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College of Arts and Sciences

Department of Biology

Faculty - Charles J. Goodnight

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Charles J. Goodnight, Professor

  • Ph.D., University of Chicago, 1983
  • University of Illinois at Chicago 83-86, Postdoctoral Research Associate
  • University of Illinois at Chicago 86-88, Visiting Assistant Professor
  • University of Vermont, Assistant Professor 88-94, Associate Professor 94 - present, Full Professor 99 - present
  • C.V. (PDF)
Area of expertise

population genetics

Contact Information
Email: Charles J. Goodnight

Office Hours: MWF 2:30-3:30
Marsh Life Science Building, Rm 115
Phone: (802) 656-8521

Research

I study genetic differentiation and evolution in structured populations. My research combines theoretical and experimental approaches to study the effects of selection among individuals, populations and communities. One of my major areas of interest is how certain types of genetic variation, such as epistatic interactions among loci, can contribute to a response to selection in a subdivided population even though they cannot contribute to a response to selection in a large panmictic population. My current research includes (1) the effect of founder events and population structure on genetic variance, (2) theoretical and experimental studies of multilevel selection, and (3) evolution and speciation in spatially structured populations. The techniques I use are drawn from the field of quantiative genetics and molecular quantitative genetics. My experimental work uses the resemblance among relatives and the response to selection to study the genetic basis of complex traits. My theoretical work uses statistical and quantitative genetic methods to study evolution in subdivided populations.

Selected Publications

  • Goodnight, C., E. Rauch, H. Sayama, M. A. M. De Aguiar, M. Branger, and Y. ar-Yam. 2008. Evolution in spatial Predator-Prey Models and the "Purdent Predatory": The inadequacy of steady-state organism fitness and the concept of the individual and group selection. In Press, Complexity.
  • Payne, J.L., Eppstein, M.J., & Goodnight, C.J. 2007. Sensitivity of Self-Organized Speciation to Long-Distance Dispersal. In Proceedings of the IEEE Symposium on Artificial Life, pp. 1-7, (winner of best student paper award).
  • Eppstein, M. J., J. L. Payne, C. J. Goodnight 2006. Speciation by self-organizing barriers to gene flow in simulated populations with localized mating. Workshop Proceedings for Genetic and Evolutionary Computation Conference (GECCO) 2006.
  • Wade, M. J., and C. J. Goodnight. 2006. Cyto-nuclear epistasis: two-locus random genetic drift in hermaphroditic and dioecious species. Evolution 60:643-659. Goodnight, C. J. 2006. News and Commentary: Peak shifts in large populations. Heredity 96:5-6
  • Goodnight, C. J. 2005. Multilevel Selection: The Evolution of Cooperation in Non Kin Groups. Population Ecology 47:3-12
  • Goodnight, C. J. 2004. Genetics and Evolution in Structured Populations. IN: Evolutionary Genetics: Concepts and Case Studies, C. Fox and J. Wolf Editors. In Press.
  • Goodnight, C. J. 2004. Gene Interaction and Selection. In: K. Lamkey ed., Long Term Selection: A Celebration Of 100 Years Of Selection For Oil And Protein In Maize
  • Goodnight, C. J. 2003. Metapopulation Quantitative Genetics. In: O. Gaggiotti ed.The Biology of Metapopulations.
  • Michael J. Wade, R. G. Winther, A. F. Agrawal, C. J. Goodnight. 2001. Alternative definitions of epistasis: dependence and interaction. Trends in Ecology & Evolution 16: 498-504
  • Goodnight, C. J. 2000, Heritability at the ecosystem level. Proceedings of the National Academy of Sciences of the United States of America, 97: 9365-9366
  • Goodnight, C. J. 2000. Modeling gene interaction in structured populations. Pp. 213-231, in J. B. Wolf, E. D. Brodie, III, M. J. Wade, eds., Epistasis and the Evolutionary Process, Oxford University Press, Oxford.
  • Goodnight, C. J., and M. J. Wade. 2000. The ongoing-synthesis: a reply to Coyne et al. (1999). Evolution 54:317-324.
  • Goodnight, C. J. 2000 Quantitative Trait Loci and Gene Interaction: The Quantitative Genetics of Metapopulations. Heredity 84:587-598.
  • Molofsky, J, S. L. Morrison, and C. J. Goodnight. 1999. Genetic and environmental controls on the establishment of the invasive grass, Phalaris arundinacea. Biological Invasions 1:181-188.
  • Wade, M. J., C. J. Goodnight, and L. Stevens. 1999. Design and interpretation of experimental studies of interdemic selection: A reply to Getty. American Naturalist 154: 599-603.
  • Goodnight, C. J. 1999. Epistasis and Heterosis. Pp. 59-68 In: James Coors and Shivaji Pandey eds., The Genetics and Exploitation of Heterosis in Crops. American Society of Agronomy, Inc/Crop Science Society of America, Inc. Madison, WI.
  • Wade, M. J. and C. J. Goodnight, 1998. Genetics and adaptation in metapopulations: When nature does many small experiments. Evolution. 52:1537-1553
  • Yan, G., L. Stevens, C. J. Goodnight and J. J. Schall 1997. Parasite mediated competition: The effect of parasites on the outcome and duration of competition and the evolution of virulence. Ecology 79:1093-1103.
  • Tonsor, S. J. , and C. J. Goodnight. 1997. Testing the effect of mating structure on the partitioning of phenotypic variance in Plantago lanceolata. Evolution 51: 1773-1784
  • Goodnight, C. J. and J. M. Schwartz. 1997. A bootstrap comparison of genetic covariance matrices. Biometrics 53:1026-1039.
  • Goodnight, C. J. and L. Stevens. 1997. Experimental studies of group selection: What do they tell us about group selection in nature. American Naturalist 150:S59-S79.

The additive genetic variance as a function of migration rate for different forms of genetic effects. Note that for gene interactions the additive genetic variance is maximized at one migrant every two to four generations.

The potential role of epistasis in speciation can be illustrated with dominance by additive epistasis. In a population segregating for the A locus, but fixed for the B2 allele the A locus will be overdominant. If a B1 allele is introduced into the metapopulation either by mutation or migration it will initially be neutral, however genetic drift at the A locus will result in directional selection favoring the B1 allele (II left and right columns). Eventually this will drive the population to fixation of the B1 allele, and one of the two A alleles.

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