	Claus O. Wilke Assistant Professor, Section of Integrative Biology, and Center for Computational Biology and Bioinformatics
Lab web site	Education \| Research Interests \| Publications
E-mail: cwilke_at_mail.utexas.edu Office: PAT 141MC (512) 471-6028 (office) (512) 471-5413 (lab) Fax: (512) 471-3878	Education Oct. 1996 Diplom (equiv. to Master's degree) in physics, Ruhr-Universitat Bochum June 1999 Ph.D. in physics, Ruhr-Universitat Bochum Research Interests I work in the areas of computational and theoretical evolutionary biology. My research can be broadly subdivided into three areas: (1) RNA virus evolution, (2) theoretical population genetics, (3) evolution of biopolymers (RNA, proteins). RNA virus evolution RNA viruses (such as influenza virus, human immunodeficiency virus, or hepatitis A, B, C virus) tend to have very high mutation rates. As a consequence, they can evolve rapidly in reaction to immune response or treatment. Frequently, they adapt to new hosts, and the majority of newly emerging infectious diseases are RNA viruses that cross the species barrier from animal host to human (examples are SARS or the avian influenza). However, a high mutation rate also implies frequent deleterious mutations. I am studying questions such as how RNA viruses can thrive under high rates of deleterious mutations, how they can mask the effect of deleterious mutations under coinfection, and how they adapt to changing hosts. Theoretical population genetics Population genetics was the first branch of biology to receive significant attention from mathematicians. The origins of theoretical population genetics date back to the early 20th century, and today the basic theory of population genetics is well understood. Nevertheless, many open questions remain. I am working mainly on the speed of adaptation in asexual populations, on neutral evolution, and on population dynamics in time-dependent environments. Evolution of biopolymers A central question of molecular biology is how biopolymers (in particular proteins) behave under mutation. We can only understand the patterns observed in genomics data, and modify and design proteins such that they serve a specific purpose, if we know which mutations are likely to disrupt a protein fold, and which are not. I am working on questions such as what is the probability that multiple mutations disrupt a protein fold, or to what extent is this probability influenced by the amino-acid sequence or the protein structure. I am also studying genome-wide patterns of evolutionary rate, and try to understand the factors that determine the evolutionary rate of genes. Publications For a complete list of publications and links to articles, see here. C. O. Wilke and D. Allan Drummond. Population genetics of translational robustness. Genetics 173:473-481. D. A. Drummond, A. Raval, and C. O. Wilke. A Single Determinant Dominates the Rate of Yeast Protein Evolution Mol. Biol. Evol. 23:327-337, 2006. C. O. Wilke, R. Forster, and I. S. Novella. Quasispecies in time-dependent environments. Curr. Topics Microbiol. Immun. 299:33-50, 2006. R. Forster and C. O. Wilke. Tradeoff between short-term and long-term adaptation in a changing environment. Phys. Rev. E 72:041922, 2005. C. O. Wilke, J. D. Bloom, D. A. Drummond, and A. Raval. Predicting the tolerance of proteins to random amino acid substitution. Biophys. J. 89:3714-3720, 2005. D. A. Drummond, J. D. Bloom, C. Adami, C. O. Wilke, and F. H. Arnold. Why highly expressed proteins evolve slowly. Proc. Natl. Acad. Sci. USA 102:14338-14343, 2005. C. O. Wilke. Quasispecies theory in the context of population genetics. BMC Evol. Biol. 5:44, 2005. C. O. Wilke. The heavy, the cold and the slow. Heredity 95:115, 2005. D. A. Drummond, J. J. Silberg, M. M. Meyer, C. O. Wilke, and F. H. Arnold. On the conservative nature of intragenic recombination. Proc. Natl. Acad. Sci. USA 102:5380-5385, 2005. J. D. Bloom, J. J. Silberg, C. O. Wilke, D. A. Drummond, C. Adami, and F. H. Arnold. Thermodynamic prediction of protein neutrality. Proc. Natl. Acad. Sci. USA 102:606-611, 2005. C. Ofria and C. O. Wilke. Avida: Evolution experiments with self-replicating computer programs. In A. Adamatzky and M. Komosinski, eds. Artificial Life Models in Software. Springer, 2005, pp. 3-36. C. O. Wilke and S. S. Chow. Exploring the evolution of ecosystems with digital organisms. In M. Pascual and J. Dunne, eds. Ecological Networks. Linking Structure to Dynamics in Food Webs. Oxford University Press, 2005. C. O. Wilke. Molecular clock in neutral protein evolution. BMC Genetics 5:25, 2004. C. O. Wilke. Supplementary materials need the right format. Nature 430:291, 2004. S. S. Chow, C. O. Wilke, C. Ofria, R. E. Lenski, and C. Adami. Adaptive Radiation from Resource Competition in Digital Organisms. Science 305:84-86, 2004. *Joint first authorship.

Claus O. Wilke

Assistant Professor, Section of Integrative Biology,
and Center for Computational Biology and Bioinformatics

Education | Research Interests | Publications

E-mail:
cwilke_at_mail.utexas.edu
Office:
PAT 141MC
(512) 471-6028 (office)
(512) 471-5413 (lab)
Fax:
(512) 471-3878

Education

Oct. 1996 Diplom (equiv. to Master's degree) in physics, Ruhr-Universitat Bochum
June 1999 Ph.D. in physics, Ruhr-Universitat Bochum

Research Interests

I work in the areas of computational and theoretical evolutionary biology. My research can be broadly subdivided into three areas: (1) RNA virus evolution, (2) theoretical population genetics, (3) evolution of biopolymers (RNA, proteins).

RNA virus evolution

RNA viruses (such as influenza virus, human immunodeficiency virus, or hepatitis A, B, C virus) tend to have very high mutation rates. As a consequence, they can evolve rapidly in reaction to immune response or treatment. Frequently, they adapt to new hosts, and the majority of newly emerging infectious diseases are RNA viruses that cross the species barrier from animal host to human (examples are SARS or the avian influenza). However, a high mutation rate also implies frequent deleterious mutations. I am studying questions such as how RNA viruses can thrive under high rates of deleterious mutations, how they can mask the effect of deleterious mutations under coinfection, and how they adapt to changing hosts.

Theoretical population genetics

Population genetics was the first branch of biology to receive significant attention from mathematicians. The origins of theoretical population genetics date back to the early 20th century, and today the basic theory of population genetics is well understood. Nevertheless, many open questions remain. I am working mainly on the speed of adaptation in asexual populations, on neutral evolution, and on population dynamics in time-dependent environments.

Evolution of biopolymers

A central question of molecular biology is how biopolymers (in particular proteins) behave under mutation. We can only understand the patterns observed in genomics data, and modify and design proteins such that they serve a specific purpose, if we know which mutations are likely to disrupt a protein fold, and which are not. I am working on questions such as what is the probability that multiple mutations disrupt a protein fold, or to what extent is this probability influenced by the amino-acid sequence or the protein structure. I am also studying genome-wide patterns of evolutionary rate, and try to understand the factors that determine the evolutionary rate of genes.

Publications

For a complete list of publications and links to articles, see here.

C. O. Wilke and D. Allan Drummond. Population genetics of translational robustness. Genetics 173:473-481.
D. A. Drummond, A. Raval, and C. O. Wilke. A Single Determinant Dominates the Rate of Yeast Protein Evolution Mol. Biol. Evol. 23:327-337, 2006.
C. O. Wilke, R. Forster, and I. S. Novella. Quasispecies in time-dependent environments. Curr. Topics Microbiol. Immun. 299:33-50, 2006.
R. Forster and C. O. Wilke. Tradeoff between short-term and long-term adaptation in a changing environment. Phys. Rev. E 72:041922, 2005.
C. O. Wilke, J. D. Bloom, D. A. Drummond, and A. Raval. Predicting the tolerance of proteins to random amino acid substitution. Biophys. J. 89:3714-3720, 2005.
D. A. Drummond, J. D. Bloom, C. Adami, C. O. Wilke, and F. H. Arnold. Why highly expressed proteins evolve slowly. Proc. Natl. Acad. Sci. USA 102:14338-14343, 2005.
C. O. Wilke. Quasispecies theory in the context of population genetics. BMC Evol. Biol. 5:44, 2005.
C. O. Wilke. The heavy, the cold and the slow. Heredity 95:115, 2005.
D. A. Drummond, J. J. Silberg, M. M. Meyer, C. O. Wilke, and F. H. Arnold. On the conservative nature of intragenic recombination. Proc. Natl. Acad. Sci. USA 102:5380-5385, 2005.
J. D. Bloom, J. J. Silberg, C. O. Wilke, D. A. Drummond, C. Adami, and F. H. Arnold. Thermodynamic prediction of protein neutrality. Proc. Natl. Acad. Sci. USA 102:606-611, 2005.
C. Ofria and C. O. Wilke. Avida: Evolution experiments with self-replicating computer programs. In A. Adamatzky and M. Komosinski, eds. Artificial Life Models in Software. Springer, 2005, pp. 3-36.
C. O. Wilke and S. S. Chow. Exploring the evolution of ecosystems with digital organisms. In M. Pascual and J. Dunne, eds. Ecological Networks. Linking Structure to Dynamics in Food Webs. Oxford University Press, 2005.
C. O. Wilke. Molecular clock in neutral protein evolution. BMC Genetics 5:25, 2004.
C. O. Wilke. Supplementary materials need the right format. Nature 430:291, 2004.
S. S. Chow*, C. O. Wilke*, C. Ofria, R. E. Lenski, and C. Adami. Adaptive Radiation from Resource Competition in Digital Organisms. Science 305:84-86, 2004. *Joint first authorship.