Find research datasets worth reusing
Search datasets from major research repositories and use ShareScore to quickly assess how well each record supports discovery, access, and reuse.
19
datasets available to search
ShareScore release 0.9.0
Dataset results
19 results for “Fitness epistasis”
Data for: Testing for fitness epistasis in a transplant experiment identifies a candidate adaptive locus in Timema stick insects
<p>Identifying the genetic basis of adaptation is a central goal of evolutionary biology. However, identifying genes and mutations affecting fitness remains challenging because a large number of traits and variants can influence fitness. Selected phenotypes can also be difficult to know <em>a priori</em>, complicating top-down genetic approaches for trait mapping that involve crosses or genome-wide association studies. In such cases, experimental genetic approaches, where one maps fitness directly and attempts to infer the traits involved afterward, can be valuable. Here, we re-analyse data from a transplant experiment involving <em>Timema</em> stick insects, where five physically clustered SNPs associated with cryptic body colouration were shown to interact to affect survival. Our analysis covers a larger genomic region than past work and revealed a locus previously not identified as associated with survival. This locus resides near a gene, <em>Punch</em> (<em>Pu</em>), involved in pteridine pigments production, implying that it could be associated with an unmeasured colouration trait. However, by combining previous and newly obtained phenotypic data, we show that this trait is not eye or body colouration. We discuss the implications of our results for the discovery of traits, genes, and mutations associated with fitness in other systems, as well as for supergene evolution.</p>
Data for: Testing for fitness epistasis in a transplant experiment identifies a candidate adaptive locus in Timema stick insects
Open the record for dataset details and reuse information.
Data from: Ecology shapes epistasis in a genotype-phenotype-fitness map for stick insect colour
<p>Genetic interactions such as epistasis are widespread in nature and can shape evolutionary dynamics. Epistasis occurs due to non-linearity in biological systems, which can arise via cellular processes that convert genotype to phenotype and via selective processes that connect phenotype to fitness. Few studies in nature have connected genotype to phenotype to fitness for multiple potentially interacting genetic variants. Thus, the causes of epistasis in the wild remain poorly understood. Here, we show that epistasis for fitness is an emergent and predictable property of non-linear selective processes. We do so by measuring the genetic basis of cryptic colouration and survival in a field experiment with stick insects. We find that colouration exhibits a largely additive genetic basis, but with some effects of epistasis that enhance differentiation between colour morphs. In terms of fitness, different combinations of loci affecting colouration confer high survival in one host-plant treatment. Specifically, non-linear correlational selection for specific combinations of colour traits in this treatment drives the emergence of pairwise and higher-order epistasis for fitness at loci underlying colour. In turn, this results in a rugged fitness landscape for genotypes. In contrast, fitness epistasis was dampened in another treatment, where selection was weaker. Patterns of epistasis that are shaped by ecologically based selection could be common, and central to understanding fitness landscapes, the dynamics of evolution, and potentially other complex systems.</p>
Data from: Mapping the fitness landscape of gene expression uncovers the cause of antagonism and sign epistasis between adaptive mutations
How do adapting populations navigate the tensions between the costs of gene expression and the benefits of gene products to optimize the levels of many genes at once? Here we combined independently-arising beneficial mutations that altered enzyme levels in the central metabolism of Methylobacterium extorquens to uncover the fitness landscape defined by gene expression levels. We found strong antagonism and sign epistasis between these beneficial mutations. Mutations with the largest individual benefit interacted the most antagonistically with other mutations, a trend we also uncovered through analyses of datasets from other model systems. However, these beneficial mutations interacted multiplicatively (i.e., no epistasis) at the level of enzyme expression. By generating a model that predicts fitness from enzyme levels we could explain the observed sign epistasis as a result of overshooting the optimum defined by a balance between enzyme catalysis benefits and fitness costs. Knowledge of the phenotypic landscape also illuminated that, although the fitness peak was phenotypically far from the ancestral state, it was not genetically distant. Single beneficial mutations jumped straight toward the global optimum rather than being constrained to change the expression phenotypes in the correlated fashion expected by the genetic architecture. Given that adaptation in nature often results from optimizing gene expression, these conclusions can be widely applicable to other organisms and selective conditions. Poor interactions between individually beneficial alleles affecting gene expression may thus compromise the benefit of sex during adaptation and promote genetic differentiation.
Data from: Mitochondrial–nuclear epistasis affects fitness within species but does not contribute to fixed incompatibilities between species of Drosophila
Efficient mitochondrial function requires physical interactions between the proteins encoded by the mitochondrial and nuclear genomes. Coevolution between these genomes may result in the accumulation of incompatibilities between divergent lineages. We test whether mitochondrial–nuclear incompatibilities have accumulated within the Drosophila melanogaster species subgroup by combining divergent mitochondrial and nuclear lineages and quantifying the effects on relative fitness. Precise placement of nine mtDNAs from D. melanogaster, D. simulans, and D. mauritiana into two D. melanogaster nuclear genetic backgrounds reveals significant mitochondrial–nuclear epistasis affecting fitness in females. Combining the mitochondrial genomes with three different D. melanogaster X chromosomes reveals significant epistasis for male fitness between X-linked and mitochondrial variation. However, we find no evidence that the more than 500 fixed differences between the mitochondrial genomes of D. melanogaster and the D. simulans species complex are incompatible with the D. melanogaster nuclear genome. Rather, the interactions of largest effect occur between mitochondrial and nuclear polymorphisms that segregate within species of the D. melanogaster species subgroup. We propose that a low mitochondrial substitution rate, resulting from a low mutation rate and/or efficient purifying selection, precludes the accumulation of mitochondrial–nuclear incompatibilities among these Drosophila species.
Data from: Epistasis buffers the fitness effects of rifampicin-resistance mutations in Pseudomonas aeruginosa
Epistatic interactions between resistance mutations in antibiotic-free environments potentially play a crucial role in the spread of resistance in pathogen populations by determining the fitness cost associated with resistance. We used an experimental evolution approach to test for epistatic interactions between 14 different pairs of rifampicin mutations in the pathogenic bacterium Pseudomonas aeruginosa in 42 different rifampicin-free environments. First, we show that epistasis between rifampicin-resistance mutations tends to be antagonistic: the fitness effect of having two mutations is generally smaller than that predicted from the effects of individual mutations on the wild type. Second, we show that sign epistasis between resistance mutations is both common and strong; most notably, pairs of deleterious resistance mutations often partially or completely compensate for each others' costs, revealing a novel mechanism for compensatory adaptation. These results suggest that antagonistic epistasis between intragenic resistance mutations may be a key determinant of the cost of antibiotic resistance and compensatory adaptation in pathogen populations.
Data from: Rates of fitness decline and rebound suggest pervasive epistasis
Unraveling the factors that determine the rate of adaptation is a major question in evolutionary biology. One key parameter is the effect of a new mutation on fitness, which invariably depends on the environment and genetic background. The fate of a mutation also depends on population size, which determines the amount of drift it will experience. Here, we manipulate both population size and genotype composition and follow adaptation of 23 distinct Escherichia coli genotypes. These have previously accumulated mutations under intense genetic drift and encompass a substantial fitness variation. A simple rule is uncovered: the net fitness change is negatively correlated with the fitness of the genotype in which new mutations appear—a signature of epistasis. We find that Fisher's geometrical model can account for the observed patterns of fitness change and infer the parameters of this model that best fit the data, using Approximate Bayesian Computation. We estimate a genomic mutation rate of 0.01 per generation for fitness altering mutations, albeit with a large confidence interval, a mean fitness effect of mutations of −0.01, and an effective number of traits nine in mutS− E. coli. This framework can be extended to confront a broader range of models with data and test different classes of fitness landscape models.
Data from: Plasticity and epistasis strongly affect bacterial fitness after losing multiple metabolic genes
Many bacterial lineages lack seemingly essential metabolic genes. Previous work suggested selective benefits could drive the loss of biosynthetic functions from bacterial genomes when the corresponding metabolites are sufficiently available in the environment. However, the factors that govern this 'genome streamlining' remain poorly understood. Here we determine the effect of plasticity and epistasis on the fitness of Escherichia coli genotypes from whose genome biosynthetic genes for one, two, or three different amino acids have been deleted. Competitive fitness experiments between auxotrophic mutants and prototrophic wild type cells in one of two carbon environments revealed that plasticity and epistasis strongly affected the mutants' fitness individually and interactively. Positive and negative epistatic interactions were prevalent, yet on average cancelled each other out. Moreover, epistasis correlated negatively with the expected effects of combined auxotrophy-causing mutations, thus producing a pattern of diminishing returns. Moreover, computationally analysing 1,432 eubacterial metabolic networks revealed that most pairs of auxotrophies co-occurred significantly more often than expected by chance, suggesting epistatic interactions and/ or environmental factors favoured these combinations. Our results demonstrate that both the genetic background and environmental conditions determine the adaptive value of a loss-of-biochemical-function mutation and that fitness gains decelerate, as more biochemical functions are lost.
Data from: Mitochondrial–nuclear epistasis affects fitness within species but does not contribute to fixed incompatibilities between species of Drosophila
Open the record for dataset details and reuse information.
Data from: Ecology shapes epistasis in a genotype-phenotype-fitness map for stick insect colour
Open the record for dataset details and reuse information.
Data from: The impact of high-order epistasis in the within-host fitness of a positive-sense plant RNA virus
Open the record for dataset details and reuse information.
Data from: Rates of fitness decline and rebound suggest pervasive epistasis
Open the record for dataset details and reuse information.
Data from: Epistasis buffers the fitness effects of rifampicin-resistance mutations in Pseudomonas aeruginosa
Open the record for dataset details and reuse information.
Data from: Mapping the fitness landscape of gene expression uncovers the cause of antagonism and sign epistasis between adaptive mutations
Open the record for dataset details and reuse information.
Data from: Plasticity and epistasis strongly affect bacterial fitness after losing multiple metabolic genes
Open the record for dataset details and reuse information.
Data from: Epistasis between antibiotic resistance mutations and genetic background shape the fitness effect of resistance across species of Pseudomonas
Open the record for dataset details and reuse information.
Extreme positive epistasis for fitness in monosomic yeast strains - part 2
GEO Series GSE276940. Saccharomyces cerevisiae. 4 samples. Type: Expression profiling by high throughput sequencing.
Extreme positive epistasis for fitness in monosomic yeast strains - part 1
GEO Series GSE217944. Saccharomyces cerevisiae. 27 samples. Type: Expression profiling by high throughput sequencing.
Combinatorial in vivo genome editing identifies widespread epistasis and an accessible fitness landscape during lung tumorigenesis
GEO Series GSE281604. Mus musculus. 74 samples. Type: Other.
ScienceDex guides
Understand access before you commit
These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.