Joanna Masel
Professor, Ecology and Evolutionary Biology
Professor, Applied Mathematics - GIDP
Professor, BIO5 Institute
Professor, Genetics - GIDP
Professor, Psychology
Professor, Statistics-GIDP
Primary Department
(520) 626-9888
Research Interest
Joanna Masel, D.Phil., is a Professor of Ecology & Evolutionary Biology, applying the tools of theoretical population genetics to diverse research problems. Her research program is divided between analytical theory, evolutionary simulations, and dry lab empirical bioinformatic work. The robustness and evolvability of living systems are major themes in her work, including questions about the origins of novelty, eg at the level of new protein-coding sequences arising during evolution from "junk" DNA. She also has interests in prion biology, and in the nature of both biological and economic competitions. She has won many awards, including a Fellowship at Wissenschaftskolleg zu Berlin, a Pew Scholarship in the Biomedical Sciences, an Alfred P. Sloan Research Fellow, a Rhodes Scholarship, and a Bronze Medal at the International Mathematical Olympiad.

Publications

Andreatta, M. E., Levine, J. A., Foy, S. G., Guzman, L. D., Kosinski, L. J., Cordes, M. H., & Masel, J. (2015). The Recent De Novo Origin of Protein C-Termini. Genome biology and evolution, 7(6), 1686-701.
BIO5 Collaborators
Matthew Hj Cordes, Joanna Masel

Protein-coding sequences can arise either from duplication and divergence of existing sequences, or de novo from noncoding DNA. Unfortunately, recently evolved de novo genes can be hard to distinguish from false positives, making their study difficult. Here, we study a more tractable version of the process of conversion of noncoding sequence into coding: the co-option of short segments of noncoding sequence into the C-termini of existing proteins via the loss of a stop codon. Because we study recent additions to potentially old genes, we are able to apply a variety of stringent quality filters to our annotations of what is a true protein-coding gene, discarding the putative proteins of unknown function that are typical of recent fully de novo genes. We identify 54 examples of C-terminal extensions in Saccharomyces and 28 in Drosophila, all of them recent enough to still be polymorphic. We find one putative gene fusion that turns out, on close inspection, to be the product of replicated assembly errors, further highlighting the issue of false positives in the study of rare events. Four of the Saccharomyces C-terminal extensions (to ADH1, ARP8, TPM2, and PIS1) that survived our quality filters are predicted to lead to significant modification of a protein domain structure.

Masel, J., A., V., Pöschel, T., Brilliantov, N. V., & Frömmel, C. (2004). Prion Kinetics (multiple letters). Biophysical Journal, 87(1), 728-729.

PMID: 15240505;PMCID: PMC1304395;

Masel, J., King, O. D., & Maughan, H. (2007). The loss of adaptive plasticity during long periods of environmental stasis. American Naturalist, 169(1), 38-46.

PMID: 17206583;PMCID: PMC1766558;Abstract:

Adaptive plasticity allows populations to adjust rapidly to environmental change. If this is useful only rarely, plasticity may undergo mutational degradation and be lost from a population. We consider a population of constant size N undergoing loss of plasticity at functional mutation rate m and with selective advantage s associated with loss. Environmental change events occur at rate θ per generation, killing all individuals that lack plasticity. The expected time until loss of plasticity in a fluctuating environment is always at least τ, the expected time until loss of plasticity in a static environment. When mN > 1 and Nθ ≫ 1, we find that plasticity will be maintained for an average of at least 108 generations in a single population, provided τ > 18/θ. In a metapopulation, plasticity is retained under the more lenient condition τ > 1.3/θ, irrespective of mN, for a modest number of demes. We calculate both exact and approximate solutions for τ and find that it is linearly dependent only on the logarithm of N, and so, surprisingly, both the population size and the number of demes in the metapopulation make little difference to the retention of plasticity. Instead, τ is dominated by the term 1/(m + s/2). © 2007 by The University of Chicago.

Griswold, C. 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).

PMID: 19521499;PMCID: PMC2686163;Abstract:

The [PSI+] prion may enhance evolvability by revealing previously cryptic genetic variation, but it is unclear whether such evolvability properties could be favored by natural selection. Sex inhibits the evolution of other putative evolvability mechanisms, such as mutator alleles. This paper explores whether sex also prevents natural selection from favoring modifier alleles that facilitate [PSI+] formation. Sex may permit the spread of "cheater" alleles that acquire the benefits of [PSI +] through mating without incurring the cost of producing [PSI+] at times when it is not adaptive. Using recent quantitative estimates of the frequency of sex in Saccharomyces paradoxus, we calculate that natural selection for evolvability can drive the evolution of the [PSI+] system, so long as yeast populations occasionally require complex adaptations involving synergistic epistasis between two loci. If adaptations are always simple and require substitution at only a single locus, then the [PSI+] system is not favored by natural selection. Obligate sex might inhibit the evolution of [PSI+]-like systems in other species. © 2009 Griswold, Masel.

King, O. D., & Masel, J. (2007). The evolution of bet-hedging adaptations to rare scenarios. Theoretical Population Biology, 72(4), 560-575.

PMID: 17915273;PMCID: PMC2118055;Abstract:

When faced with a variable environment, organisms may switch between different strategies according to some probabilistic rule. In an infinite population, evolution is expected to favor the rule that maximizes geometric mean fitness. If some environments are encountered only rarely, selection may not be strong enough for optimal switching probabilities to evolve. Here we calculate the evolution of switching probabilities in a finite population by analyzing fixation probabilities of alleles specifying switching rules. We calculate the conditions required for the evolution of phenotypic switching as a form of bet-hedging as a function of the population size N, the rate θ at which a rare environment is encountered, and the selective advantage s associated with switching in the rare environment. We consider a simplified model in which environmental switching and phenotypic switching are one-way processes, and mutation is symmetric and rare with respect to the timescale of fixation events. In this case, the approximate requirements for bet-hedging to be favored by a ratio of at least R are that sN>log(R) and θ N > sqrt(R) . © 2007 Elsevier Inc. All rights reserved.