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

Hazelton, N. W., Bennett, L. M., & Masel, J. (1992). Topological structures for 4-dimensional geographic information systems. Computers, Environment and Urban Systems, 16(3), 227-237.

Abstract:

The purpose of this paper is to extend the framework for binary topological interactions to spaces up to 4-D. It includes descriptions of the various interactions between objects of various dimensions in various spaces, covering all interactions between all types of objects up to 4-D, in spaces up to 4-D. The need for topology in GIS is briefly discussed, in the instance of a vector-based 4-D GIS. The requirements for spatio-temporal indexing of data in a 4-D GIS are discussed briefly, together with the current dearth of information on query types and temporal analysis needs. This absence limits how well system designers can optimize the indexing, and consequently performance, of a 4-D GIS. This information will become available only after systems are in regular use and their modes of use analyzed. © 1992.

Masel, J. (2004). Genetic assimilation can occur in the absence of selection for the assimilating phenotype, suggesting a role for the canalization heuristic. Journal of Evolutionary Biology, 17(5), 1106-1110.

PMID: 15312082;Abstract:

Genetic assimilation occurs when an acquired trait loses dependency on its environmental trigger and becomes an inherited trait. According to the standard quantitative genetic model for genetic assimilation, the trait is determined by the contributions of multiple genes. Trait expression occurs at a lower threshold with the trigger. Selection for the trait in the presence of the trigger increases the frequency of the trait-determining alleles. Eventually these alleles become frequent enough to breach the higher threshold for expression in the absence of the trigger. This loss of dependence on the trigger signifies genetic assimilation. Here I show that genetic assimilation can occur in the absence of selection for the trait in an evolutionary simulation of a gene network model. This contradicts the prediction of the standard quantitative genetic model, but is consistent with an explanation in terms of the canalization heuristic.

Wilson, B. A., & Masel, J. (2011). Putatively noncoding transcripts show extensive association with ribosomes. Genome Biology and Evolution, 3(1), 1245-1252.

PMID: 21948395;PMCID: PMC3209793;Abstract:

There have been recent surprising reports that whole genes can evolve de novo from noncoding sequences. This would be extraordinary if the noncoding sequences were random with respect to amino acid identity. However, if the noncoding sequences were previously translated at low rates, with the most strongly deleterious cryptic polypeptides purged by selection, then de novo gene origination would be more plausible. Here we analyze Saccharomyces cerevisiae data on noncoding transcripts found in association with ribosomes. We find many such transcripts. Although their average ribosomal densities are lower than those of protein-coding genes, a significant proportion of noncoding transcripts nevertheless have ribosomal densities comparable to those of coding genes. Most show increased ribosomal association in response to starvation, as has been previously reported for other noncoding sequences such as untranslated regions and introns. In rich media, ribosomal association is correlated with start codons but is not usually consistent and contiguous beyond that, suggesting that translation occurs only at low rates. One transcript contains a 28-codon open reading frame, which we name RDT1, which shows evidence of translation, and may be a new protein-coding gene that originated de novo from noncoding sequence. But the bulk of the ribosomal association cannot be attributed to unannotated protein-coding genes. Our primary finding of extensive ribosome association shows that a necessary precondition for selective purging is met, making de novo gene evolution more plausible. Our analysis is also proof of principle of the utility of ribosomal profiling data for the purpose of gene annotation. © The Author(s) 2010.