Dissecting the genetic basis of an evolved acute heat stress and oxidative stress resistance in the nematode Caenorhabditis remanei reveals a complex and unique genetic architecture
Ontology highlight
ABSTRACT:
ORGANISM(S): Caenorhabditis remanei
PROVIDER: GSE108235 | GEO | 2017/12/19
SECONDARY ACCESSION(S): PRJNA422896
REPOSITORIES: GEO
Similar Datasets
Project description:In response to changing environmental conditions, organisms can acclimate through phenotypic plasticity or adapt by evolving mechanisms to cope with novel stressors. Changes in gene expression, whether dynamic or evolved, are an important way in which environmental responses are mediated; however, much is still unknown about how the molecular networks underlying plastic phenotypes evolve. Here, we compare transcriptional responses to acute heat stress among four populations of the nematode Caenorhabditis remanei-one selected to withstand heat stress, one selected under oxidative stress, an unselected control, and the ancestral population. We used a weighted gene coexpression network analysis within these lines to identify transcriptional modules, which are sets of genes that respond similarly to stress via plastic responses, evolutionary responses, or both. The transcriptional response to acute heat stress is dominated by a plastic response that is shared in the ancestor and all evolved populations. However, we also identified several modules that respond to artificial selection by (1) changing the baseline level of expression, (2) altering the magnitude of the plastic response, or (3) a combination of the two. Our findings reveal that while it is possible to perturb the nature of the transcriptional response network with short bouts of intense selection, the overall structure of transcriptional plasticity is dominated by inherent, ancestral regulatory systems.
2019-02-04 | GSE115496 | GEO
Project description:Many organisms can acclimate to new environments through phenotypic plasticity, a complex trait that can be heritable, subject to selection, and evolve. However, the rate and genetic basis of plasticity evolution remain largely unknown. We experimentally evolved outbred populations of the nematode Caenorhabditis remanei under an acute heat shock during early larval development. When raised in a non-stressful environment, ancestral populations were highly sensitive to a 36.8°C heat shock and exhibited high mortality. However, initial exposure to a non-lethal high temperature environment resulted in significantly reduced mortality during heat shock (hormesis). Lines selected for heat shock resistance rapidly evolved the capacity to withstand heat shock in the native environment without any initial exposure to high temperatures, and early exposure to high temperatures did not lead to further increases in heat resistance. This loss of plasticity would appear to have resulted from the genetic assimilation of the heat induction response in the non-inducing environment. However, analyses of transcriptional variation via RNA-sequencing from the selected populations revealed no global changes in gene regulation correlated with the observed changes in heat stress resistance. Instead, assays of the phenotypic response across a broader range of temperatures revealed that the induced plasticity was not fixed across environments, but rather the threshold for the response was shifted to higher temperatures over evolutionary time. These results demonstrate that apparent genetic assimilation can result from shifting thresholds of induction across environments and that analysis of the broader environmental context is critically important for understanding the evolution of phenotypic plasticity. mRNA profiles of ancestral and two experimentally evolved populations of C. remanei at 20°C or 30°C, 6 replicates/temperature for each population
2014-05-04 | E-GEOD-56510 | biostudies-arrayexpress
Project description:Many organisms can acclimate to new environments through phenotypic plasticity, a complex trait that can be heritable, subject to selection, and evolve. However, the rate and genetic basis of plasticity evolution remain largely unknown. We experimentally evolved outbred populations of the nematode Caenorhabditis remanei under an acute heat shock during early larval development. When raised in a non-stressful environment, ancestral populations were highly sensitive to a 36.8°C heat shock and exhibited high mortality. However, initial exposure to a non-lethal high temperature environment resulted in significantly reduced mortality during heat shock (hormesis). Lines selected for heat shock resistance rapidly evolved the capacity to withstand heat shock in the native environment without any initial exposure to high temperatures, and early exposure to high temperatures did not lead to further increases in heat resistance. This loss of plasticity would appear to have resulted from the genetic assimilation of the heat induction response in the non-inducing environment. However, analyses of transcriptional variation via RNA-sequencing from the selected populations revealed no global changes in gene regulation correlated with the observed changes in heat stress resistance. Instead, assays of the phenotypic response across a broader range of temperatures revealed that the induced plasticity was not fixed across environments, but rather the threshold for the response was shifted to higher temperatures over evolutionary time. These results demonstrate that apparent genetic assimilation can result from shifting thresholds of induction across environments and that analysis of the broader environmental context is critically important for understanding the evolution of phenotypic plasticity.
2014-05-04 | GSE56510 | GEO
Project description:gene expression was measured in five independent heat resistance selected replicate lines and five control lines. The genetic architecture underlying heat resistance remains partly unclear despite the well documented involvement of heat shock proteins (Hsps). It was previously shown that factors besides Hsps are likely to play an important role for heat resistance. In this study, gene expression arrays were used to make replicate measurements of gene expression before and up to 64h after a mild heat stress treatment, in flies selected for heat resistance and unselected control flies, to identify genes differentially expressed in heat resistance selected flies. We found 108 genes upregulated and 10 downregulated using the Affymetrix gene expression platform. Among the upregulated genes, a substantial number are involved in the phototransduction process. Another group of genes upregulated in selected flies is characterized by also responding to heat shock treatment several hours after peak induction of known Hsps revert to non-stress levels. These findings suggest phototransduction genes to be critically involved in heat resistance, and support a role for components of the phototransduction process in stress sensing mechanisms. In addition the results suggest yet uncharacterized genes responding to heat stress several hours after treatment to be involved in heat stress resistance. These findings mark an important increase in the understanding of heat resistance. Keywords: control versus selected
2006-08-01 | GSE5146 | GEO
Project description:Environmental stress, such as oxidative or heat stress, induces the activation of the heat shock response
(HSR) and leads to an increase in the heat shock proteins (HSPs) level. These HSPs act as molecular
chaperones to maintain cellular proteostasis. Controlled by highly intricate regulatory mechanisms,
having stress-induced activation and feedback regulations with multiple partners, the HSR is still
incompletely understood. In this context, we propose a minimal molecular model for the gene
regulatory network of the HSR that reproduces quantitatively different heat shock experiments both
on heat shock factor 1 (HSF1) and HSPs activities. This model, which is based on chemical kinetics
laws, is kept with a low dimensionality without altering the biological interpretation of the model
dynamics. This simplistic model highlights the titration of HSF1 by chaperones as the guiding line of
the network. Moreover, by a steady states analysis of the network, three different temperature stress
regimes appear: normal, acute, and chronic, where normal stress corresponds to pseudo thermal
adaption. The protein triage that governs the fate of damaged proteins or the different stress regimes
are consequences of the titration mechanism. The simplicity of the present model is of interest in
order to study detailed modelling of cross regulation between the HSR and other major genetic
networks like the cell cycle or the circadian clock.
Sivéry, A., Courtade, E., Thommen, Q. (2016). A minimal titration model of the mammalian dynamical heat shock response. Physical biology, 13(6), 066008.
2022-01-25 | MODEL2201210001 | BioModels
Project description:Dinoflagellates have evolved a nuclear organization unlike that of any other eukaryotic group. Recent studies find a predominance of post-transcriptional control of dinoflagellate gene expression. This study investigated regulation of the environmental stress response in the red tide dinoflagellate, Karenia brevis using an Agilent custom oligonucleotide microarray. K. brevis cultures were exposed to 5°C or 10°C heat shock, or three different sources of oxidative stress: 60 µM H2O2, 10 mM NaNO2, or 12 µM PbCl2 over acute time courses. Ribosomal genes, genes involved in RNA processing, translation, and chaperones were among the classes of genes consistently downregulated across treatments, although within these functional classes the same genes did not always respond to different stressors. Genes involved in the photosystem and mitochondrial and chloroplast ATP generation dominated the down-regulated genes. Heat shock and oxidative stress response genes were not induced under any treatment, even under conditions that resulted in decreased viability. We subsequently identified the presence of a trans-spliced leader sequence on many stress response gene transcripts, which suggests that they may be transcribed constitutively and their expression regulated at the level of translation. Cultures of were grown to mid-log phase. For each treatment, five replicate untreated control cultures and five replicate treated cultures were harvested at several time points following treatment. The following time courses were used: 5°C heat shock - 5, 15, 30, 60, and 240 min; 10°C heat shock - 60 min; 60 µM H2O2 - 5, 15, 30, 60, and 240 min; 10 mM NaNO2 -1, 4, and 7 hours; 12 µM PbCl2 -1, 4, and 7 hours. For each treatment, RNA was pooled from the controls and treated cultures at each timepoint. Two color arrays were then run comparing each the transcriptome at timepoint with the pooled control for that treatment. A technical dye swap array was run at each timepoint.
2010-12-01 | E-GEOD-13961 | biostudies-arrayexpress
Project description:We evolved Escherichia coli cells over 500 generations under five environments that include four abiotic stressors: osmotic, acidic, oxidative, n-butanol, and control The goal of the experiment: Bacterial populations have a remarkable capacity to cope with extreme environmental fluctuations in their natural environments. In certain cases, adaptation to one stressful environment provides a fitness advantage when cells are exposed to a second stressor, a phenomenon that has been coined as cross-stress protection. A tantalizing question in bacterial physiology is how the cross-stress behavior emerges during adaptation and what the genetic basis of acquired stress resistance is. RNA profiles were obtained for six E. coli strains evolved for 500 generations under abiotic stressors; two technical replicates for each strain where sequenced by Illumina GAII analyzer
2013-02-28 | E-GEOD-39926 | biostudies-arrayexpress
Project description:A data-independent acquisition assay library was used to examine proteome wide changes in liver of two populations of threespine stickleback (Gasterosteus aculeatus) after acute thermal stress. Experimental fish were held at 28°C for two hours and allowed to recover back at the acclimation temperature of 15°C for either six or 24 hours, while controls remained at 15°C. The Big Lagoon population (BL) had a large response at six hours after acute heat stress but had mostly regained protein homeostasis by 24 hours after the heat stress. The Klamath population showed very little response to acute thermal stress at either time point, highlighting major differences between the two populations in their response to acute heat stress. Functional enrichment analyses using STRING aided in identifying larger networks and domains that were significantly enriched in the different groups beyond the individual significantly different proteins, and KEGG pathway analysis was conducted on the large number of significantly different proteins for the BL28-6hr vs BL15-6hr comparison. DnaJ/Hsp40 B1b was the one protein that was significantly higher in abundance for both populations at both time points, suggesting a key role for this protein in regulating and orchestrating the response to acute temperature stress for this species. At six hours after acute heat stress, the main themes from the significant protein changes in the Big Lagoon population were the regulation of multiple levels of gene expression, reduction of reactive oxygen species (ROS) production, and structural changes.
2021-06-21 | PXD024677 | panorama
Project description:Analysis of evolved changes in transcriptional plasticity and parental effects on plasticity induced by mild heat stress in the nematode Caenorhabditis remanei. Results of this study highlight the importance of the broad environmental context of an organism and its influence on phenotypic plasticity, parental effects, and evolutionary responses. mRNA profiles of ancestral and two experimentally evolved populations of C. remanei. Parents of the sampled worms were raised at either 20°C or 30°C, then the resulting embryos were divided and reared at either 20°C or 30°C prior to collection (as L1 larvae). 6 replicates/larval temperature for each population if the parents were raised at 20°C, and 2 replicates/larval temperature for each population if the parents were raised at 30°C.
2014-10-30 | E-GEOD-62841 | biostudies-arrayexpress
Project description:Dissecting the genetic basis of an evolved acute heat stress and oxidative stress resistance in the nematode Caenorhabditis remanei reveals a complex and unique genetic architecture
| PRJNA422896 | ENA