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6,363 results for “Mutations”
Association between susceptibility of Thrips palmi to spinetoram and frequency of G275E mutation provides basis for molecular diagnostics of field-evolved resistance
<p><b><span>Background</span></b><span>: Spinosyn resistance is an increasing problem in field control of targeted pests. While putative mechanisms underlying spinosyn resistance have been identified in controlled studies on many species, mechanisms underlying field-evolved resistance and the development of a molecular diagnostic method for monitoring field resistance have lagged behind. Here, we examined levels of resistance of melon thrips, <i>Thrips palmi,</i> to spinetoram as well as target site mutations in field populations across China to identify potential mechanisms and useful molecular markers for diagnostic purposes.</span></p> <p><b><span>Results</span></b><span>: LC<sub>50</sub> </span><span>of 16 field-collected populations to the spinetoram varied from 0.12 to 759.34 </span>mg L<sup>-1</sup><span>. In resistant populations, we identified the G275E mutation, which has previously been linked to spinosyns resistance, as well as another nonsynonymous mutation, F314V, both located in the <i>α</i>6 subunit of the nicotinic acetylcholine receptor. There was a strong correlation between levels of spinetoram resistance and allele frequency of G275E mutation in field-collected populations (<i>r<sup>2</sup></i> = 0.84) and those reared under laboratory conditions for two to five generations (<i>r<sup>2</sup></i> = 0.91). LC<sub>50</sub> ranged from 0.12 to 0.66 </span>mg L<sup>-1</sup><span> in populations without </span><span>G275E mutation, while it ranged from </span>33.12<span> to 39.91</span> mg L<sup>-1</sup><span> in most populations with a </span><span>G275E mutation frequency > 90%, with the exception of one field-collected population which had an G275E frequency of 92% and a very high LC<sub>50</sub> value of 759.34</span> mg L<sup>-1</sup><span>, suggesting additional mechanisms.</span></p> <p><b><span>Conclusions: </span></b><span>Our results indicate that field-evolved resistance of <i>T. palmi</i> to spinetoram in China is mainly conferred by the G275E mutation, with other mechanisms contributing to a higher level of resistance. The frequency of the G275E mutation provides a useful diagnostic for quantifying resistance levels in field populations of <i>T. palmi</i>.</span></p>
Fast and exact single and double mutation-response scanning of proteins: data and results
<p>Data, data analysis code, and results accompanying the manuscript: <strong>Fast and exact single and double mutation-response scanning of proteins: </strong>https://doi.org/10.1101/2020.10.23.352955</p> <p>In addition, the code needed to generate the data must be downloaded from <a href="https://doi.org/10.5281/zenodo.4123149">https://doi.org/10.5281/zenodo.4123149</a> and put in a subfolder named mutenm/</p>
Pretreatment Neutrophil-to-Lymphocyte Ratio, Mutational Load, and Outcomes in Patients Treated with Immune Checkpoint Inhibitors
<p>This dataset has been used to analyze the association between pre-treatment neutrophil-to-lymphocyte ratio and tumour mutational burden with survival and response to treatment in immunotherapy-treated patients with cancer. The dataset contains clinical and genomic data for 2,037 patients with 18 cancer types.</p>
Response Rates to Anti–PD-1 Immunotherapy in Microsatellite-Stable Solid Tumors With 10 or More Mutations per Megabase
<p>This dataset has been used to analyze the association between tumor mutational burden and response to treatment in immunotherapy-treated patients with microsatellite-stable solid tumors. The dataset contains clinical and genomic data for 1,678 patients with 16 cancer types.</p> <p> </p>
Elevated temperature increases genome-wide selection on de novo mutations
<p>Adaptation in new environments depends on the amount of genetic variation available for evolution, and the efficacy by which natural selection discriminates among this variation. However, whether some ecological factors reveal more genetic variation, or impose stronger selection pressures than others, is typically not known. Here, we apply enzyme kinetic theory to show that rising global temperatures are predicted to intensify natural selection throughout the genome by increasing the effects of DNA sequence variation on protein stability. We test this prediction by i) estimating temperature-dependent fitness effects of induced mutations in seed beetles adapted to ancestral or elevated temperature, ii) calculate 100 paired selection estimates on mutations in benign versus stressful environments from unicellular and multicellular organisms. Environmental stress per se did not increase mean selection on de novo mutation, suggesting that the cost of adaptation does not generally increase in new ecological settings to which the organism is maladapted. However, elevated temperature increased the mean strength of selection on genome-wide polymorphism, signified by increases in both mutation load and mutational variance in fitness. These results have important implications for genetic diversity gradients and the rate and repeatability of evolution under climate change.</p>
The evolutionary advantage of fitness-dependent recombination in diploids: a deterministic mutation–selection–balance model
<p>Recombination's omnipresence in nature is one of the most intriguing problems in evolutionary biology. The question of why recombination exhibits certain general features is no less interesting than that of why it exists at all. One such feature is recombination's fitness dependence (FD). The so far developed population-genetics models have focused on the evolution of FD recombination mainly in haploids, although the empirical evidence for this phenomenon comes mostly from diploids. Using numerical analysis of modifier models for infinite panmictic populations, we show here that FD recombination can be evolutionarily advantageous in diploids subjected to purifying selection. We ascribe this advantage to the differential rate of disruption of lower- vs higher-fitness genotypes, which can be manifested in selected systems with at least three loci. We also show that if the modifier is linked to such selected system, it can additionally benefit from modifying this linkage in a fitness-dependent manner. The revealed evolutionary advantage of FD recombination appeared robust to crossover interference within the selected system, either positive or negative. Remarkably, FD recombination was often favored in situations where any constant non-zero recombination was evolutionarily disfavored, implying a relaxation of the rather strict constraints on major parameters (e.g., selection intensity and epistasis) required for the evolutionary advantage of non-zero recombination formulated by classical models.</p>
Low immunogenicity of common cancer hot spot mutations resulting in false immunogenic selection signals
<p>Downstream data used for the analysis as reported in the corresponding manuscript.</p>
The burden of post-translational modification (PTM) – disrupting mutations in the tumor matrisome
<p>A Pan-cancer analysis of the post-translational modification (PTM) – disrupting mutations in the tumor matrisome</p>
Data from: Costs of selfing prevent the spread of a self-compatibility mutation that causes reproductive assurance
In flowering plants, shifts from outcrossing to partial or complete self-fertilization have occurred independently thousands of times, yet the underlying adaptive processes are difficult to discern. Selfing's ability to provide reproductive assurance when pollination is uncertain is an oft-cited ecological explanation for its evolution, but this benefit may be outweighed by genetic costs diminishing its selective advantage over outcrossing. We directly studied the fitness effects of a self-compatibility (SC) mutation that was backcrossed into a self-incompatible (SI) population of Leavenworthia alabamica, illuminating the direction and magnitude of selection on the mating-system modifier. In array experiments conducted in two years, SC plants produced 17-26% more seed, but this advantage was counteracted by extensive seed discounting -- the replacement of high-quality outcrossed seeds by selfed seeds. Using a simple model and simulations, we demonstrate that SC mutations with these attributes rarely spread to high frequency in natural populations, unless inbreeding depression falls below a threshold value (0.57 ≤ threshold ≤ 0.70) in SI populations. A combination of heavy seed discounting and moderate inbreeding depression likely explains why outcrossing adaptations such as self-incompatibility are maintained generally, despite persistent input of selfing mutations and frequent limits on outcross seed production in nature.
Spectrum of mutational signatures in T-cell lymphoma reveals a key role for UV radiation in mycosis fungoides and Sezary syndrome
<p>T-cell non-Hodgkin's lymphomas (NHL) develop following transformation of tissue resident T-cells. We performed a meta-analysis of mutational catalogues derived from whole exome sequencing data from 403 patients with eight subtypes of T-cell NHL to identify mutational signatures and recurrent gene mutations associated with specific causal peaks within these signatures. Signature 1, indicative of age-related deamination, was prevalent across all T-cell NHL subtypes, reflecting the derivation of these malignancies from memory T-cell subsets. Adult T-cell leukemia-lymphoma (ATLL) was specifically associated with signature 17, which was found to strongly correlate with the IRF4 K59R mutation that is exclusive to ATLL. Signature 7, implicating UV exposure as a potential initiating factor was uniquely identified in cutaneous T-cell lymphoma, contributing 52% of the mutational burden in mycosis fungoides and 23% in Sezary syndrome. Importantly this UV signature was observed in CD4+ T-cells isolated from blood suggesting extensive re-circulation of these T-cells through both skin and blood and strongly implicating a role for UV in the pathogenesis of cutaneous T-cell lymphoma.</p>
Data from: Effects of a titin mutation on force enhancement and force depression in mouse soleus muscles
The force produced by muscles varies with muscle length. Compared to isometric contractions at the same final length, force increases after lengthening, known as force enhancement, and decreases after shortening, known as force depression. The mechanisms of force enhancement remain unexplained by the sliding-filament and cross-bridge theories of muscle contraction. Although cross-bridge mechanisms have been proposed to account for force depression, so too have other mechanisms. In addition to cross bridges, titin has been suggested to contribute to both force enhancement and depression. Although titin is too compliant in passive muscles to contribute to active stiffness, recent evidence suggests that calcium activation increases titin stiffness. To test the hypothesis that titin plays a role in force enhancement and depression, we investigated muscle force in active and passive wild type and mdm soleus muscles after isovelocity stretching and shortening at three activation levels. Muscles from mdm mice (muscular dystrophy with myositis) have a predicted 83 amino acid deletion in the N2A region of titin and show no increase in stiffness when activated. We found that: 1) force enhancement and depression were reduced in mdm soleus compared to wild type muscles; 2) force enhancement increased with the amplitude of stretch across all activation levels in wild type and mdm muscles, while force depression increased with amplitude in wild type but not in mdm muscles; and 3) maximal shortening velocity of wild type and mdm muscles was similar, although active stress was reduced in mdm compared to wild type muscles. The results of this study suggest a role for titin in force enhancement and depression, which contribute importantly to regulation of muscle force during natural movements.
Data used to produce figures in "Monotonicity of Fitness Landscapes and Mutation Rate Control"
<p>Data used in Figures 2, 3, 4, 6, 7, 8, 9 and 10 of the manuscript "Monotonicity of Fitness Landscapes and Mutation Rate Control"</p>
Involvement of the optic nerve in mutated CSF1R-induced hereditary diffuse leukoencephalopathy with axonal spheroids
<p><strong>Figure 1:</strong> Family pedigree. The arrow indicates the proband (present patient). Her mother developed a motor disorder at 40 years of age and died at 60 years of age. Her grandparents, father, brothers, sisters, and daughters were not affected.</p> <p><strong>Figure 2: Brain MRI, DWI, DTI, and MRS images. T2/Flair showed multifocal periventricular white matter lesions (A, B, and C), without enhancement (D). DWI shows high-signal intensities in periventricular white matters and corpus callosum (E, F). DTI shows decreased numbers of corpus callosum fibers, while subcortical arcuate fibers are spared (G). MRS shows increased Cho levels, while NAA levels are decreased in the white matter lesions (H, I).</strong></p> <p><strong>Figure 3: </strong>Optic nerves on MRI, showing that bilateral optic nerves are injured (red arrows). </p> <p><strong>Figure 4: </strong>OCT shows that the right peripapillary retinal nerve fiber layer (pRNFL) is atrophic in the temporal quadrant, and the left pRNFL is thinning in the temporal superior quadrants. Green represents pRNFL thickness, which is within normal limits; yellow represents pRNFL thickness, which is below borderline; red represents pRNFL thickness, which is below normal limits.</p> <p><strong>Figure 5:</strong> VEP shows reduced bilateral P100 amplitudes, although P100 latencies are normal in both eyes.</p> <p><strong>Figure 6:</strong> Visual fields in the right eye are partially missing in the upper right, lower right, and lower left quadrants, especially in the lower right quadrant. Visual fields in the left eye are partially missing in the four quadrants, especially in the upper left and lower right quadrants.</p> <p><strong>Figure 7:</strong> Gene analysis of <em>CSF1R</em>. The sequencing result from exon 18 of <em>CSF1R</em> (NM_005211.3) indicates a heterozygous c.2345 G>A (p.782Arg>His) substitution in the patient.</p>
Aminergic G protein-coupled receptor (GPCR) mutation data set
<p>Curated set of 6553 quantitative mutation data points covering 34 aminergic G protein-coupled receptors, annotated according to GPCRdb standards (http://gpcrdb.org/) building from the data set published by Kooistra et al. in BJP 2013, 170, 101.</p>
Chemokine G protein-coupled receptor (GPCR) mutation data set
<p>Curated set of 2004 quantitative mutation data points covering 10 chemokine G protein-coupled receptors, annotated according to GPCRdb standards (http://gpcrdb.org/) building from the data set published by Scholten et al. in BJP 2012, 165, 1617.</p>
Data S1. Human PGBD5 DNA transposase promotes site-specific oncogenic mutations in rhabdoid tumors
<p>Supplementary data S1 for Henssen et al. "</p> <p>Human PGBD5 DNA transposase promotes site-specific oncogenic mutations in rhabdoid tumors"</p>
Mutation Testing Operators
<p>Overview of Data</p> <p>This dataset lists the mutation operators for C-programming language</p> <p>Paper Abstract</p> <p>Safety-critical software must adhere to stringent quality standards and is expected to be thoroughly tested. However, exhaustive testing of software is usually impractical. The two main challenges faced by a software testing team are generation of effective test cases and demonstration of testing adequacy.</p> <p>This paper proposes an intuitive and conservative approach to determine the test adequacy in safety-critical software. The approach is demonstrated through a case study: the core temperature monitoring system of a nuclear reactor. We combine conservative test coverage of unique execution path test cases, and the results from mutation testing to determine the test adequacy.</p> <p>Although mutation testing is a powerful technique, the difficulty in identifying equivalent mutants has limited its practical utility. To gain confidence on the computed test adequacy: (i) faults during mutation testing must be induced at all possible execution paths of the code, (ii) properties of unkilled mutants must be studied, and (iii) all equivalent mutants must be detected. In this regard; results of static, dynamic and coverage analysis of the mutants is presented, and a technique to identify the likely equivalent mutants is proposed.</p> <p> </p>
Chemokine G protein-coupled receptor (GPCR) mutation data set - revision
<p>Curated set of 2004 quantitative mutation data points covering 10 chemokine G protein-coupled receptors, annotated according to GPCRdb standards (http://gpcrdb.org/) building from the data set published by Scholten et al. in BJP 2012, 165, 1617.</p> <p>Errors in the previous version were corrected and new data points for CCR2 and CCR9 were added.</p>
Figure 2. - Phylogenetic relationships among Dicronocephalus species reconstructed with Bayesian inference using COI sequences. Numbers above branches indicate ML bootstrap values and Bayesian posterior probabilities. Numbers below branches are bootstrap, symmetric resampling, and jacknife support from parsimony searches, respectively. Scale bar represents 10% nucleotide mutation rate.
Figure 2. - Phylogenetic relationships among Dicronocephalus species reconstructed with Bayesian inference using COI sequences. Numbers above branches indicate ML bootstrap values and Bayesian posterior probabilities. Numbers below branches are bootstrap, symmetric resampling, and jacknife support from parsimony searches, respectively. Scale bar represents 10% nucleotide mutation rate.
Figure 4. - Phylogenetic relationships among Dicronocephalus species reconstructed with Bayesian inference using COI and 16S rRNA sequences. Numbers above branches indicate ML bootstrap values and Bayesian posterior probabilities. Numbers below branches are bootstrap, symmetric resampling, and jacknife support from parsimony searches, respectively. Scale bar represents 10% nucleotide mutation rate.
Figure 4. - Phylogenetic relationships among Dicronocephalus species reconstructed with Bayesian inference using COI and 16S rRNA sequences. Numbers above branches indicate ML bootstrap values and Bayesian posterior probabilities. Numbers below branches are bootstrap, symmetric resampling, and jacknife support from parsimony searches, respectively. Scale bar represents 10% nucleotide mutation rate.
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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.