James J. Bull

University of Idaho


Primary Section: 27, Evolutionary Biology
Membership Type:
Member (elected 2016)

Biosketch

Jim Bull is an evolutionary biologist recognized for work on evolution of sex determination and viral evolution. Specific contributions on the evolution of sex determination lie at understanding the selective processes governing the transition between different mechanisms, such as sex chromosome systems, haplo-diploidy, and environmental sex determination. Contributions on viral evolution include understanding evolution at high mutation rate (lethal mutagenesis), molecular mechanisms of viral attenuation, and parallel molecular evolution. Bull was born in and grew up in Waukesha, Wisconsin. His undergraduate work was at Texas Tech University (mentored by RJ Baker), PhD from University of Utah (advisor J Legler, mentor E. Charnov), with postdocs at the University of Wisconsin (J F Crow) and University of Sussex (J Maynard Smith). He started his first job at the University of Texas in 1983 and has been there ever since. He served on the Science board of reviewing editors for 13 years, chaired the NIH GVE study section for two years, and is a member of the American Academy of Arts and Sciences and National Academy of Sciences.

Research Interests

Bull currently works on (i) the use of phages and phage products to treat bacterial infections, (ii) the engineering of viral genomes to achieve long term attenuation that will not revert to high virulence, and (iii) evolution of resistance to gene drive systems. The phage work uses a combination of purely in vitro studies with E. coli, Pseudomonas, Vibrio, and others to discover how best to suppress bacterial numbers with phages. Mouse infections are used to test treatment efficacy, both with phages and enzymes derived from phages. The engineering of attenuation is also done with phages, where the goal is to suppress viral fitness and then subject the engineered phages to long term growth, observing whether fitness recovers. Some genomic designs lead to effectively permanent attenuation, such that the virus would not be able to recover original fitness levels. The work on evolution of resistance to gene drive systems is in its infancy and is so far limited to population genetics models to predict the various ways that a population may evolve in response to a gene drive system that harms the population.

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