Dr. Mia Levine

Curriculum Vitae

Mia seeks to understand the causes and consequences of heterochromatic sequence evolution.  She focuses primarily on the model system, Drosophila melanogaster, but has recently applied these questions to humans and our close relatives.

Heterochromatin is that gene-poor, satellite-rich eukaryotic genome compartment that supports manMia Leviney essential cellular processes, from chromosome segregation to genome defense.  Extensive tracts of repetitive DNA in heterochromatin, however, challenge traditional methods of sequence assembly and experimental manipulation. Fortunately, the functional diversity of proteins that bind and often epigenetically define heterochromatic DNA sequence mirrors the diverse functions supported by this elusive genome compartment.  

To identify new such surrogates for dissecting heterochromatin function and evolution, Mia, along with several collaborators at FHCRC, has conducted a comprehensive phylogenomic analysis of the Heterochromatin Protein 1 gene family over 40 million years of Drosophila evolution.  This analysis has uncovered numerous germline line restricted, chromatin-binding proteins encoded by genes evolving under positive selection, purifying selection, or lack of functional constraint.  This expanded compendium of surrogates and their corresponding signatures of selection direct Mia’s functional analyses of heterochromatin, especially in the male germline. Moreover, these analyses are guiding her exploration of HP1 family dynamics in humans.

Mia’s curiosity about the mechanisms that generate and maintain biological diversity originated as an undergraduate and with of the most accessible manifestations of variation—spatial and temporal distributions of natural plant populations. After graduating from the University of Pennsylvania, Mia pursued this interest along the sub-estuaries of the Chesapeake Bay (under Dr. Candy Feller, Smithsonian Environmental Research Center) and in the alpine meadows near Flagstaff, Arizona (MSc under Dr. Ken Paige, University of Illinois).  While investigating the roles of abiotic and biotic factors shaping the reproductive success and distributions of plant populations across ecological timescales, Mia developed a deeper curiosity about the forces shaping variation across evolutionary time scales.   She followed this interest to the Center for Population Biology at UC Davis, where Mia received training in molecular population genetics and evolution (PhD under Dr. David Begun).  She used Drosophila melanogaster and its close relatives to investigate both the evolution of novel genes and the role of chromatin remodeling factors in adaptation to novel habitat.  The latter research program sparked Mia’s maturing interest in how natural selection shapes chromosome structure and organization over evolutionary time.

When Mia is not in the lab, she in enjoying her son, Harry, her husband, James, and her dog, Ernest.  They typically can be found working in the garden, building with Legos, and re-visiting Seattle’s kid-tolerant museums, parks, and cafes.

Email Dr. Mia Levine 

Selected publications 

Levine, M.T., McCoy, C., Lee, G., Vermaak, D., Hiatt, M.A., Matsen, F., and H.S. Malik. 2012. “Phylogenomic analysis reveals dynamic evolutionary history of the Drosophila Heterochromatin Protein 1 (HP1) gene family. PLoS Genetics: 8(6): e1002729.

Moyle, L.C., Levine, M.T., Stanton, M.L. and J.W. Wright. 2012. Hybrid sterility over tens of meters between ecotypes adapted to serpentine and non-serpentine soils. Evolutionary Biology, 39:207-2318.

Levine, M.T. and H.S. Malik. 2011. Learning to protect your genome on the fly. Cell: 147:1440-1441.  Preview of “Adaptation to transposon invasion in Drosophila melanogaster.”

Levine, M.T., Eckert, M., Begun, D.J., 2011. Whole genome expression plasticity across tropical and temperate Drosophila melanogaster populations from eastern Australia. Molecular Biology and Evolution: 28:249–256

Levine, M.T. and D.J. Begun 2008. Evidence of spatially varying selection at four chromatin-remodeling loci in Drosophila melanogaster. Genetics: 179: 455-473.

Turner, L.T., Levine, M.T., and D.J.Begun. 2008. Genomic analysis of adaptive differentiation in Drosophila melanogaster. Genetics: 179: 475-485

Levine, M.T., Holloway, A.K., Arshad, U., and D.J. Begun. 2007. Pervasive and largely lineage-specific adaptive protein evolution in the dosage compensation complex of Drosophila melanogaster.  Genetics: 177: 1959–1962.

Levine, M.T. and D.J. Begun. 2007. Comparative Population Genetics of the Immunity Gene, Relish: Is Adaptive Evolution Idiosyncratic?.  PLoS ONE: 2(5): e442.

Levine, M.T., C. D. Jones, A. D. Kern, H. A. Lindfors, and D. J. Begun. 2006. Novel genes derived from noncoding DNA in Drosophila melanogaster are frequently X-linked and exhibit testis-biased expression. Proceedings of the National Academy of Sciences 103: 9935-9939. 
   

Fred Hutchinson Cancer Research Center
1100 Fairview Ave. N. PO Box 19024 Seattle, WA 98109
©2013 Fred Hutchinson Cancer Research Center, a 501(c)(3) nonprofit organization.
Terms of Use & Privacy Policy.