Joanna Masel

Joanna Masel

Professor, Ecology and Evolutionary Biology
Professor, Genetics - GIDP
Professor, Statistics-GIDP
Professor, Applied Mathematics - GIDP
Professor, Psychology
Member of the Graduate Faculty
Professor, BIO5 Institute
Primary Department
Contact
(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

Giacomelli, M. G., Hancock, A. S., & Masel, J. (2007). The conversion of 3′ UTRs into coding regions. Molecular Biology and Evolution, 24(2), 457-464.

PMID: 17099057;PMCID: PMC1808353;Abstract:

A possible origin of novel coding sequences is the removal of stop codons, leading to the inclusion of 3′ untranslated regions (3′ UTRs) within genes. We classified changes in the position of stop codons in closely related Saccharomyces species and in a mouse/rat comparison as either additions to or subtractions from coding regions. In both cases, the position of stop codons is highly labile, with more subtractions than additions found. The subtraction bias may be balanced by the input of new coding regions through gene duplication. Saccharomyces shows less stop codon lability than rodents, probably due to greater selective constraint. A higher proportion of 3′ UTR incorporation events preserve frame in Saccharomyces. This higher proportion is consistent with the action of the [PSI+] prion as an evolutionary capacitor to facilitate 3′ UTR incorporation in yeast. © 2006 The Authors.

Masel, J., & Trotter, M. V. (2010). Robustness and evolvability. Trends in Genetics, 26(9), 406-414.

PMID: 20598394;PMCID: PMC3198833;Abstract:

Why isn't random variation always deleterious? Are there factors that sometimes make adaptation easier? Biological systems are extraordinarily robust to perturbation by mutations, recombination and the environment. It has been proposed that this robustness might make them more evolvable. Robustness to mutation allows genetic variation to accumulate in a cryptic state. Switching mechanisms known as evolutionary capacitors mean that the amount of heritable phenotypic variation available can be correlated to the degree of stress and hence to the novelty of the environment and remaining potential for adaptation. There have been two somewhat separate literatures relating robustness to evolvability. One has focused on molecular phenotypes and new mutations, the other on morphology and cryptic genetic variation. Here, we review both literatures, and show that the true distinction is whether recombination rates are high or low. In both cases, the evidence supports the claim that robustness promotes evolvability. © 2010 Elsevier Ltd.

Masel, J. (2013). Q&A: Evolutionary capacitance. BMC Biology, 11.

PMID: 24228631;PMCID: PMC3849687;