BAR HARBOR, Maine -- Research conducted at The Jackson Laboratory has confirmed an important role in embryonic development for the Lunatic fringe gene, part of a cell communication mechanism known as the Notch signaling pathway that is critical to the normal implementation of the body "blueprint" in mammals and other organisms.
The findings are reported in the July 23, 1998, issue of the scientific journal Nature by a team led by Dr. Thomas Gridley, Staff Scientist at The Jackson Laboratory. "Defects in Somite Formation in Lunatic fringe Deficient Mice" is co-published in Nature with a complementary research paper on Lunatic fringe by Dr. Randy Johnson and his colleagues at the University of Texas M.D. Anderson Cancer Center.
Dr. Gridley, who has conducted extensive research in mice on the Notch family of genes, describes the Notch signaling pathway as an evolutionarily conserved mechanism first studied in the fruit fly, Drosophila. Mutations in this pathway disrupt essential signaling between cells during early embryonic development that helps choreograph implementation of the segmented body plan in organisms as diverse as insects, nematodes, and mammals. In humans, Notch mutations have been implicated in cancer and in several inherited disease syndromes.
Recent studies have demonstrated that the Notch signaling pathway specifically helps regulate development of the somite, the primary unit of segmentation in mammals. Somites are present only transiently in embryos and are arranged as clusters of cells on either side of the neural tube. They form sequentially, starting at the head, and give rise to muscle, vertebrae, and skin. In adults, the influence of the primary segmentation of the embryo can be observed in the segmented pattern of the vertebrae and spinal nerves.
The Drosophila fringe gene, which encodes a secreted signaling molecule
required for Notch activation during wing formation in the fruit fly, has three
Contact: Luther Young