Our initiatives bring the tools and concepts of genomics into the undergraduate and high school biology curricula. Starting in 2002, we added genomic investigations to several biology courses at WUSTL. The first, a short bioinformatics laboratory, introduces students to a suite of web-based informatics tools to explore the impact of a particular mutation on protein structure, metabolic function, and human health http://gep.wustl.edu/curriculum/course_materials_WU/introduction_to_genomics/bio3055/. The following course, Research Explorations in Genomics, provides juniors / seniors with an opportunity to work as a team on a large-scale sequencing project. Students begin by analyzing and refining raw sequence data, then annotate the genes and explore other features. The course enables students to become comfortable thinking about large data sets as a research tool in biology—how to generate them, how to analyze them, and how to use them. The work has led to publication of two student-authored papers, with a third in preparation. Our current project is a comparative genomics analysis of the dot chromosomes (Muller F elements) of different species of Drosophila, the fruit fly.
To provide insight into WUSTL’s Genome Institute, we developed a video, available at www.nslc.wustl.edu/elgin/genomics/gsc.html, which offers a guided tour of the facility and provides an up-close look at the people and equipment involved in the Sanger sequencing of the human genome. Animations show the processes at the molecular level. We have updated by adding a video explaining “next generation” sequencing machines. All college materials are freely available at http://gep.wustl.edu, while some adaptations for high school students are available through the WUSTL Institute for School Partnership, http://schoolpartnership.wustl.edu/instructional-materials/ (see Modern Genetics, Significant Sequences, Building Food).
In 2006, we started the Genomics Education Partnership (GEP), establishing a collaboration with faculty and students from primarily undergraduate institutions. GEP participation requires only access to the Web and computers for student use. Students enrolled at Partner schools are able to work on the same large-scale genome sequencing project using data available through web-based repositories on the GEP website. In addition to learning about genes and genomes, and developing skills in using genomics databases, students contribute to scientific knowledge (currently through an analysis of the dot chromosomes of Drosophila), and their work is deposited in public databases. Our next scientific paper will have more than 500 student co-authors!
Interested faculty joined GEP by participating in a 3- to 5-day workshop at Wash U, and return subsequent summers to work jointly on publications and curriculum development, including genomics course materials, assessment resources, and research projects, all made available on GEP's website. More than 100 faculty have implemented the curriculum materials and approaches in a variety of course formats, including as a lab component in a genetics course, as a stand-alone course, and as independent research for a small group of students.
The program is flourishing in diverse educational settings, including small and large schools, commuter and residential schools, schools with a high proportion of first-generation students and/or a high proportion of underrepresented minority students. Blending an introduction to genomics with a research experience appears to be cost-effective and pedagogically successful. Assessment data show that GEP students (more than 1300 in 2012-2013) improve their understanding of genes and genomes, gain skill with genomics tools, and exhibit gains in attitude and learning that equal those gains attributed to summer undergraduate research experiences. The GEP faculty have published three papers in the science education literature on using genomics research as a teaching strategy.
Research in the Elgin Lab
I’m interested in the role that chromatin structure plays in gene regulation, both the effects from packaging large domains and local effects of the nucleosome array. Our earlier work, using the fruit fly Drosophila melanogaster, generated a detailed picture of the chromatin structure of hsp26, a heat shock gene, demonstrating that formation of 5’ DNase hypersensitive sites (DH sites) is necessary for gene activation and requires both GAGA factor and RNA polymerase II. Immunofluorescent staining of polytene chromosomes led to identification of heterochromatin protein 1 (HP1), located predominantly in the pericentric heterochromatin and small fourth chromosome (Muller F element). Using genetic and biochemical analysis, we have shown that HP1 plays a key role in heterochromatin formation and gene silencing. We have mapped heterochromatin domains using a transposable element carrying an hsp70-white reporter gene, allowing us to score variegated expression of white, a determinant of eye pigmentation. Variegation indicates that the gene has been silenced in some of the cells where it is normally active, and is a good indicator of heterochromatin formation; this silencing is dependent on HP1. When the hsp26 gene is packaged into heterochromatin, it has a more uniform nucleosome array, with loss of DH sites. Mapping experiments with the hsp70-white reporter showed that the F element is primarily heterochromatic, even though it contains ~80 genes. More recently we have participated in the modENCODE project to map histone modifications and chromosomal proteins across the entire D. melanogaster genome. This map shows that while the bulk of the F element is packaged as heterochromatin, the active genes have the typical marks of active chromatin specifically at the 5’ transcription start site. How these F element genes function and evolve in a heterochromatic domain is under study in collaboration with the faculty and students of the GEP.
In a related project, we have found that ectopic heterochromatin formation can be induced by the presence of repetitious element 1360, and probably other repeats, when that repeat is inserted close to a block of heterochromatin. Ongoing work suggests that this targeting occurs through a piRNA mechanism during blastoderm formation, the time when heterochromatin formation first occurs. Work continues to determine the targeting mechanism, and to analyze the role of critical heterochromatin-associated proteins, including HP1 and its partners.
Last updated May 2014