensors of land plant cells. Disruption of CNGCb or CNGC2 produced a hyper-thermosensitive phenotype, giving rise to a HSR and acquired thermotolerance at significantly milder heat-priming treatments than in wild type plants. In an aequorin-expressing moss, CNGCb loss-of-function caused altered Ca2+ signaling and a sustained Ca2+ influx. Patch clamp recordings on moss protoplasts showed the presence of three distinct thermo-responsive Ca2+-channels in wild type cells. Deletion of CNGCb led to a total absence of one, and it increased the open probability of the remaining two thermo-responsive Ca2+ channels. Thus, both in Arabidopsis and moss, CNGC2 and CNGCb are expected to form with other related CNGCs, heteromeric Ca2+ channels in the plasma membrane that respond to mild increments in the ambient temperature by triggering an optimal HSR, leading to the onset of plant acquired thermotolerance. The WT moss tissues were heat-shocked for a half an hour at 34°C and 38°C and CNGCb at 25and 34°C followed by liquid nitrogen freezing. Total RNA was isolated using RNeasy Mini Kit (QIAGEN, Hilden, Germany) and two biological replicate samples for each treatment, were extracted. An Agilent-certified microarray service lab (MOgene, LC, St. Louis, MO, USA) was used to verify the integrity of the RNA and perform the microarray experiments. Two biological replicates were performed.
2012-03-06 | E-GEOD-36301 | biostudies-arrayexpress
Project description:During thermotolerance development, B. subtilis cells can be primed by a short mild heat shock to survive a subsequent severe, otherwise lethal, heat stress. We wanted to assess the influence of transcriptional regulation during thermotolerance development in B. subtilis. We prepared total RNA of four differently treated samples of B. subtilis cells. For this purpose, exponential B. subtilis cells grown at 37 °C were divided and exposed for additional 15 min to temperatures of 37 °C, 48 °C, 53 °C or 15 min 48 °C followed by 15 min at 53 °C.
2014-05-01 | GSE45972 | GEO
Project description:Honey bee colonies in the United States have suffered from a higher than usual rate of die-off in the last few years with a complex set of interacting stresses playing a key role. With changing climate, an increase in the frequency of severe weather events, such as heat waves, is anticipated and understanding how these changes may contribute to stress in the bee is of crucial. Individual honey bees appear to have a high capacity to endure thermal stress. One reason for this high-level endurance is likely their robust HSR which contributes to thermotolerance at the cellular level. To elucidate other determinants of this resilience, we used thermal stress coupled with RNAseq and identified broad transcriptional remodeling of a number of key signaling pathways in the honey bee in response to tissue damage, including those pathways known to be involved in digestive tract regeneration in the fruit fly such as the Hippo and JAK-STAT pathways. We also observe cell death and shedding of epithelial cells, which likely leads to induction of this regenerative program. We found that thermal stress affects many of these pathways in other tissues, suggesting a shared program of damage response. In addition to allowing for important foundational characterization of damage response program in this key pollinating species, this study suggest that a robust regeneration program may also be a critical contributor to thermotolerance at the tissue level.
2021-09-08 | GSE159083 | GEO
Project description:Thermotolerance development of robust Saccharomyces cerevisiae is necessary to enhance enzyme activity of cellulase, lower cooling costs, and reduce cell harm from the bad-distributed heat transfer in large-scale fermentation. The process-based studies of adaptive evolution have been well documented, but it remains unknown for the underlying molecular mechanism of the improved thermotolerance and the facilitated ethanol fermentability derived from adaptive evolution. Genome requencing was used to investigate the molecular mechanism for the evolved S. cerevisiae. It proved that the outstanding thermotolerance performance of the evolved strain brought about less single-nucleotide polymorphisms (SNPs) through genome resequencing. The key mutation derived from adaptive evolution would provide a robust thermotolerant S. cerevisiae for bioethanol production and an important clue for future synthetic biology to thermotolerance engineering of fermentation strains.
2021-09-03 | PRJEB47268 | EVA
Project description:During thermotolerance development, B. subtilis cells can be primed by a short mild heat shock to survive a subsequent severe, otherwise lethal, heat stress. We wanted to assess the influence of transcriptional regulation during thermotolerance development in B. subtilis. We prepared total RNA of four differently treated samples of B. subtilis cells. For this purpose, exponential B. subtilis cells grown at 37 °C were divided and exposed for additional 15 min to temperatures of 37 °C, 48 °C, 53 °C or 15 min 48 °C followed by 15 min at 53 °C. Using four different merged dye swap experiments of red or green labelled cDNA of the above described RNA preparations, we compared and analyzed the transcriptional change of the conditions 48 °C vs. 53/48 °C (array 1), 37 °C vs. 53 °C (array 2), 37 °C vs. 48 °C (array 3) and especially 37/53°C vs. 53/48 °C (array 4)
2014-05-01 | E-GEOD-45972 | biostudies-arrayexpress