Dr. Joanna Masel

Positions and Education: 
  • Professor, Ecology and Evolutionary Biology, University of Arizona, 2016-present
  • Associate Professor, Ecology and Evolutionary Biology, University of Arizona, 2010-2016
  • Assistant Professor, Ecology and Evolutionary Biology, University of Arizona, 2004-2010
  • Postdoctoral Researcher, Biological Sciences, Stanford University 2000-2003
  • D. Phil. Zoology, Oxford University 2001
  • B.Sc. (Hons) University of Melbourne 1996
Honors and Awards: 
  • Fellow, Wissenschaftskolleg zu Berlin, 2012-13
  • Outstanding Faculty Mentor, Honorable Mention, University of Arizona Undergraduate Biology Research Program, 2011
  • Pew Scholar in the Biomedical Sciences, 2007
  • Alfred P. Sloan Research Fellow, 2007
  • Merton College Prize Scholarship, 1999
  • Rhodes Scholarship, 1997
  • International Mathematical Olympiad: Bronze Medal, 1991
Research Interests: 

Why does evolution work? Randomly switching 0s and 1s in the assembly language of a computer program will essentially never improve its function. Nevertheless, a seemingly similar mutation process in DNA gives rise to the remarkable diversity of life we see around us. Why does one work so well and the other so badly? This question of evolvability is central to our work (Masel & Trotter 2010).

We study evolvability using theoretical models, especially those that explicitly capture mechanistic constraints, usually from biochemistry or genetics, and calculate their evolutionary consequences. We also use existing genome data to bioinformatically test hypotheses that come out of our theories.

The partial robustness of biological systems is important to their evolvability. Most biological variants either break a component, or tinker with it: their effects are rarely in between. Adaptation always comes from tinkering mutations, never from breaking: there is no environment in which lethal mutations are adaptive. When the phenotypic effects of mutations are partially suppressed, selection remains strong enough to weed out the most deleterious mutations, enriching the pool of cryptic variants, by a process of elimination, for those most likely to contribute to evolvability (Masel 2006; Rajon & Masel 2011). This process may be important in the origin of de novo coding sequences from noncoding ancestors (Giacomelli et al. 2007; Wilson & Masel 2011). We also study “evolutionary capacitors” such as the yeast prion [PSI+], which seems to be an adaptation to tap into and exploit such pre-adapted stocks of variation (Masel & Bergman 2003; Griswold & Masel 2009; Lancaster et al. 2010).

We study a variety of other topics in theoretical population genetics, including the molecular clock (Peterson & Masel 2009), bet-hedging (King & Masel 2007), mutation accumulation (Masel et al. 2007; Maughan et al. 2007), genetic drift (Masel 2012), and evolutionary rescue in the context of density-dependent hard selection and the substitutional load.

Selected Publications: 

PubMed list of publications for Joanna Masel


  1. Brettner LM, Masel J. (2012) Protein stickiness, rather than number of functional protein-protein interactions, predicts expression noise and plasticity in yeast, BMC Systems Biology, 6:128.
  2. Masel J. (2012) Rethinking Hardy-Weinberg and genetic drift in undergraduate biology, BioEssays, 34:701-710.
  3. Wilson BA, Masel J. (2011) Putatively noncoding transcripts show extensive association with ribosomes, Genome Biology & Evolution, 3:1245-1252.
  4. Masel J, Lyttle DN. (2011) The consequences of rare sexual reproduction by means of selfing in an otherwise clonal species, Theoretical Population Biology, 80: 317-322.
  5. Rajon, E., Masel, J. (2011). Evolution of molecular error rates and the consequences for evolvability, PNAS, 108: 1082-1087.
  6. Masel, J., Trotter, M., (2010). Robustness and evolvability, Trends in Genetics, 26: 406-414.
  7. Masel, J., Siegal M.L. (2009) Robustness: mechanisms and consequences, Trends in Genetics, 25:395-403.
  8. Peterson, G. I., Masel, J. (2009). Quantitative prediction of molecular clock and Ka/Ks at short timescales. Mol. Biol. Evol., 26:2595-2603.
  9. Griswold, G.K., Masel, J., (2009) Complex adaptations can drive the evolution of the capacitor [PSI+], even with realistic rates of yeast sex, PLoS Genetics, 5(6): e1000517.
  10. King, O.D., Masel, J. (2007) The evolution of bet-hedging adaptations to rare scenarios, Theor. Pop. Biol.,72:560-575.
  11. Giacomelli, M., Hancock, A., Masel, J. (2007) The conversion of 3' UTRs into coding regions. Molecular Biology & Evolution, 24:457-464.
  12. Masel, J., King, O.D., Maughan, H. (2007) The loss of adaptive plasticity during long periods of environmental stasis. The American Naturalist 169:38-46.
  13. Maughan, H., Masel, J., Birky, C.W., Nicholson, W.L. (2007) The roles of mutation accumulation and selection in loss of sporulation in experimental populations of Bacillus subtilis, Genetics, 177:937-948.
  14. Masel, J. A Bayesian model of quasi-magical thinking can explain observed co-operation in the public good game (2007) Journal of Economic Behavior & Organization 64:216-231.
  15. Masel, J., (2006) Cryptic genetic variation is enriched for potential adaptations, Genetics 172, 1985-1991.
  16. Masel, J., Jansen, V.A.A., (2000). Designing drugs to stop the formation of prion aggregates and other amyloids. Biophys. Chem., 88, 47-59.
  17. Masel, J., Jansen, V.A.A., Nowak, M.A. (1999). Quantifying the kinetic parameters of prion replication. Biophys. Chem., 77, 139-152.


Contact Information

Lab Phone: 
(520) 626-1727
Office Phone: 
(520) 626-9888
Office Location: 
Lab Location: