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

Siegal, M. L., & Masel, J. (2012). Hsp90 depletion goes wild. BMC Biology, 10.

Abstract:

Hsp90 reveals phenotypic variation in the laboratory, but is Hsp90 depletion important in the wild? Recent work from Chen and Wagner in BMC Evolutionary Biology has discovered a naturally occurring Drosophila allele that downregulates Hsp90, creating sensitivity to cryptic genetic variation. Laboratory studies suggest that the exact magnitude of Hsp90 downregulation is important. Extreme Hsp90 depletion might reactivate transposable elements and/or induce aneuploidy, in addition to revealing cryptic genetic variation.See research article http://wwww.biomedcentral.com/1471-2148/12/25. © 2012 Siegal and Masel; licensee BioMed Central Ltd.

Masel, J., & Jansen, V. A. (2001). The measured level of prion infectivity varies in a predictable way according to the aggregation state of the infectious agent. Biochimica et Biophysica Acta - Molecular Basis of Disease, 1535(2), 164-173.

PMID: 11342005;Abstract:

Transmissible spongiform encephalopathies are believed to be caused by an infectious form of the prion protein, designated PrPSc. The concentration of PrPSc is often poorly correlated to the level of infectivity. Infectivity can be measured in two ways, namely endpoint titration and the incubation time assay, but patterns of infectivity vary depending on which method is used. These discrepancies can be explained by variation in the aggregation state of PrPSc. Both methods of measuring infectivity are modelled mathematically, and the theoretical results are in agreement with published data. It was found to be theoretically impossible to characterise prion infectivity by a multiple of a single quantity representing 'one prion', no matter how it is measured. Infectivity is instead characterised by both the number and sizes of the PrPSc aggregates. Apparent discrepancies arise when these complexities are reduced to a single number. © 2001 Elsevier Science B.V.

Masel, J., & Siegal, M. L. (2009). Robustness: mechanisms and consequences. Trends in Genetics, 25(9), 395-403.

PMID: 19717203;PMCID: PMC2770586;Abstract:

Biological systems are robust to perturbation by mutations and environmental fluctuations. New data are shedding light on the biochemical and network-level mechanisms responsible for robustness. Robustness to mutation might have evolved as an adaptation to reduce the effect of mutations, as a congruent byproduct of adaptive robustness to environmental variation, or as an intrinsic property of biological systems selected for their primary functions. Whatever its mechanism or origin, robustness to mutation results in the accumulation of phenotypically cryptic genetic variation. Partial robustness can lead to pre-adaptation, and thereby might contribute to evolvability. The identification and characterization of phenotypic capacitors - which act as switches of the degree of robustness - are critical to understanding the mechanisms and consequences of robustness. © 2009 Elsevier Ltd. All rights reserved.