Project description:Environmental stress is detrimental to plants viability and requires an adequate reprogramming of cellular activities to maximize plant survival. We present a global analysis of the adaptive stress response of Arabidopsis thaliana to prolonged heat stress. We combine deep sequencing of RNA and ribosome protected fragments to provide genome wide map of adaptation to heat stress on at transcriptional and translational level. Our analysis shows that the genes with the highest upregulation upon heat stress are known heat-responsive gene, chaperons and other genes involved in protein folding control. Majority of these genes exhibits increase on both transcriptional and translational level. No translational inhibition or ribosome stalling was observed, which can be observed in the early thermal stress response, indicating that plants alter their cellular composition in order to adapt to the prolonged exposure to increased temperatures.
Project description:Microarray analysis was performed to identify the differentially expressed genes during heat stress by comparing the transcriptome of L. monocytogenes under optimal temperature (37°C), and prolonged heat shock (60°C for 9 minutes) conditions.
Project description:This experiment broadens our understanding of the temporal dynamics underlying the transcriptional response to heat stress. Using C. elegans hermaphrodite N2 populations, we have created a high-resolution time series of gene expression profiles taken at different time points during prolonged heat stress (35 C) conditions. Samples ware taken after 0h, 0.5h, 1h, 2h, 3h, 4h, 6h, 8h, and 12h of heat exposure with 3-5 biological replicas per time point.
Project description:We sequenced mRNA from leaves of Arabidopsis under the control (CK), warming (W) and heat (H) treatments using the Illumina HiSeq4000 platform to generate the transcriptome dynamics that may serve as a gene expression profile blueprint for different response patterns under prolonged warming versus rapid-onset heat stress in Arabidopsis.
Project description:FBXW7 modulates stress response by post-translational modification of HSF1 HSF1 orchestrates the heat-shock response upon exposure to heat stress and activates a transcriptional program vital for cancer cells. Genes positively regulated by HSF1 show increeased expression during heat shock while their expression is reduced during recovery. Genes negatively regulated by HSF1 show the opposite pattern. In this study we utilized the HCT116 FBXW7 KO colon cell line and its wild type counterpart to monitor gene expression changes during heat shock (42oC, 1 hour) and recovery (37oC for 2 hours post heat shock) using RNA sequencing. These results revealed that the heat-shock response pathway is prolonged in cells deficient for FBXW7.
Project description:We generated a comprehensive RNAseq expression atlas for several stress conditions in order to analyze changes in the gene expression during adaptation to mild stresses. The stresses are divided into two main groups: the “nutrient stresses” and the “environmental stresses”. Nutrient stresses include nutrient depletion (-N, -P, -S, -micronutrients), salt stress (+NaCl), osmotic stress (+mannitol) and control. The environmental stresses consist of high light, prolonged darkness, heat, cold and control.
Project description:The role of stress-induced increases in SUMO2/3 conjugation during the Heat Shock Response (HSR) has remained enigmatic. We investigated SUMO signal transduction at the proteomic and functional level during the HSR in the context of cells depleted of proteostasis network components via chronic Heat Shock Factor 1 inhibition versus cells with normal pro-teostasis networks. In the recovery phase post-heat shock, SUMO2/3 conjugation remained high for a prolonged time in cells lacking sufficient chaperones. Similar results were obtained upon inhibiting HSP90, indicating that increased chaperone activity during the HSR is critical for the recovery of SUMO2/3 levels post-heat shock. Proteasome inhibition during the re-covery phase likewise prolonged SUMO2/3 conjugation, indicating that stress-induced SU-MO2/3 targets are subsequently degraded by the ubiquitin-proteasome system. Functionally, we show that SUMOylation profoundly enhances solubility of target proteins upon heat shock in vitro. Collectively, our results implicate SUMO2/3 as a rapid response factor protecting the proteome from aggregation upon proteotoxic stress.
Project description:Mild stress could help cells to survive more severe environmental or pathophysiological conditions. In the current study, we investigated the cellular mechanisms which contribute to the development of stress tolerance upon a prolonged (0-12h) fever-like (40 °C) or a moderate (42.5 °C) hyperthermia in mammalian CHO cells. Our results indicate that mild heat triggers a distinct, dose dependent remodeling of the cellular lipidome followed by the expression of heat shock proteins only at higher heat dosages. A significant elevation in the relative concentration of sat-urated membrane lipid species, specific lysophosphatidylinositol and sphingolipid species sug-gests prompt membrane microdomain reorganization and an overall membrane rigidification in response to the fluidizing heat in a time dependent manner. RNAseq experiments reveal that mild heat initiate endoplasmic reticulum stress-related signaling cascades resulting in lipid re-arrangement and ultimately in an elevated resistance against membrane fluidization by benzyl alcohol. To protect cells against lethal, protein denaturing high temperatures the classical heat shock protein response was required. The different layers of stress response elicited by different heat dosages highlights the capability of cells to utilize multiple tools to gain resistance against or to survive lethal stress conditions.
Project description:Prolonged exposure to high temperatures may cause heat-related illnesses, such as cramps, syncope, exhaustion or even stroke in some individuals. Heat-related injuries remain a threat to the health and operational effectiveness of military personnel, athletes and the general public. Heat injury victims experience long-term complications that may include multi-system organ (liver, kidney, muscle) and neurologic damage, as well as reduced exercise capacity and heat intolerance. Findings from our laboratory using a developed heat stress model show that about 1/3 of mice are heat-intolerant and vulnerable to heat injury even though they are from the same mice litter. We examined if there is any genetic causation to this pattern of observation between the two groups of mice classified (Heat Intolerant and Heat Tolerant). We would like to screen Heat Tolerant and Heat Intolerant mice samples using microarray technology and examine their microRNA and mRNA for possible gene-specific differences between the two groups (6 mice per group). The results from this proposed animal research will help identify and select potential markers that can be used as a pre-screen to identify heat intolerance and assess heat injury recovery in humans.