HEADY Role in Hydra
Hydra, a multicellular, lower-eukaryotic, freshwater polyp, is known for its developmental idiosyncrasies. Slice off its head or its foot, and within two days either regenerates perfectly at the proper location. Although developmental biologists have some understanding of the molecular machinery involved in this feat, they have yet to isolate and prioritize many of the factors that play a role. In a recent paper, two scientists report the discovery of a signaling peptide called HEADY that appears to be very important for setting up axis formation in Hydra and other lower metazoans (J.U. Lohmann, T.C. Bosch, "The novel peptide HEADY specifies apical fate in a simple radially symmetric metazoan," Genes and Development, 14:2771-7, Nov. 1, 2000). Because Hydra does not lend itself to mutagenesis, investigators employed a screening strategy using differential display PCR. They split the organisms into balls of cells, let them form intact polyps, and noted which genes were differentially regulated during the development process. After identifying HEADY, investigators showed that the peptide could trigger the formation of a second head when HEADY-treated tissue was grafted onto an untreated Hydra. Importantly, HEADY appears to only set up axis formation while other peptides maintain it. HEADY's role as a developmental switch provides the first insight into how lower metazoans specify initial asymmetry. "This really supports the view that the lower you go in evolution, the more important the smaller peptides actually are," says lead author Jan Lohmann, now an associate researcher at the Salk Institute in La Jolla, Calif. By contrast, higher organisms such as the mouse and fruit fly employ growth factors.
Although Burkitt's lymphoma is uncommon in the United States, the disease accounts for more than half of all childhood cancers in Africa. Research to define mouse models of this human non-Hodgkin's lymphoma has continued for more than 15 years. Now scientists are hopeful that a new transgenic Burkitt's mouse (A.L. Kovalchuk et al., Burkitt's lymphoma in the mouse, Journal of Experimental Medicine, 192:1183-90, Oct. 16, 2000) will hold clues to the treatment and prevention of the disease. "It was a true scientific high to see that our mice develop lymphomas with so many parallels to human Burkitt's," says lead investigator Herbert C. Morse, chief of the immunopathology lab at the National Institute of Allergy and Infectious Diseases (NIAID). The Burkitt's mouse is expected to facilitate a deeper understanding of the pathogenesis of Burkitt's lymphoma, and alternative modes of treatment, comments Morse. Many aspects of the disease remain a mystery, including how genetic mutations, environmental factors, and infectious agents work together to cause the cancer. Scientists do know, however, that Burkitt's lymphoma arises from the immune system and occurs when a gene called MYC moves from its regular location on chromosome 8 to a new location, often chromosome 14. This move allows MYC, a cell growth gene that is normally controlled by regulator genes, to evade controls and causes rapid growth of the immune system's B cells. These B cells in turn lead to lymphomas, or tumors. Several laboratories have already approached the authors on the report about using the mouse in their research. Morse's group is making the animals freely available to the research community.
--Jennifer Fisher Wilson