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This paper aims to systematically analyze the peptides and proteins from Asini Corii Colla(ACC) through shotgun proteomics. After high-pH reversed-phase fractionation, the proteins and peptides in the hydrolysate of ACC were further separated by nano LC-Q-Exactive-MS/MS under the following conditions: Thermo Scientific EASY column(100 μm×2 cm, 5 μm, C_(18)) as precolumn, Thermo Scientific EASY column(75 μm×100 mm, 3 μm, C_(18)) for solid phase extraction, gradient elution with 0.1% formic acid in water(mobile phase A) and 84% acetonitrile in water containing 0.1% formic acid(mobile phase B), and MS in positive ion mode. Based on Uniprot_Equus caballus, MS data, and literature, 2 291 peptides were identified from ACC by MaxQuant, with 255 Maillard reactions(AML, CML, CEL)-modified peptides identified for the first time. Through alignment, the peptides were found to belong to 678 equine proteins. In conclusion, the combination of nano LC-Q-Exactive-MS/MS and shotgun proteomics achieved rapid and accurate identification of the proteins and peptides in ACC, which provides the key information and new insights for further investigation of chemicals and effective substances in ACC.

CRISPR-Cas9-based gene drive systems possess the inherent capacity to spread progressively throughout target populations. Here we describe two self-copying (or active) guide RNA-only genetic elements, called e-CHACRs and ERACRs. These elements use Cas9 produced in trans by a gene drive either to inactivate the cas9 transgene (e-CHACRs) or to delete and replace the gene drive (ERACRs). e-CHACRs can be inserted at various genomic locations and carry two or more gRNAs, the first copying the e-CHACR and the second mutating and inactivating the cas9 transgene. Alternatively, ERACRs are inserted at the same genomic location as a gene drive, carrying two gRNAs that cut on either side of the gene drive to excise it. e-CHACRs efficiently inactivate Cas9 and can drive to completion in cage experiments. Similarly, ERACRs, particularly those carrying a recoded cDNA-restoring endogenous gene activity, can drive reliably to fully replace a gene drive. We compare the strengths of these two systems.

Photoneutron cross sections were measured for $^{137}$Ba and $^{138}$Ba at energies below two-neutron threshold using quasi-monochromatic $��$-ray beams produced in laser Compton-scattering at the NewSUBARU synchrotron radiation facility. The photoneutron data are used to constrain the $��$-ray strength function on the basis of the Hartree-Fock-Bogolyubov plus quasi-particle random phase approximation using the Gogny D1M interaction. Supplementing the experimentally constrained $��$-ray strength function with the zero-limit E1 and M1 contributions which are unique to the deexcitation mode, we discuss radiative neutron capture cross sections relevant to the s-process nucleosynthesis of barium isotopes in the vicinity of the neutron magic number 82., arXiv admin note: substantial text overlap with arXiv:1811.00291, arXiv:1804.07654

A gene drive biases the transmission of a particular allele of a gene such that it is inherited at a greater frequency than by random assortment. Recently, a highly efficient gene drive was developed in insects, which leverages the sequence-targeted DNA cleavage activity of CRISPR/Cas9 and endogenous homology directed repair mechanisms to convert heterozygous genotypes to homozygosity. If implemented in laboratory rodents, this powerful system would enable the rapid assembly of genotypes that involve multiple genes (e.g., to model multigenic human diseases). Such complex genetic models are currently precluded by time, cost, and a requirement for a large number of animals to obtain a few individuals of the desired genotype. However, the efficiency of a CRISPR/Cas9 gene drive system in mammals has not yet been determined. Here, we utilize an active genetic “CopyCat” element embedded in the mouse Tyrosinase gene to detect genotype conversions after Cas9 activity in the embryo and in the germline. Although Cas9 efficiently induces double strand DNA breaks in the early embryo and is therefore highly mutagenic, these breaks are not resolved by homology directed repair. However, when Cas9 expression is limited to the developing female germline, resulting double strand breaks are resolved by homology directed repair that copies the CopyCat allele from the donor to the receiver chromosome and leads to its super-Mendelian inheritance. These results demonstrate that the CRISPR/Cas9 gene drive mechanism can be implemented to simplify complex genetic crosses in laboratory mice and also contribute valuable data to the ongoing debate about applications to combat invasive rodent populations in island communities.

A gene drive biases the transmission of one of the two copies of a gene such that it is inherited more frequently than by random segregation. Highly efficient gene drive systems have recently been developed in insects, which leverage the sequence-targeted DNA cleavage activity of CRISPR-Cas9 and endogenous homology-directed repair mechanisms to convert heterozygous genotypes to homozygosity

BACKGROUND: Aerobic capacity is a powerful predictor of cardiovascular disease and all‐cause mortality, and it declines with advancing age. HYPOTHESIS: Since physical activity alters body metabolism, metabolism markers will likely differ between subjects with high vs low aerobic capacities. METHODS: Community‐based participants without physician‐diagnosed heart disease, stroke or cancer underwent same‐day multimodal assessment of cardiovascular function (by echocardiography and magnetic resonance feature tracking of left atrium) and aerobic capacity by peak oxygen uptake (VO(2)) metrics. Associations between VO(2) and cardiovascular and metabolomics profiles were studied in adjusted models including standard covariates. RESULTS: We studied 141 participants, of whom 82 (58.2%) had low VO(2), while 59 (41.8%) had high VO(2). Compared to participants with high VO(2), participants with low VO(2) had more adverse cardiovascular parameters, such as lower ratio of peak velocity flow in early diastole to peak velocity flow in late diastole by atrial contraction of >0.8 (76% vs 35%, adjusted odd ratio [OR] = 4.1, 95% confidence interval [CI] [1.7‐9.5], P = 0.001) and lower left atrial conduit strain (11.3 ± 4.0 vs 15.6 ± 6.1%, adjusted OR = 1.1, 95% CI [1.002‐1.3], P = 0.045). High VO(2) was associated with lower accumulation of wide‐spectrum acyl‐carnitines (OR = 0.6, 95% CI [0.4‐0.9], P = 0.013), alanine (OR = 0.1, 95% CI [0.01‐0.9], P = 0.044) and glutamine /glutamate (OR = 0.1, 95% CI [0.01‐0.5], P = 0.007), compared to low VO(2.) CONCLUSION: Elderly adults with low VO(2) have adverse cardiovascular and metabolic parameters compared to their counterparts with high VO(2). Combined cardiac and metabolomics phenotyping may be a promising tool to provide insights into physiological states, useful for tracking future interventions related to physical activity among community cohorts.

Photoneutron cross sections were measured for $^{58}$Ni, $^{60}$Ni, $^{61}$Ni, and $^{64}$Ni at energies between the one-neutron and two-neutron thresholds using quasi-monochromatic $��$-ray beams produced in laser Compton-scattering at the NewSUBARU synchrotron radiation facility. The new photoneutron data are used to extract the $��$-ray strength function above the neutron threshold complementing the information obtained by the Oslo method below the threshold. We discuss radiative neutron capture cross sections and the Maxwellian-averaged cross sections for Ni isotopes including $^{63}$Ni, a branching point nucleus along the weak s-process path. The cross sections are calculated with the experimentally constrained $��$-ray strength functions from the Hartree-Fock-Bogolyubov plus quasi-particle-random phase approximation based on the Gogny D1M interaction for both $E1$ and $M1$ components and supplemented with the $M1$ upbend., 9 pages, 7 figures, re-submitted to PRC

Photoneutron cross sections were measured for $^{203}$Tl and $^{205}$Tl at energies between the one- and two-neutron thresholds using quasi-monochromatic $��$-ray beams produced in laser Compton-scattering at the NewSUBARU synchrotron radiation facility. Our new measurement results in cross sections significantly different from the previously reported bremsstrahlung experiment, leading to rather different GDR parameters, in particular to lower GDR peak energies and higher peak cross sections. The photoneutron data are used to constrain the $��$-ray strength function on the basis of the Hartree-Fock-Bogolyubov plus quasi-particle random phase approximation using the Gogny D1M interaction. Supplementing the experimentally constrained $��$-ray strength function with the zero-limit E1 and M1 contributions for the de-excitation mode, we estimate the Maxwellian-averaged cross section for the s-process branching-point nucleus $^{204}$Tl in the context of the $^{205}$Pb - $^{205}$Tl chronometry., 8 pages, 10 figures, to be submitted to PRC

The knirps (kni) locus encodes transcription factors required for induction of the L2 wing vein in Drosophila. Here, we employ diverse CRISPR/Cas9 genome editing tools to generate a series of targeted lesions within the endogenous cis-regulatory module (CRM) required for kni expression in the L2 vein primordium. Phenotypic analysis of these ‘in locus’ mutations based on both expression of Kni protein and adult wing phenotypes, reveals novel unexpected features of L2-CRM function including evidence for a chromosome pairing-dependent process that promotes transcription. We also demonstrate that self-propagating active genetic elements (CopyCat elements) can efficiently delete and replace the L2-CRM with orthologous sequences from other divergent fly species. Wing vein phenotypes resulting from these trans-species enhancer replacements parallel features of the respective donor fly species. This highly sensitive phenotypic readout of enhancer function in a native genomic context reveals novel features of CRM function undetected by traditional reporter gene analysis., eLife digest Gregor Mendel was an Austrian monk and botanist whose work with pea plants in the 19th century founded the field of genetics. Though he was not aware of genes at the time, Mendel essentially worked out that pea plants had two copies of each gene, and that each copy had a 50% chance of being passed on to any one offspring. Yet not all genes actually follow this pattern of inheritance. In 2015, researchers reported that they had used components of the CRISPR/Cas9 genome editing system to edit genes so that they could propagate in a “Super-Mendelian” fashion. Indeed, when it was engineered into fruit flies, any parent carrying this active genetic element passed it on to almost every offspring. Active genetic elements have potential applications in many different fields of scientific research. These include providing new ways to explore how genes control the formation and activity of different organisms. Now, Xu, Gantz et al. – including the two researchers involved in the 2015 work – have used a new active genetic element called a CopyCat element and more traditional genome editing to analyze the control of a gene that coordinates the formation of a simple structure in a fruit fly – a vein in the wing. The goal was to understand which sections of DNA controlled where and when genes are activated to result in this structure being reliably located in its correct position. First, Xu, Gantz et al. used genome editing to make mutations in a stretch of DNA that regulates the gene involved in wing vein formation. The effects of these mutations unexpectedly suggested that pairs of chromosomes might be interacting to control the activity of this gene. This was something that had not been seen before, which shows the advantage of editing a gene’s regulatory sequence at its normal location within the genome. Next, Xu, Gantz et al. used the CopyCat tool to delete the regulatory sequence and replace it with sequences from three other species of flies. When the sequence was replaced with that of a housefly, a complete vein formed but it was further forward than normal for a fruit fly, and more closely matched the position of the wing vein in a housefly. These findings show how gene activity can affect the position of a simple structure; they also suggest that this strategy could help scientists to understand how the genomes of different species have evolved. Xu, Gantz et al. hope these advances will encourage other researchers to use active genetic elements in a broad range of organisms to enable and accelerate their research. Since these tools fundamentally change the rules of genetic inheritance, they have many applications beyond research too. These applications are not without their risks and would need careful consideration, but could include engineering wild mosquito populations to combat diseases like malaria, dengue fever, chikungunya and Zika.

A load-independent index of myocardial contractility provides a measure of cardiac function. Previous contractility indices have been shown to be either load-dependent or invasive. We sought to determine the extent of load (preload and afterload)-independence of d σ*/d tmax( σ* is pressure-normalized stress) in comparison with other well-established indices. Six anaesthetized pigs underwent left ventricular pressure–volume measurements under various load conditions. The average preload was decreased by 70.0 ± 15.0% (from 39.2 ± 6.4 mL to 11.7 ± 7.7 mL) and increased by 49.3 ± 5.9% (from 35.1 ± 7.4 mL to 51.7 ± 8.9 mL). The average afterload was increased by 74.3 ± 43.5% (from 3.3 ± 0.6 mmHg/mL to 5.7 ± 1.7 mmHg/mL). When preload was reduced within an average of 21.7% (39.2 ± 6.4 mL to 30.7 ± 6.2 mL) using occlusion of the inferior vena cava, d σ*/d tmaxdid not change significantly (6.50 ± 1.10 s−1vs 6.60 ± 0.90 s−1, P = non-significant [NS]). When preload was increased within an average of 29.3% (35.1 ± 7.4 mL to 45.4 ± 7.3 mL) from infusion of normal saline, d σ*/d tmaxdid not change significantly (7.04 ± 1.00 s−1vs 7.29 ± 1.10 s−1, P = NS). When afterload was increased within an average of 42.4% (3.3 ± 0.6 mmHg/mL to 4.7 ± 1.0 mmHg/mL) using intra-aortic balloon occlusion, d σ*/d tmaxdid not change significantly (6.72 ± 1.18 s−1vs 6.89 ± 1.28 s−1, P = NS). As expected, d σ*/d tmaxwas significantly increased with dobutamine. A linear regression showed no correlation between d σ*/d tmaxand preload ( r2 = 0.02, P = 0.17) within a maximum range of −30% to +50% of preload change, or between d σ*/d tmaxand afterload ( r2 = 0.03, P = 0.36) within maximum range of 0–100% of afterload increase, respectively. In conclusion, d σ*/d tmaxis independent of loading conditions within an average of 21.7% of preload decrease, 29.3% of preload increase, 42.4% of afterload increase, and sensitive to dobutamine infusion.

Digital oriented front-end and signal processing interface for capacitive MEMS sensor is an attractive alternative to the conventional analog intensive design. The main challenge comes from improving the noise performance of digitally oriented front-end which will dictate the performance of the entire system. We are proposing a new interface that uses an RC relaxation oscillator front-end as a capacitance to duty cycle converter, followed by a phase locked loop time-to-digital converter which provides fine/coarse resolution digital output. Utilizing the RC relaxation oscillator output as the input reference to the phase locked loop, the time-to-digital conversion becomes synchronized with the front-end thus significantly improves the overall system noise performance. From measurement, our design has a flat output noise density profile of −103 dBFS with an Allan Deviation floor of −104 dBFS, non-linearity of ≤0.35 %FS across a wide bandwidth of 0.5 MHz. Our design can be used directly as an interface for any differential capacitive MEMS sensor to achieve high-performance sensing with direct digital output.

Valuable theoretical predictions of nuclear dipole excitations in the whole chart are of great interest for different nuclear applications, including in particular nuclear astrophysics. Here we present large-scale calculations of the $E1$ $��$-ray strength function obtained in the framework of the axially-symmetric deformed QRPA based on the finite-range Gogny force. This approach is applied to even-even nuclei, the strength function for odd nuclei being derived by interpolation. The convergence with respect to the adopted number of harmonic oscillator shells and the cut-off energy introduced in the 2-quasiparticle (2-$qp$) excitation space is analyzed. The calculations performed with two different Gogny interactions, namely D1S and D1M, are compared. A systematic energy shift of the $E1$ strength is found for D1M relative to D1S, leading to a lower energy centroid and a smaller energy-weighted sum rule for D1M. When comparing with experimental photoabsorption data, the Gogny-QRPA predictions are found to overestimate the giant dipole energy by typically $\sim$2 MeV. Despite the microscopic nature of our self-consistent Hartree-Fock-Bogoliubov plus QRPA calculation, some phenomenological corrections need to be included to take into account the effects beyond the standard 2-$qp$ QRPA excitations and the coupling between the single-particle and low-lying collective phonon degrees of freedom. For this purpose, three prescriptions of folding procedure are considered and adjusted to reproduce experimental photoabsorption data at best. All of them are shown to lead to rather similar predictions of the $E1$ strength, both at low energies and for exotic neutron-rich nuclei. Predictions of $��$-ray strength functions and Maxwellian-averaged neutron capture rates for the whole Sn isotopic chain are also discussed and compared with previous theoretical calculations.

There has been much characterization of the heart as a pump by means of models based on elastance and compliance. The present paper puts forward the new concept of time-varying passive and active elastance. The biomechanical basis of cyclic elastances of the left ventricle (LV) is presented. Elastance is defined in terms of the relationship between ventricular pressure and volume as d P = Ed V + Vd E, where E includes passive elastance, Ep, and active elastance, Ea. By incorporating this concept in LV models to simulate diastolic (filling) and systolic phases, a time-varying expression has been obtained for Ea, and an LV volume dependent expression has been obtained for Ep. It is proposed to use these two elastances Ea and Ep to represent the intrinsic LV properties. The active elastance, Ea, can be used to characterize the LV contractile state and represents LV pressure variation due to LV volume variation (such as during the filling and ejection phases). The passive elastance, Ep, can serve as a measure of LV resistance to filling. Furthermore, it has been demonstrated how the LV pressure dynamics (and LV pressure response to LV volume) can be explained in terms of Ea and Ep.

The uptake mechanisms and kinetics of gold nanoparticles (AuNPs) by mouse calvaria osteoblastic cells have been studied by transmission electron microscopy (TEM). The average size of the as-synthesized AuNPs used in this study was 12.2 (± 1.3) nm, and they were used to expose MC3T3-E1 osteoblastic cells at two concentrations (10 and 160 μg/ml) for 6, 24, and 96 hours before TEM imaging. Based on this analysis, we propose that the uptake mechanism of AuNPs is concentration-dependent. At the higher concentration (160 μg/ml), the particles seem to penetrate inside the cells primarily by endocytosis as the cells engulf AuNPs as agglomerates formed on the outer cellular membrane. At the lower concentrations of 10 μg/ml, AuNPs are more likely to cross the plasma membrane individually through diffusion. Therefore, the average diameters of the nanoparticles are expected to have a significant role only when exposed to cells in low concentrations. Moreover, cytotoxicity assays showed no toxic effects of the AuNPs when MC3T3-E1 cells were exposed to concentrations used in the experiments.

In this paper, the left ventricle (LV) is modeled as a cylinder with myocardial fibers located helically within its wall. A fiber is modeled into myocardial structural units (MSUs); the core entity of each MSU is the sarcomeric contractile element. The relationship between the sarcomere unit's contractile force and shortening velocity is expressed in terms of the LV model's wall stress and deformation, and hence in terms of the monitored LV pressure and volume. Then, the LV systolic performance is investigated in terms of a mechatronic (excitation-contraction) model of the sarcomere unit located within the LV cylindrical model wall.The governing equation of dynamics of the LV myocardial structural unit (MSU) is developed, involving the parameters of the series-elastic element (SE), the viscous element (VE) and the contractile element (CE). We then relate the MSU's force and displacement variables (in terms of SE, VE and CE parameters) to the LV pressure and volume, using the patient's catheterization-ventriculogram data. We thereby evaluate the MSU elements' parameters.We then determine the sarcomere (CE) 'force vs. shortening-velocity' characteristics as well as the power generated by the sarcomere (or CE) element. These are deemed to be important LV functional indices. When our computed sarcomeric peak-power is compared against the traditional LV contractility indices (by linear regression), a high degree of correlation is obtained.We have provided herein, a LV systolic-phase (cylindrical geometry) model whose wall contains the myocardial fibers having sarcomere units. We have expressed the LV myocardial sarcomere's CE (force vs. shortening-velocity) characteristics in terms of the LV pressure-volume data. These CE properties express the intrinsic performance capacity of the LV. Hence, indices containing these properties are deemed to reflect LV performance. In this regard, our new LV contractility index correlates very well with the traditional LV contractility index dP/dt(max).

Background Approximately 60,000 people are born with thalassaemia major every year. The average life expectancy of thalassaemia major patients is 35 years due to iron overload Cardiomyopathy. The cardiomyopathy is reversible when treated early, but once heart failure is established it is often rapidly progressive, and unresponsive to treatment. The single breath hold (SBH) T2* technique has been validated as the most robust and reproducible non-invasive measurement of myocardial and iron load. Our aim in this study was to validate the transferability and reproducibility of this technique in different scanners worldwide. Methods We aim to compare the reproducibility in six different sites worldwide as part of an NIH funded grant (R01-DK66084-01). So far, two of these sites have been validated: Singapore (Siemens Sonata, 1.5T scanner) and Cagliari, Italy (GE Signa, 1.5 T scanner). At both validation sites, 10 patients were scanned for heart and liver T2*, and scans were repeated for interstudy reproducibility. All patients then flew to London to be rescanned on our reference Siemens Sonata scanner. Results Of the 20 patients scanned, 70% had myocardial iron loading (T2* Liver iron loading was present in 65% of patients and in 30% this was severe. The coefficient of variation (COV) for the heart T2* measurements between the local sites and London was 5.9% and 4.9% yielding an average coefficient of variation across both sites of 5.4% (figure 1). The coefficient of variation (COV) for the liver T2* measurements between the local sites and London was 11.3% and 3.9% yielding an average coefficient of variation across both sites of 7.6% (figure 2). There was no significant correlation between liver and myocardial loading. Conclusion These are the first data demonstrating the transferability of the SBH T2* technique and the clinical validation from the 2 collaborating centers were excellent for both heart and liver measurements. Further MR sites confirmed for validation include Children’s Hospital of Philadelphia (USA); Ramathibodi Hospital, Bangkok (Thailand); and Chinese University Hong Kong. Figure 1 Figure 1. Figure 2 Figure 2.

Pdf of the poster (HAG_TAGC2020 Poster.pdf) and Video/Audio walk through (HAG_TAGC2020_Poster_Vid.mov)Title:Super-Mendelian inheritance mediated by CRISPR–Cas9 in the female mouse germline.Abstract:A gene drive biases the transmission of one of the two copies of a gene such that it is inherited more frequently than by random segregation. Highly efficient gene drive systems that have recently been developed in insects, which leverage the sequence-targeted DNA cleavage activity of CRISPR–Cas9 and endogenous homology- directed repair mechanisms to convert heterozygous genotypes to homozygosity. If implemented in laboratory rodents, similar systems would enable the rapid assembly of currently impractical genotypes that involve multiple homozygous genes (for example, to model multigenic human diseases). To our knowledge, however, such a system has not yet been demonstrated in mammals. Here we use an active genetic element that encodes a guide RNA, which is embedded in the mouse tyrosinase (Tyr) gene, to evaluate whether targeted gene conversion can occur when CRISPR–Cas9 is active in the early embryo or in the developing germline. Although Cas9 efficiently induces double-stranded DNA breaks in the early embryo and male germline, these breaks are not corrected by homology- directed repair. By contrast, Cas9 expression limited to the female germline induces double-stranded breaks that are corrected by homology-directed repair, which copies the active genetic element from the donor to the receiver chromosome and increases its rate of inheritance in the next generation. These results demonstrate the feasibility of CRISPR–Cas9-mediated systems that bias inheritance of desired alleles in mice and that have the potential to transform the use of rodent models in basic and biomedical research.

Pdf of the poster (HAG_TAGC2020 Poster.pdf) and Video/Audio walk through (HAG_TAGC2020_Poster_Vid.mov)Title:Super-Mendelian inheritance mediated by CRISPR–Cas9 in the female mouse germline.Abstract:A gene drive biases the transmission of one of the two copies of a gene such that it is inherited more frequently than by random segregation. Highly efficient gene drive systems that have recently been developed in insects, which leverage the sequence-targeted DNA cleavage activity of CRISPR–Cas9 and endogenous homology- directed repair mechanisms to convert heterozygous genotypes to homozygosity. If implemented in laboratory rodents, similar systems would enable the rapid assembly of currently impractical genotypes that involve multiple homozygous genes (for example, to model multigenic human diseases). To our knowledge, however, such a system has not yet been demonstrated in mammals. Here we use an active genetic element that encodes a guide RNA, which is embedded in the mouse tyrosinase (Tyr) gene, to evaluate whether targeted gene conversion can occur when CRISPR–Cas9 is active in the early embryo or in the developing germline. Although Cas9 efficiently induces double-stranded DNA breaks in the early embryo and male germline, these breaks are not corrected by homology- directed repair. By contrast, Cas9 expression limited to the female germline induces double-stranded breaks that are corrected by homology-directed repair, which copies the active genetic element from the donor to the receiver chromosome and increases its rate of inheritance in the next generation. These results demonstrate the feasibility of CRISPR–Cas9-mediated systems that bias inheritance of desired alleles in mice and that have the potential to transform the use of rodent models in basic and biomedical research.

This is the dataset for all genotyping for the paper "Super-Mendelian inheritance mediated by CRISPR/Cas9 in the female mouse germline." Abstract:A gene drive biases the transmission of a particular allele of a gene such that it is inherited at a greater frequency than by Mendelian segregation. Recently, highly efficient gene drive systems were developed in insects, which leverage the sequence-targeted DNA cleavage activity of CRISPR/Cas9 and endogenous homology directed repair mechanisms to convert heterozygous genotypes to homozygosity. If implemented in laboratory rodents, similarly powerful systems would enable the rapid assembly of genotypes that involve multiple genes (e.g., to model multigenic human diseases). Such complex genetic models are currently precluded by time, cost, and a requirement for a large number of animals to obtain a few individuals of the desired genotype. However, the efficiency of a CRISPR/Cas9 gene drive system in mammals has not yet been determined. Here, we utilize an active genetic “CopyCat” element embedded in the mouse Tyrosinase gene to detect genotype conversions after Cas9 activity in the embryo and in the germline. Although Cas9 efficiently induces double strand DNA breaks in the early embryo and is therefore highly mutagenic, these breaks are not resolved by homology directed repair. However, when Cas9expression is limited to the developing female germline, resulting double strand breaks are resolved by homology directed repair that copies the CopyCat allele from the donor to the receiver chromosome and leads to its super-Mendelian inheritance. These results demonstrate feasibility of the CRISPR/Cas9 gene drive mechanism in mice, which has potential to transform the use of rodent models in basic and biomedical research and also contributes valuable data to the ongoing discussion of possible approaches to suppress invasive and disease-harboring wild rodent populations., Please use the Word.docx file titled "Instructions" for instructions on how to navigate this dataset., {"references":["https://www.biorxiv.org/content/early/2018/07/04/362558"]}