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Anthea Letsou

Associate Professor of Human Genetics

A.B. Harvard University

Ph.D. Yale University

Research

References

 

 

Research

In a second set of experiments, we are applying traditional genetic methods to our studies of the Dpp/TGF-ß and DJNK signaling cascades that are required for the morphogenetic process of dorsal closure in Drosophila embryos, and more generally for the control of changes in cell shape and migration in virtually all organisms. Data from several labs, including my own, have led to the model for dorsal closure that is shown in the accompanying figure. In this model, two signaling pathways function sequentially to coordinate morphogenesis. First, an as yet uncharacterized signal (or event) activates DJNK signaling in leading edge epidermal cells. Next, DJNK signaling induces elongation of leading edge cells and secretion of Dpp from leading edge cells. Finally, the Dpp cytokine activates signaling in adjacent epidermal cells and induces their elongation. Our recent progress in identifying dorsal-open group gene products and characterizing their roles in signal transduction provided the first evidence for dual ligand specific Dpp/TGF-ß receptors. In addition, our research provided the first identification of a transcriptional effector of a Dpp/TGF-ß signaling pathway.

In the long term, we seek to understand how the Drosophila DJNK and Dpp/TGF-b signaling cascades control embryonic cell motility. We continue to exploit Drosophila as a genetically tractable system to: (1) mechanistically characterize the sequential activities of these two signaling cascades, and (2) gain significant insights into their biologically relevant roles in eliciting the changes in cell motility that are required for embryonic dorsal closure. Since the cellular acquisition of motility oftentimes leads to metastasis, what we learn about dorsal closure in Drosophila is likely to be applicable to models of tumorigenesis in human disease as well.

In a second set of experiments, we are applying traditional genetic methods to our studies of the Dpp/TGF-ß and DJNK signaling cascades that are required for the morphogenetic process of dorsal closure in Drosophila embryos, and more generally for the control of changes in cell shape and migration in virtually all organisms. Data from several labs, including my own, have led to the model for dorsal closure that is shown in the accompanying figure. In this model, two signaling pathways function sequentially to coordinate morphogenesis. First, an as yet uncharacterized signal (or event) activates DJNK signaling in leading edge epidermal cells. Next, DJNK signaling induces elongation of leading edge cells and secretion of Dpp from leading edge cells. Finally, the Dpp cytokine activates signaling in adjacent epidermal cells and induces their elongation. Our recent progress in identifying dorsal-open group gene products and characterizing their roles in signal transduction provided the first evidence for dual ligand specific Dpp/TGF-ß receptors. In addition, our research provided the first identification of a transcriptional effector of a Dpp/TGF-ß signaling pathway.

In the long term, we seek to understand how the Drosophila DJNK and Dpp/TGF-b signaling cascades control embryonic cell motility. We continue to exploit Drosophila as a genetically tractable system to: (1) mechanistically characterize the sequential activities of these two signaling cascades, and (2) gain significant insights into their biologically relevant roles in eliciting the changes in cell motility that are required for embryonic dorsal closure. Since the cellular acquisition of motility oftentimes leads to metastasis, what we learn about dorsal closure in Drosophila is likely to be applicable to models of tumorigenesis in human disease as well.

References