Genomics is not only essential for students to understand biology but also provides unprecedented opportunities for undergraduate research. The goal of the Genomics Education Partnership (GEP), a collaboration between a growing number of colleges and universities around the country and the Department of Biology and Genome Center of Washington University in St. Louis, is to provide such research opportunities. Using a versatile curriculum that has been adapted to many different class settings, GEP undergraduates undertake projects to bring draft-quality genomic sequence up to high quality and/or participate in the annotation of these sequences. GEP undergraduates have improved more than 2 million bases of draft genomic sequence from several species of Drosophila and have produced hundreds of gene models using evidence-based manual annotation. Students appreciate their ability to make a contribution to ongoing research, and report increased independence and a more active learning approach after participation in GEP projects. They show knowledge gains on pre- and postcourse quizzes about genes and genomes and in bioinformatic analysis. Participating faculty also report professional gains, increased access to genomics-related technology, and an overall positive experience. We have found that using a genomics research project as the core of a laboratory course is rewarding for both faculty and students.

While course-based research in genomics can generate both knowledge gains and a greater appreciation for how science is done, a significant investment of course time is required to enable students to show gains commensurate to a summer research experience. Nonetheless, this is a very cost-effective way to reach larger numbers of students.

Germ cells must develop along distinct male or female paths to produce the sperm or eggs required for sexual reproduction. In both mouse and Drosophila, sexual identity of germ cells is influenced by the sex of the surrounding somatic tissue (e.g. 1 , 2 ; reviewed in 3, 4 ), but little is known about how the soma controls germline sex determination. Here we show that the JAK/STAT pathway provides a sex-specific signal from the soma to the germline in the Drosophila embryonic gonad. The somatic gonad expresses a JAK/STAT ligand, unpaired (upd), in a male-specific manner, and activates the JAK/STAT pathway in male germ cells at the time of gonad formation. Furthermore, the JAK/STAT pathway is necessary for male-specific germ cell behavior during early gonad development, and is sufficient to activate aspects of male germ cell behavior in female germ cells. This work provides direct evidence that the JAK/STAT pathway mediates a key signal from the somatic gonad that regulates male germline sexual development.While investigating communication between the somatic gonad and germline, we found that the JAK/STAT pathway is specifically activated in male, but not female, germ cells. In Drosophila, JAK/STAT signaling (reviewed in 5 ) is initiated when an UPD or UPD-like ligand binds a transmembrane receptor (Domeless), activating the janus kinase (JAK), Hopscotch (HOP), which phosphorylates the STAT92E transcription factor. STAT activation has been shown to regulate stat gene expression 6 and can induce upregulation of the STAT92E protein, which can be used as an assay for JAK/STAT pathway activation. We found that STAT92E is upregulated specifically in male, but not female germ cells at the time of gonad formation ( Fig. 1 a,b). This reflects male-specific activation of the JAK/STAT pathway since (i) the activated form of STAT92E (phospho-STAT92E) was also only detected in male germ cells ( Fig. 1 c,d), and (ii) JAK activity is necessary and sufficient for STAT92E expression. Expression of a JAK inhibitor, Socs36E 7 , resulted in loss of STAT92E expression in male germ cells (Fig. 1e) and expression of constitutively active JAK 8 (hop TumL ) induced STAT92E in female germ cells (Fig. 1f). The male-specific activation of STAT92E at this time is distinct from STAT92E activation in germ cells in the early embryo, which is not sex-specific and is regulated by the MAP kinase pathway 9 .We also found that STAT92E expression in male germ cells is dependent on their association with the somatic gonad. STAT92E was not detected in germ cells that were migrating to the gonad (Fig. 2a), but was detected in male germ cells after they contact the somatic gonad (Fig. 2b). STAT92E expression was greatly reduced or absent in eya mutants (data not shown), where somatic gonad identity is initiated, but not maintained 10 . Furthermore, STAT92E was (Fig. 2b, arrows) or in mis-localized germ cells in wunen (Fig. 2c) and HMG-CoA reductase (data not shown) mutants which lack guidance cues that target germ cells to the somatic gonad 1...