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John Yin
Professor
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| John Yin |
| 3633 Engineering Hall 1415 Engineering Drive Madison, WI 53706-1691 |
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Tel: 608/265-3779 Fax: 608/262-5434 E-mail: yin@engr.wisc.edu |
What might you gain while pursuing post-doctoral research in the Yin lab?
(1) Hands-on training in the emerging and exciting area of systems biology, focusing on virus-host interactions,
(2) Experience in how to integrate research, teaching and learning (see www.delta.wisc.edu) --- skills that are highly valued by academic employers and funding agencies,
(3) Guidance by a mentor who has a strong record of placing students and post-docs in stimulating academic (Caltech, Duke, Harvard, MIT, Stanford, Tufts, UConn-Storrs, UC-Berkeley), government, and industry positions,
(4) Opportunities for personal growth at a world-class university, located in safe, attractive and affordable city surrounded by beautiful lakes.
We are advancing new technologies to better understand the growth, spread and evolution of viruses. Active NIH-supported projects are in three areas: (1) flow-enhanced spread and characterization of infections in microfluidic devices, (2) phenotype distributions from measurements and models of infections initiated by single virus particles, (3) dynamics of virus populations in anti-viral environments. Systems of current interest are influenza virus and vesicular stomatitis virus. The most competitive applicants will be exceptionally creative, highly-motivated individuals with experience in:
Quantitative biology: methods to detect and/or quantify nucleic acids, proteins, viruses, virus-like particles, activation of innate immunity. Experience in microscopy, construction or characterization of live-cell reporters of gene expression, quantitative imaging and image analysis would be especially valuable.
Madison, Wisconsin routinely ranks at the top of national surveys of 'best places to live,' and post-docs here thrive on a rich diversity of outdoor and cultural opportunities. Forward your CV with cover letter, and have three letters of reference sent to John Yin by e-mail (yin@engr.wisc.edu), fax (608/262-5434) or regular mail: Department of Chemical and Biological Engineering, University of Wisconsin, Madison, WI 53706-1607 USA.
Viruses cause a diversity of human diseases including acquired immunodeficiency syndrome(AIDS), influenza, hepatitis, and cancer. The focus of our research is to develop new experimental and computational methods to better understand how viruses grow and how their infections spread. Our ultimate goal is to apply these methods to create more effective vaccines, design potent anti-viral therapies, and engineer useful viruses. We currently study influenza A virus, which has the potential to cause a global epidemic, and vesicular stomatitis virus (VSV), a virus that may be engineered to destroy cancers.
As the smallest organisms viruses range from 20 to 300 nanometers in diameter and carry genomes that encode from 5 to 200 genes. To grow, a virus must develop an intimate relationship with a living cell. After docking with receptors at the cell surface the virus enters the cell, releases its genome, and thereby sets in motion processes that ultimately divert resources of the cell toward the mass production of virus proteins and virus genomes. Self-assembly of these parts give rise to progeny viruses that, following release, may encounter and infect other susceptible cells. Despite the small size and relative simplicity of virus genomes, the network of molecular transformations that define virus growth within the cell remain complex. Thus it is a major challenge to predict how engineered differences, natural mutations, virus-targeted drugs or cell differences can influence how viruses grow.
Integration of diverse information. We address the complexity of virus growth by casting the molecular interactions in the mathematical and computable language of chemical reaction engineering, a process that enables us to weave together mechanisms and data drawn from biochemical, biophysical and genetic studies spanning the last 40 years. Through our model building we integrate themes of molecular synthesis and decay, template-directed information transfers, physical interactions and regulatory feedbacks, and macro-molecular assembly. Our models provide a functional link between static genomes of viruses and the dynamic processes of infection that they encode.
Nature versus nurture. Our genome-to-organism models of virus growth have opened the door to better understanding how interactions between virus genomes and their intracellular environments influence virus development. Specifically, we have shown that protein synthesis is the limiting resource for virus growth, quantified how interactions among genes contribute to virus fitness and robustness, and identified conditions under which wild-type genome designs perform optimally. On the applications side we have used these models to suggest novel anti-viral strategies that resist escape.
Challenging paradigms and taking risks. The modus operandi in biology employs average measures of molecular levels to elucidate mechanisms. However, in the study of viruses, where genetic variability can be rampant, such average measures can mask variations that are likely to be central to viral growth and persistence. We are beginning to address such issues by probing virus growth and host-cell responses at the single-cell level, using flow cytometry to sort and analyze single infected cells, computer modeling to test potential mechanisms, and novel experimental methods to visualize and quantify the dynamics of virus populations from single infected cells. In the process we are identifying and illuminating new themes and variations as the smallest genomes come to life.
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Copyright 2009 The Board of Regents of the University of Wisconsin System Date last modified: 03-Nov-2009 Content by: yin@engr.wisc.edu Accessibility Web services |