Dataset Information

Warmer temperatures enhance beneficial mutation effects.

ABSTRACT: Temperature determines the rates of all biochemical and biophysical processes, and is also believed to be a key driver of macroevolutionary patterns. It is suggested that physiological constraints at low temperatures may diminish the fitness advantages of otherwise beneficial mutations; by contrast, relatively high, benign, temperatures allow beneficial mutations to efficiently show their phenotypic effects. To experimentally test this "mutational effects" mechanism, we examined the fitness effects of mutations across a temperature gradient using bacterial genotypes from the early stage of a mutation accumulation experiment with Escherichia coli. While the incidence of beneficial mutations did not significantly change across environmental temperatures, the number of mutations that conferred strong beneficial fitness effects was greater at higher temperatures. The results therefore support the hypothesis that warmer temperatures increase the chance and magnitude of positive selection, with implications for explaining the geographic patterns in evolutionary rates and understanding contemporary evolution under global warming.

SUBMITTER: Chu XL

PROVIDER: S-EPMC7496171 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Warmer temperatures enhance beneficial mutation effects.

Chu Xiao-Lin XL Zhang Da-Yong DY Buckling Angus A Zhang Quan-Guo QG

Journal of evolutionary biology 20200623 8

Temperature determines the rates of all biochemical and biophysical processes, and is also believed to be a key driver of macroevolutionary patterns. It is suggested that physiological constraints at low temperatures may diminish the fitness advantages of otherwise beneficial mutations; by contrast, relatively high, benign, temperatures allow beneficial mutations to efficiently show their phenotypic effects. To experimentally test this "mutational effects" mechanism, we examined the fitness effe ...[more]

PMID: 32424908

Similar Datasets

Project description:Short periods of heat (>37°C) are extremely damaging to non-acclimated plants and their capacity to acclimate to and recover from heat stress is a key parameter for their survival and longevity. To acclimate, the Heat Shock transcription Factor A1 (HSFA1) subfamily activates a transcriptional response that resolves the heat stress-induced protein damage. Importantly, HSFA1 activity is also critical for Arabidopsis to withstand sustained warmer periods of 28°C, a non-detrimental condition that triggers a thermomorphogenesis response. We find that SUMO, a protein modification whose adduct levels increase as a result of acute heat stress in eukaryotes, is also critical for plant longevity during warmer periods, in particular for shoot meristem development. The known E3 and E4 SUMO ligases (SIZ1, HPY1/MMS21, PIAL1/2) were not essential to endure these warmer periods, alone or in combination. Thermo-lethality was also not seen when plants lacked certain SUMO proteases (ESD4, OTS1/OTS2, SPF1/SPF2 combined) or when SUMO chain formation was blocked. Furthermore, SUMO thermo-resilience is not connected to the autoimmune phenotype found in the corresponding SUMO knockdown and a SIZ1 loss-of-function mutant. As acquired thermotolerance was normal in the SUMO knockdown mutant, we thus conclude that the role of SUMO in heat acclimation differs from that of HSFA1 and SIZ1. Combined, this study reveals that SUMO appears to be critical for shoot meristem integrity during warmer periods. This experiment we have examined how gene expression is affected in two SUMO mutants (siz1-2; sumo1 amiR-SUMO1 [aka. sumo1/2KD] ), and a HsfA1a,b,d triple mutant, when the plants are placed at 28C constant ambient temperature, which is a condition normally used to induce thermomorphogenesis. We used as control the pad1-4 background, as the siz1-2 and sumo1/2KD mutants normally suffer from constitutive defence signalling due hyperaccumulation of SA, which is suppressed by introgression of pad4 in these backgrounds.

Project description:Most studies using murine disease models are conducted at a housing temperature of 20ºC that is sub-optimal (ST) for mice, eliciting changes in metabolism and response to disease. Experiments performed at a thermoneutral temperature (TT) of 37ºC have revealed an altered immune response to pathogens and experimental treatments in disease models (e.g. cancer, obesity, Alzheimer’s disease). These alterations in metabolic activity have implications for the use of murine models to understand human diseases and their translation to clinical research. How such conditions affect the inflammatory response to infection with Plasmodium berghei ANKA (PbA) and subsequent disease progression is unknown. We hypothesized that changes in environmental temperature modulate immune cells and modify host response to malaria disease. To test this hypothesis, we conducted two sets of experiments to determine: (1) the inflammatory response of bone-marrow derived macrophages (BMDM) to infectious agents at different environmental temperatures and (2a) the inflammatory response to malarial agents injection in a peritonitis model and (2b) disease progression in PbA-infected mice at TT compared to ST. Firstly, BMDMs were incubated and stimulated with LPS at a fever-like temperature (FT; 39ºC), TT (37ºC) or low-temperatures (LT; 30ºC) mimicking ST for 6, 12 and 24 hours. We observed an that BMDMs released increased inflammation markers (i.e. nitric oxide and pro-inflammatory cytokine at FT and TT compared to LT, with an increase overtime. Secondly, C57BL6 mice were acclimatized for 3 weeks at TT (28 – 31ºC) or ST (20 – 22ºC). In one study, mice were injected intraperitoneally with nHZ or Leishmania at both temperatures, and immune cells were counted and subtyped from the peritoneal cavity (PEC) fluid. Cytokine concentrations and extracellular vesicle (EV) profiles were also determined from the PEC. Apart from Leishmania injection resulting in decreased cell recruitment and a higher phagocytosis of nHZ in mice housed at TT, we did not observe many temperature-based differences. We found 398 upregulated and 293 downregulated pro-inflammatory genes in mice injected with nHZ, that were similar to those previously elicite with Leishmania injections, at both temperatures. EV profile did not differ significantly at TT compared to ST but we report the presence of proteosome-derived and platelet-derived EVs in a murine parasitic murine model at both temperatures. In another study, mice were injected with luciferase-tagged PbA-infected RBCs and monitored until death. We observed metabolic changes (i.e. lower body weight and temperature loss) in mice housed at TT but these did not result to noticeable changes in survivability, parasite organ sequestration or serum cytokine levels compared to ST. To our knowledge, these experiments are the first to investigate the effect of thermoneutrality on a malaria murine model. Despite results suggesting that thermoneutrality does not significantly alter severe malarial disease progression or host inflammatory response to parasitic agents, we found important metabolic difference in mice housed at TT. Our results offer insights on how thermoneutrality might impact a severe malaria murine model and directions for more targeted investigations. This constitutes a first step in elucidating factors that may explain the lack of translatability to clinical trial.

Dataset Information

Warmer temperatures enhance beneficial mutation effects.

Publications

Warmer temperatures enhance beneficial mutation effects.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure