Sarah C. Elgin

Washington University in St. Louis

Election Year: 2018
Primary Section: 26, Genetics
Secondary Section: 21, Biochemistry
Membership Type: Member


Sarah C. R. Elgin is a molecular geneticist recognized for her work on chromatin structure and its impact on gene expression. Early work in the Elgin lab developed a number of tools to characterize chromatin in Drosophila, including both a method to determine the distribution of specific proteins in the polytene chromosomes using immunofluorescence, and methods for analyzing the nucleosome array, including identification of accessible regulatory sites. Using these approaches led to a detailed picture of the chromatin structure of an inducible gene, hsp26, and to the identification of Heterochromatin Protein 1 (HP1a), shown by genetic and cytological analysis to play a key role in heterochromatin formation and gene silencing. Current work focuses on the establishment of heterochromatin, investigating both targeting mechanisms, maintenance, and epigenetic memory. Elgin was born in Washington, DC and grew up in Salem, Oregon. She graduated from Pomona College, Claremont CA in 1967 with a degree in chemistry and from the California Institute of Technology in 1972 with a PhD in biochemistry.  She was a junior faculty member in the Harvard Department of Biochemistry & Molecular Biology, and joined the faculty of Washington University in St Louis in 1981. In addition to her scientific work, Elgin has been very active in science education, and has received numerous awards for her efforts to bring research experiences into the undergraduate curriculum. She is a member of both the American Academy of Arts & Sciences and the National Academy of Sciences.

Research Interests

Dr. Elgin’s laboratory is interested in how heterochromatin is assembled, specifically how the cell knows which portions of the genome to package as heterochromatin, how that decision is maintained, and the impact of that packaging on regulation of gene expression. Using Drosophila as a model system, the lab has focused on the F element, a small “dot” chromosome that appears entirely heterochromatic by many criteria, but carries ~80 active/activatable genes, despite the silencing environment. Using a P-element reporter, the lab identified the TE (transposable element) remnant 1360 as a cis-acting target for heterochromatin formation. Following studies provided evidence for the role of piRNA in targeting heterochromatin formation in Drosophila, showing that while this apparently occurs in the early embryo, the impact on gene silencing can be seen in the adult. Somewhat different mechanisms of targeting and of heterochromatin assembly are observed when looking at tandem arrays of repeated sequence, from the trinucleotide GAA (source of the Friedreich’s Ataxia mutation in humans) to a 36 bp bacterial DNA fragment. How the dot chromosome genes escape silencing, despite their association with HP1a and H3K9me3, is under active investigation. Given that HP1a and the histone modification system linked together in heterochromatin formation are highly conserved, the results are likely to be broadly applicable.

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