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6,171 results for “mutant”
Source data: Native American ataxia medicines rescue ataxia-linked mutant potassium channel activity via binding to the voltage sensing domain
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The KRASG12C Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients
<p>We directly interrogated the role of selected genes in mediating therapeutic response to MRTX849 utilizing a focused CRISPR/Cas9 knockout screen targeting approximately 400 genes including many genes involved in KRAS signaling. This was conducted in H358 and H2122 cells in vitro and in H2122 xenografts in vivo in presence and absence of MRTX849 treatment.</p> <p>Three independent drug anchored CRISPR studies were performed and two data files have been provided for each study. The .csv metadata files contain sample IDs, replicate number, sample descriptions and various experimental conditions. The .xlsx data files contain guide labels, guide sequences and NGS guide counts.Three independent drug anchored CRISPR studies were performed and two data files have been provided for each study. The .csv metadata files contain sample IDs, replicate number, sample descriptions and various experimental conditions. The .xlsx data files contain guide labels, guide sequences and NGS guide counts.</p>
Mutant phenotypes of candidate genes from Fv'/Fm' and QY max loci identified using GWAS in Arabidopsis HapMap population
<p>The phenotypes of T-DNA insertion lines and background line (Col-0), located in the loci identified using GWAS, corresponding to maximum quantum yield (QY max) and light-adapted quantum yield (Fv'/Fm') under salt stress. The data was collected using high-throughput phenotyping of plants and is part of a manuscript currently in preparation. </p>
Data-driven models reveal mutant cell behaviors important for myxobacterial aggregation
<p>Single mutations frequently alter several aspects of cell behavior but rarely reveal whether a particular statistically significant change is biologically significant. To determine which behavioral changes are most important for multicellular self-organization, we devised a new methodology using <em>Myxococcus xanthus</em> as a model system. During development, myxobacteria coordinate their movement to aggregate into spore-filled fruiting bodies. We investigate how aggregation is restored in two mutants, <em>csgA</em> and <em>pilC</em>, that cannot aggregate unless mixed with wild type (WT) cells. To this end, we use cell tracking to follow the movement of fluorescently labeled cells in combination with data-driven agent-based modeling. The results indicate that just like WT cells, both mutants bias their movement toward aggregates and reduce motility inside aggregates. However, several aspects of mutant behavior remain uncorrected by WT demonstrating that perfect recreation of WT behavior is unnecessary. In fact, synergies between errant behaviors can make aggregation robust.</p>
nkx3.2 mutant zebrafish accommodate jaw joint loss through a phenocopy of the head shapes of Paleozoic jawless fish
The vertebrate jaw is a versatile feeding apparatus. To function, it requires a joint between the upper and lower jaws, so jaw joint defects are often highly disruptive and difficult to study. To describe the consequences of jaw-joint dysfunction, we engineered two independent null alleles of a single jaw-joint marker gene, <i>nkx3.2</i>, in zebrafish. These mutations caused zebrafish to become functionally jawless via fusion of the upper and lower jaw cartilages (ankylosis). Despite lacking jaw joints, <i>nkx3.2</i> mutants survived to adulthood and accommodated this defect by: a) remodeling their skulls; and b) altering their behavior from suction feeding to ram feeding. As a result, <i>nkx3.2</i> mutants developed skull shapes superficially similar to those observed in two lineages of ancient jawless vertebrates (anaspids and furcacaudiid thelodonts), including: a fixed open gape, reduced snout, and enlarged branchial region. However, no homology exists in individual skull elements between these taxa, and most of the modified elements in the mutant zebrafish occur outside known expression domains of <i>nkx3.2</i>. Therefore, we interpret the adult <i>nkx3.2</i> phenotype not as a reversal to an ancestral state, but as convergence due to similar functional requirements of feeding without moveable jaws. This remarkable convergence strongly suggests that jaw movements themselves dramatically influence the development of jawed vertebrate skulls. Thus, these mutants provide a unique model with which to: a) investigate adaptive responses to perturbation in skeletal development; b) re-evaluate evolutionarily inspired interpretations of phenocopies generated by gene knockdowns and knockouts; and c) gain insights into feeding mechanics of the extinct agnathans.
NMR data for titration of various mutants in a highly charge depleted protein EXG:CBM
<p>Supporting Information for</p> <p><strong>Charge Interactions in a Highly Charge-depleted Protein</strong></p> <p>Stefan Hervø-Hansen<sup>a,b,1</sup>, Casper Højgaard<sup>a,1</sup>, Kristoffer Enøe Johansson<sup>a</sup>, Yong Wang<sup>a</sup>, Khadija Wahni<sup>c,d,e</sup>, David Young<sup>c,d,e,§</sup>, Joris Messens<sup>c,d,e</sup>, Kaare Teilum<sup>a</sup>, Kresten Lindorff-Larsen<sup>a**</sup>, and Jakob Rahr Winther<sup>a*</sup></p> <p><sup>a</sup>Linderstrøm-Lang Centre of Protein Science, Department of Biology, University of Copenhagen, DK-2200 Copenhagen N, Denmark, <sup>b</sup>Division of Theoretical Chemistry, Department of Chemistry, Lund University, SE 221 00 Lund, Sweden, <sup>c</sup>VIB-VUB Center for Structural Biology, Vlaams Instituut voor Biotechnologie - Vrije Universiteit Brussel, B-1050 Brussels, Belgium, <sup>d</sup>Brussels Center for Redox Biology, Vrije Universiteit Brussel, B-1050 Brussels, Belgium, <sup>e</sup>Structural Biology Brussels, Vrije Universiteit Brussel, B-1050 Brussels, Belgium</p> <p><sup>*</sup>To whom correspondence may be addressed <a href="mailto:jrwinther@bio.ku.dk">jrwinther@bio.ku.dk</a></p> <p><sup>**</sup>Co-corresponding author, <a href="mailto:lindorff@bio.ku.dk">lindorff@bio.ku.dk</a></p> <p><sup>1 </sup>These authors contributed equally to this work.</p> <p> </p> <p>Preprint available on BioRXiv</p>
A Lightweight Technique to Identify Equivalent Mutants
<p>Mutation analysis is a popular but costly approach to assess the quality of test suites. Equivalent mutants are useless and contribute to increase costs. We propose a lightweight technique to identify equivalent mutants by proving equivalences with Z3 in the context of weak mutation testing. To evaluate our approach, we apply our technique for 40 mutation targets (mutations of an expression or statement) and automatically identify 13 equivalent mutations for seven mutation targets. We manually confirm that the equivalent mutants detected by our technique are indeed equivalent. Moreover, we evaluate our approach in the context of strong mutation testing against mutants generated by MuJava for 5 projects. Our technique detects all equivalent mutants detected by TCE. The results of our technique can be useful to improve mutation testing tools by avoiding the application of 13 mutations for 7 mutation targets.</p>
Raw diffraction images of hollow-forming cypovirus polyhedra mutant crystals (H3L2 deletion)
<p>Crystal structure of cypovirus polyhedra mutant (H3L2 deletion) to form hollow inside (PDB code: <a href="https://www.rcsb.org/structure/6LEE">6LEE</a>).</p> <p>Small-wedge (5° or 10°/each) datasets were collected from loop-harvested microcrystals using <a href="https://github.com/keitaroyam/yamtbx/blob/master/doc/eiger-en.md">EIGER</a> X 9M detector at a wavelength of 1 Å using a microbeam on BL32XU, SPring-8. </p> <p>All diffraction images were processed using XDS through <a href="https://github.com/keitaroyam/yamtbx/blob/master/doc/kamo-en.md">KAMO</a> pipeline, and merged using XSCALE with kamo.multi_merge. The crystals belong to space group I23 with a=103.8 Å. Finally 45 datasets were merged at 1.95 Å resolution in the published result. </p>
Data from: Mutant invasions and adaptive dynamics in variable environments
The evolution of natural organisms is ultimately driven by the invasion and possible fixation of mutant alleles. The invasion process is highly stochastic, however, and the probability of success is generally low, even for advantageous alleles. Additionally, all organisms live in a stochastic environment, which may have a large influence on what alleles are favorable, but also contributes to the uncertainty of the invasion process. We calculate the invasion probability of a beneficial, mutant allele in a monomorphic, large population subject to stochastic environmental fluctuations, taking into account density- and frequency-dependent selection, stochastic population dynamics and temporal autocorrelation of the environment. We treat both discrete and continuous time population dynamics, and allow for overlapping generations in the continuous time case. The results can be generalized to diploid, sexually reproducing organisms embedded in communities of interacting species. We further use these results to derive an extended canonical equation of adaptive dynamics, predicting the rate of evolutionary change of a heritable trait on long evolutionary time scales.
Data from: Drosophila FoxP mutants are deficient in operant self-learning
Intact function of the Forkhead Box P2 (FOXP2) gene is necessary for normal development of speech and language. This important role has recently been extended, first to other forms of vocal learning in animals and then also to other forms of motor learning. The homology in structure and in function among the FoxP gene members raises the possibility that the ancestral FoxP gene may have evolved as a crucial component of the neural circuitry mediating motor learning. Here we report that genetic manipulations of the single Drosophila orthologue, dFoxP, disrupt operant self-learning, a form of motor learning sharing several conceptually analogous features with language acquisition. Structural alterations of the dFoxP locus uncovered the role of dFoxP in operant self-learning and habit formation, as well as the dispensability of dFoxP for operant world-learning, in which no motor learning occurs. These manipulations also led to subtle alterations in the brain anatomy, including a reduced volume of the optic glomeruli. RNAi-mediated interference with dFoxP expression levels copied the behavioral phenotype of the mutant flies, even in the absence of mRNA degradation. Our results provide evidence that motor learning and language acquisition share a common ancestral trait still present in extant invertebrates, manifest in operant self-learning. This 'deep' homology probably traces back to before the split between vertebrate and invertebrate animals.
Data from: Within-host stochastic emergence dynamics of immune-escape mutants
Predicting the emergence of new pathogenic strains is a key goal of evolutionary epidemiology. However, the majority of existing studies have focussed on emergence at the population level, and not within a host. In particular, the coexistence of pre-existing and mutated strains triggers a heightened immune response due to the larger total pathogen population; this feedback can smother mutated strains before they reach an ample size and establish. Here, we extend previous work for measuring emergence probabilities in non-equilibrium populations, to within-host models of acute infections. We create a mathematical model to investigate the emergence probability of a fitter strain if it mutates from a self-limiting strain that is guaranteed to go extinct in the long-term. We show that ongoing immune cell proliferation during the initial stages of infection causes a drastic reduction in the probability of emergence of mutated strains; we further outline how this effect can be accurately measured. Further analysis of the model shows that, in the short-term, mutant strains that enlarge their replication rate due to evolving an increased growth rate are more favoured than strains that suffer a lower immune-mediated death rate ('immune tolerance'), as the latter does not completely evade ongoing immune proliferation due to inter-parasitic competition. We end by discussing the model in relation to within-host evolution of human pathogens (including HIV, hepatitis C virus, and cancer), and how ongoing immune growth can affect their evolutionary dynamics.
Data from: The fitness effects of a pale mutant in the aposematic seed bug Lygaeus simulans indicate pleiotropy between warning coloration and life history
Conspicuous warning colours that signal chemical or other defences are common in the natural world. For instance, such aposematic warning patterns of red-and-black or yellow-and-black are common among insect taxa, particularly in the order Hemiptera, often forming the basis of Batesian and/or Müllerian mimicry rings. In addition, it has been repeatedly noted that colour polymorphisms or mutants that influence pigmentation can show pleiotropy with other behavioural, physiological or life-history traits. Here we describe a pale mutant of the seed bug Lygaeus simulans that appeared in our lab population in 2012, which differs in colour to the wild-type bugs. Through multigenerational experimental crosses between wild-type and pale mutant L. simulans, we first show that the pale phenotype segregates as a single Mendelian locus, with the pale allele being recessive to the wild-type. Next, we show (1) that there is a large heterozygous advantage in terms of fecundity, (2) that pale females suffer reduced longevity, and (3) that pale males have increased body length compared to wild-type homozygotes. Our data therefore suggest that the colour locus is pleiotropic with a number of life-history traits, opening the door for a more complete genetic analysis of aposematic colouration in this species. In addition, this phenotype will be useful as a visible genetic marker, providing a tool for investigating sperm competition and other post-copulatory drivers of sexual selection in this species.
Comparative genomic analysis of the mutant Rhodotorula mucilaginosa JH-R23 provides insight into the high-yield carotenoid mechanism
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Double and triple thermodynamic mutant cycles reveal the basis for specific MsbA-lipid interactions
<p>Raw native MS data for manuscript</p>
Luminal STIM1 Mutants that Cause Tubular Aggregate Myopathy Promote Autophagic Processes
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Targeting Myc-driven stress vulnerability in mutant KRAS colorectal cancer (Ruan et al.)
<p>Mutant <em>KRAS </em>is a key driver in colorectal cancer (CRC) and promotes Myc translation and Myc-dependent stress adaptation and proliferation. Here, we report that the combination of two FDA-approved drugs Bortezomib and Everolimus (RAD001) (BR) is highly efficacious against mutant <em>KRAS </em>CRC cells. Mechanistically, the combination, not single agent, rapidly depletes Myc protein, not mRNA, and leads to GCN2- and p-eIF2a-dependent cell death through the activation of extrinsic and intrinsic apoptotic pathways. Cell death is selectively induced in mutant <em>KRAS </em>CRC cells with elevated basal Myc and p-eIF2a and is characterized by CHOP induction and transcriptional signatures in proteotoxicity, oxidative stress, metabolic inhibition, and immune activation. BR-induced p-GCN2/p-eIF2a elevation and cell death are strongly attenuated by <em>MYC </em>knockdown and enhanced by <em>MYC </em>overexpression. The BR combination is efficacious against mutant <em>KRAS </em>patient derived organoids (PDO) and xenografts (PDX) by inducing p-eIF2a/CHOP and cell death. Interestingly, an elevated four-gene (DDIT3, GADD45B, CRYBA4 and HSPA1L) stress signature is linked to shortened overall survival in CRC patients. These data support that Myc-dependent stress adaptation drives the progression of mutant <em>KRAS </em>CRC and serves as a therapeutic vulnerability, which can be targeted using dual translational inhibitors.</p>
SI Reduction of phosphoribulokinase amount and re-routing me-tabolism in Chlamydomonas reinhardtii CP12 mutants.
<p>Supplementary material associated with the manuscript<strong>: </strong>Reduction of phosphoribulokinase amount and re-routing me-tabolism in Chlamydomonas reinhardtii CP12 mutants</p>
Direct access to millions of mutations by Whole Genome Sequencing of an oilseed rape mutant population
<p>Induced mutations are an essential source of genetic variation in plant breeding. EMS mutagenesis has been frequently applied, and mutants have been detected by phenotypic or genotypic screening of large populations. In this study, a rapeseed M<sub>2</sub> population was derived from M<sub>1</sub> parent cultivar “Express” treated with EMS. Whole genomes were sequenced from fourfold (4x) pools of 1,988 M<sub>2</sub> plants representing 497 M<sub>2</sub> families. Detected mutations were not evenly distributed and displayed distinct patterns across the 19 chromosomes with lower mutation rates towards the ends. Mutation frequencies ranged from 32/Mb to 48/Mb. On average, 284,442 single nucleotide polymorphisms per M<sub>2</sub> DNA pool were found resulting from EMS mutagenesis. 55% were C→T and G→A transitions, characteristic for EMS induced (‘canonical’) mutations, whereas the remaining SNPs were ‘non-canonical’ transitions (15%) or transversions (30%). Additionally, we detected 88,725 high confidence insertions and deletions (InDels) per pool. On average, each M<sub>2</sub> plant carried 39,120 canonical mutations, corresponding to a frequency of one mutation per 23.6 kb. Roughly 82% of such mutations were located either 5 kb upstream or downstream (~56%) of gene coding regions or within intergenic regions (26%). The remaining 18% were located within regions coding for genes. All mutations detected by whole-genome sequencing could be verified by comparison with known mutations. Furthermore, all sequences are accessible via the online tool “EMS Brassica” (<a href="http://www.emsbrassica.plantbreeding.uni-kiel.de/">http://www.emsbrassica.plantbreeding.uni-kiel.de/</a>), which enables direct identification of mutations in any target sequence. The sequence resource described here will further add value for functional gene studies in rapeseed breeding.</p>
Atomistic Predictions and Network-Based Allosteric Analysis of Conformational Ensembles for the State-Switching ABL Kinase Mutants Using Combination of Alanine Sequence Scanning and Shallow Subsampling in AlphaFold2
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Lopez and Alward_2023_RSOS_Female aromatase_AR mutants_datasets
<p>Contains data used in statistical analyses and figure generation in Lopez and Alward 2024 published in Royal Society Open Science. </p>
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