NOV 02, 2017 10:00 AM PDT
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WEBINAR: Rapid Development and Functional Analysis of Mouse Models Using CRISPR/Cas
SPONSORED BY: Synthego
CONTINUING EDUCATION (CME/CE/CEU) CREDITS: P.A.C.E. CE | Florida CE
1 7 400

Speakers:
  • Professor & Associate Director, Aab Cardiovascular Research Institute, University of Rochester.
    Biography
      Joseph Miano received his Ph.D. in Experimental Pathology from New York Medical College and did post-doctoral training with Eric Olson at the M.D. Anderson Cancer Center in Houston. His first faculty appointment was at the Medical College of Wisconsin where he worked mainly on the role of retinoids as a therapeutic for vascular diseases. He was then recruited to the University of Rochester School of Medicine and Dentistry where he is a Full Professor and Associate Director of the Aab Cardiovascular Research Institute. Dr. Miano serves as an editorial board member for several journals and is an Associate Editor of Vascular Pharmacology. He is a past Associate Editor of ATVB and Consulting Editor for Circulation Research. He is a Fellow of the American Heart Association and a member of the Vascular Cell and Molecular Biology Study Section at NIH. Current research in the Miano Lab focuses on deciphering how small snippets of code in our genome give cells exquisite control over the level of gene activity, much like a thermostat controlling the heat in a home. Passionate about new technology that drives research, Dr. Miano's lab was among the first wave of labs in 2013 to exploit the revolutionary CRISPR-Cas9 genome editing technology for purposes of altering the mouse genome and within a year, the lab generated the first CRISPR animal model carrying subtle mutations in a control element that turns on a gene.

    Abstract:

    DATE: November 2, 2017
    TIME: 10:00am PDT, 1:00pm EDT

    A CRISPR Way of Making Mice

    The bulk of genetic variation associated with human disease exists in the noncoding genome, much of which comprises transcribed long noncoding RNAs and non-transcribed regulatory sequences. While headway has been made in elucidating the function of some non-coding sequences, we have much to learn and we know virtually nothing about how sequence variants (such as SNPs) in regulatory sequences contribute to human disease.

     

    CRISPR/Cas-mediated genome editing offers unprecedented ease and efficiency in generating mice carrying small (100s of nucleotides) or large (several kilobases) deletions as well as subtle substitutions of regulatory sequences in their native genomic milieu. Delivering synthetic single guide RNAs (sgRNA) and Cas9 protein (as RNPs) to the 1-cell mouse embryo has resulted in the rapid production of new genetic mouse models that previously would be considered risky or even challenging to engineer.

     

    Optimized approaches to generating, genotyping, and phenotyping ‘CRISPRized’ mice carrying multiple types of genomic sequence edits will be discussed. Data will be presented demonstrating high efficiency editing with synthetic sgRNA leading to nearly 100% success rate of germline transmission, driving rapid generation of mouse models. This new wave of mouse models will accelerate discovery of genomic sequence function, including the role of coding and non-coding sequence variants associated with human disease.

    Learning Objectives:

    • Explain mouse model generation using CRISPR/Cas9
    • Optimized approaches to generating, genotyping, and phenotyping ‘CRISPRized’ mice
    • Use of mouse models to study function and disease impact of coding & non-coding sequence variation

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