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259 results for “mouse genetics”
Data related to research article: Towards mouse genetic-specific RNA-sequencing read mapping
<p>This dataset contains data related to the research article: "Towards mouse genetic-specific RNA-sequencing read mapping".</p>
Genetic variation in mouse islet Ca2+ oscillations reveals novel regulators of islet function
<p class="MsoNormal">Insufficient insulin secretion to meet metabolic demand results in diabetes. The intracellular flux of Ca<sup>2+</sup> into β-cells triggers insulin release. Since genetics strongly influences variation in islet secretory responses, we surveyed islet Ca<sup>2+</sup> dynamics in eight genetically diverse mouse strains. We found high strain variation in response to four conditions: 1) 8 mM glucose; 2) 8 mM glucose plus amino acids; 3) 8 mM glucose, amino acids, plus 10nM GIP; and 4) 2 mM glucose. These stimuli interrogate β-cell function, α-cell to β-cell signaling, and incretin responses. We then correlated components of the Ca<sup>2+</sup> waveforms to islet protein abundances in the same strains used for the Ca<sup>2+</sup> measurements. To focus on proteins relevant to human islet function, we identified human orthologues of correlated mouse proteins that are proximal to glycemic-associated SNPs in human GWAS. Several orthologues have previously been shown to regulate insulin secretion (e.g. ABCC8, PCSK1, and GCK), supporting our mouse-to-human integration as a discovery platform. By integrating these data, we nominated novel regulators of islet Ca<sup>2+</sup> oscillations and insulin secretion with potential relevance for human islet function. We also provide a resource for identifying appropriate mouse strains in which to study these regulators.</p>
Genetic variation in mouse islet Ca2+ oscillations reveals novel regulators of islet function
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Feature attention graph neural network for estimating brain age and identifying important neural connections in mouse models of genetic risk for Alzheimer's disease
<p>Connectome, traits and behavior data for APOE234 mice.</p> <ul> <li>1. connectome.zip: mouse brain structural connectivity matrices from diffusion MRI.</li> <li>2. FAGNN_Phenotype.csv: a sheet of trait information of mice used in the study.</li> </ul> <p>columns: winding numbers, total distance, normalized NE time, normalized NE distance, normalized NW time, normalized NW distance, normalized SE time, normalized SE distance, normlaized SW time, normalized SW distance, island latency to first entry, island entries, normalized thigmataxis time, and normalized thigmotaxis distance</p> <div>rows: 4 trials for each day from day 1 to day 5 with 1 probing test each at day 5 and day 8</div> <ul> <li>3. mouse_anatomy.csv: brain region information regarding the connectivity matrix.</li> <li>4. behavior.zip: behavioral data for each mouse from Morris Water Maze experiments.</li> </ul>
Modelling the genetic aetiology of complex disease: human-mouse conservation of noncoding features and disease-associated loci
<p>Understanding the genetic aetiology of loci associated with disease is crucial for developing preventative measures and effective treatments. Mouse models are used extensively to understand human pathobiology and mechanistic functions of disease-associated loci. However, the utility of mouse models is limited by evolutionary divergence in transcription regulation for pathways of interest. Here, we summarise the conservation of genomic (exonic and multi-cell regulatory) features and complex disease associated variant sites between humans and mice. Our results highlight the importance of understanding evolutionary divergence in transcription regulation when interpreting functional studies using mice as models for human disease variants.</p>
Millions of lung tumors harboring KRAS, BRAF, EGFR, and tumor suppressor alterations from genetically engineered mouse models
<p><span>Tumors acquire alterations in oncogenes and tumor suppressor genes in an adaptive walk through the fitness landscape of tumorigenesis. However, the <a>interactions </a></span><span>between oncogenes and tumor suppressor genes that shape this landscape remain poorly resolved and cannot be revealed by human cancer genomics alone. Here, we use a multiplexed, autochthonous mouse platform to model and quantify the initiation and growth of more than one hundred genotypes of lung tumors across four oncogenic contexts: KRAS G12D, KRAS G12C, BRAF V600E, and EGFR L858R. We show that the fitness landscape is rugged—the effect of tumor suppressor inactivation often switches between beneficial and deleterious depending on the oncogenic context—and shows no evidence of diminishing-returns epistasis within variants of the same oncogene. These findings argue against a simple linear signaling relationship amongst these three oncogenes and imply a critical role for off-axis signaling in determining the fitness effects of inactivating tumor suppressors.</span></p>
Pleiotropic effects of trisomy and pharmacologic modulation on structural, functional, molecular, and genetic systems in a Down syndrome mouse model
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Modelling the genetic aetiology of complex disease: human-mouse conservation of noncoding features and disease-associated loci
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Data for: Desert landscape features influencing the microgeographic genetic structure of Nelson’s pocket mouse Chaetodipus nelsoni
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Data from: Keratinocyte-TRPV1 sensory neuron interactions in a genetically controllable mouse model of chronic neuropathic itch
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Millions of lung tumors harboring KRAS, BRAF, EGFR, and tumor suppressor alterations from genetically engineered mouse models
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Data from: Polyandry and the decrease of a selfish genetic element in a wild house mouse population
Despite deleterious effects on individuals, the t haplotype is a selfish genetic element present in many house mouse populations. By distorting the transmission ratio, +/t males transmit the t haplotype to up to 90% of their offspring. However, t/t individuals perish in utero. Theoretical models based on these properties predict a much higher t frequency than observed, leading to the t paradox. Here, we use empirical field data and theoretical approaches to investigate whether polyandry is a female counterstrategy against the negative fitness consequences of such distorters. We found a significant decrease of the t frequency over a period of 5.5 years that cannot be explained by the effect of transmission ratio distortion and recessive lethals, despite significantly higher life expectancy of +/t females compared to +/+ females. We quantified life history data and homozygous and heterozygous fitness effects. Population subdivision and inbreeding were excluded as evolutionary force influencing the t system. The possible influence of polyandry on the t system was then investigated by applying a stochastic model to this situation. Simulations show that polyandry can explain the observed t dynamics, making it a biologically plausible explanation for low t frequencies in natural populations in general.
Data from: Rapid, pervasive genetic differentiation of urban white-footed mouse (Peromyscus leucopus) populations in New York City
We investigated genetic diversity and structure of urban white-footed mouse, Peromyscus leucopus, populations in New York City (NYC) using variation at 18 microsatellite loci. White-footed mice are "urban adapters" that occur at higher population densities as habitat fragments are reduced in area, but have a limited ability to disperse through urbanized areas. We hypothesized that this combination of traits has produced substantial genetic structure but minimal loss of genetic variation over the last century in NYC. Allelic diversity and heterozygosity in fourteen NYC populations were high, and nearly all of our NYC study sites contained genetically distinct populations of white-footed mice as measured by pairwise FST, assignment tests, and Bayesian clustering analyses performed by Structure and BAPS. Analysis of molecular variance revealed that genetic differences between populations separated by a few km are more significant than differences between prehistorically isolated landmasses (i.e. Bronx, Queens, and Manhattan). Allele size permutation tests and lack of isolation-by-distance indicated that mutation and migration are less important than drift as explanations for structure in urban, fragmented P. leucopus populations. Peromyscus often exhibit little genetic structure over even regional scales, prompting us to conclude that urbanization is a particularly potent driver of genetic differentiation compared to natural fragmentation.
Data from: Challenges of NGS in conservation management: insights from long-term monitoring of corridor effects on the genetic diversity of mouse lemurs in a fragmented landscape
Long-term genetic monitoring of populations is essential for efforts aimed at preserving genetic diversity of endangered species. Here, we employ a framework of long-term genetic monitoring to evaluate the effects of fragmentation and the effectiveness of the establishment of corridors in restoring population connectivity and genetic diversity of mouse lemurs Micocebus ganzhorni. To this end, we supplement estimates of neutral genetic diversity with the assessment of adaptive genetic variability of the MHC. In addition, we address the challenges of long-term genetic monitoring of functional diversity by comparing the genotyping performance and estimates of MHC variability generated by SSCP/Sanger-sequencing with those obtained by high throughput sequencing (NGS, Illumina), an issue that is particularly relevant when previous work serves as a baseline for planning management strategies that aim to ensure the viability of a population. We report that SSCP greatly underestimates individual diversity and that discrepancies in estimates of MHC diversity attributable to the comparisons of traditional and NGS genotyping techniques can influence the conclusions drawn from conservation management scenarios. Evidence of migration among fragments in Mandena suggests that mouse lemurs are robust to the process of fragmentation and that the effect of corridors is masked by ongoing gene flow. Nonetheless, results based on a larger number of shared private alleles at neutral loci between fragment pairs found after the establishment of corridors in Mandena suggest that gene flow is augmented as a result of enhanced connectivity. Our data points out that despite low effective population size, M. ganzhorni maintains high individual heterozygosity at neutral loci and at MHC II DRB gene and that selection plays a predominant role in maintaining MHC diversity. These findings highlight the importance of long-term genetic monitoring in order to disentangle between the processes of drift and selection maintaining adaptive genetic diversity in small populations.
Data from: Urban landscape genetics: canopy cover predicts gene flow between white-footed mouse (Peromyscus leucopus) populations in New York City
In this study, I examine the influence of urban canopy cover on gene flow between 15 white-footed mouse (Peromyscus leucopus) populations in New York City. Nm calculated from F_ST and recent migration estimated in BayesAss+, but not historic migration estimated in Migrate-n, exhibited significant isolation-by-distance (IBD). Gene flow was also associated with "effective distances" between populations that were calculated based on percent canopy cover using two different approaches: 1) isolation-by-effective-distance (IED) that calculates the single best pathway to minimize passage through high-resistance (i.e. low canopy cover) areas, and 2) isolation-by-resistance (IBR), an implementation of circuit theory that identifies all low-resistance paths through the landscape. IBR, but not IED, models were still significantly associated with all three measures of gene flow after factoring out the influence of IBD using partial Mantel tests. In cases where both IBR and IED explained gene flow independently of IBD, an additional partial Mantel test indicated that the IBR models still explained gene flow after factoring out IED. The IBR models that explained the most variation in recent migration after factoring out IBD (r = 0.70 – 0.90) included landscape cells with at least 60-80% canopy cover as low resistance habitat. These results have implications for understanding the impacts of urbanization trends on native wildlife, as well as for urban reforestation efforts that aim to improve urban ecosystem processes.
Data from: Heritability and genetic correlations of personality, life history, and morphology in the grey mouse lemur (M. murinus)
<p class="Style1">The recent interest in animal personality has sparked a number of studies on the heritability of personality traits. Yet, how the sources variance these traits can be decomposed remains unclear. Moreover, whether genetic correlations with life-history traits, personality traits and other phenotypic traits exist as predicted by the pace-of-life syndrome hypothesis remains poorly understood. Our aim was to compare the heritability of personality, life-history, and morphological traits and their potential genetic correlations in a small primate (<i>Microcebus murinus</i>). We performed an animal model analysis on six traits measured in a large sample of captive mouse lemurs (<i>N</i>=486). We chose two personality traits, two life history traits, and two morphological traits to 1) estimate the genetic and/or environmental contribution to their variance, and 2) test for genetic correlations between these traits. We found modest narrow-sense heritability for personality traits, morphological traits, and life history traits. Other factors including maternal effects also influence the sources of variation in life history and morphological traits. We found genetic correlations between emergence latency on the one hand and radius length and growth rate on the other hand. Emergence latency was also genetically correlated with birth weight and was influenced by maternal identity. These results provide insights into the influence of genes and maternal effects on the partitioning of sources of variation in personality, life-history, and morphological traits in a captive primate model and suggest that the pace-of-life syndrome may be partly explained by genetic trait covariances.</p>
Data from: Seeking signatures of reinforcement at the genetic level: a hitchhiking mapping and candidate gene approach in the house mouse
Reinforcement is the process by which prezygotic isolation is strengthened as a response to selection against hybridization. Most empirical support for reinforcement comes from the observation of its possible phenotypic signature: an accentuated degree of prezygotic isolation in the hybrid zone as compared to allopatry. Here, we implemented a novel approach to this question by seeking for the signature of reinforcement at the genetic level. In the house mouse, selection against hybrids and enhanced olfactory-based assortative mate preferences are observed in a hybrid zone between the two European subspecies Mus musculus musculus and M. m. domesticus, suggesting a possible recent reinforcement event. To test for the genetic signature of reinforcing selection and identify genes involved in sexual isolation, we adopted a hitchhiking mapping approach targeting genomic regions containing candidate genes for assortative mating in mice. We densely scanned these genomic regions in hybrid zone and allopatric samples using a large number of fast evolving microsatellite loci that allow the detection of recent selection events. We found a handful of loci showing the expected pattern of significant reduction in variability in populations close to the hybrid zone, showing assortative odour preference in mate choice experiments as compared to populations further away and displaying no such preference. These loci lie close to genes that we pinpoint as testable candidates for further investigation.
Genetic and cellular/biochemical data for mouse Pycard gene differences altering mRNA turnover and IL-1b release
<p>Quantitative trait locus mapping for interleukin-1b release after inflammasome priming and activation was performed on bone marrow-derived macrophages (BMDM) from an AKRxDBA/2 strain intercross. The strongest associated locus mapped very close to the <i>Pycard</i> gene on chromosome 7, which codes for the inflammasome adaptor protein apoptosis-associated speck-like protein containing a CARD (ASC). The DBA/2 and AKR <i>Pycard</i> genes only differ at single nucleotide polymorphism (SNP) in their 3' untranslated region (UTR). DBA/2 vs. AKR BMDM had increased levels of <i>Pycard</i> mRNA expression and ASC protein, and increased inflammasome speck formation, which was associated with increased <i>Pycard</i> mRNA stability without an increased transcription rate. CRIPSR/Cas9 gene editing was performed on DBA/2 embryonic stem cells to change the <i>Pycard</i> 3'UTR SNP from the DBA/2 to the AKR allele. This single base change significantly reduced <i>Pycard</i> expression and inflammasome activity after cells were differentiated into macrophages due to reduced <i>Pycard</i> mRNA stability.</p>
Data from: Rapid, pervasive genetic differentiation of urban white-footed mouse (Peromyscus leucopus) populations in New York City
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Data from: Challenges of NGS in conservation management: insights from long-term monitoring of corridor effects on the genetic diversity of mouse lemurs in a fragmented landscape
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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.