----, Sept. 3 (UPI) -- THEY CAN'T BITE YOU IF THEY CAN'T SMELL YOU
Insects, including disease-carrying mosquitoes, rely on their sense of smell to find humans to bite. Researchers at Rockefeller University report insects' ability to detect odors depends on a single gene, known as Or83b. Fruit flies lacking the gene cannot smell. Or83b is unique in two ways: first, nearly all the olfactory neurons in the fly -- and other insects -- have receptors for the gene. Second, the gene is found in widely divergent species of insects, including locusts, mosquitoes and moths. The researchers said the finding has direct applied potential in developing repellents as insects are the primary carriers for malaria, dengue fever, yellow fever and West Nile encephalitis, and they locate human hosts largely through their very sensitive olfactory systems. This study appeared in the Sept. 2 issue of the journal Neuron.
A CLOSER LOOK AT GENOME CONTROL
A genome's sequence is little more than a list of parts, so now researchers are focusing on what makes those parts work. For the first time, researchers at the Whitehead Institute for Biomedical Research have revealed all the "controlling elements" of an entire genome. The researchers combined the latest biological tools with new computational methods to uncover the 203 gene regulators, or transcription factors, at work in the yeast genome. Their findings may soon contribute to a new way of understanding human health and disease. They call it the next stage in human genome research. Human cells have roughly 10 times the number of regulators that yeast cells do, but the researchers are confident analyzing the human genome regulators is not far off. This paper appeared in the Sept. 2 issue of Nature.
GENETIC FIRST STEP TO PROSTATE CANCER DISCOVERED
A new mouse study uncovered what appears to be the first genetic step in prostate cancer development. Researchers at the Fred Hutchinson Cancer Research Center discovered that when mice were engineered to lose just a single copy of the Rb gene in the prostate they developed a precancerous condition similar to the earliest stages of human prostate cancer. They also found that in the absence of other genetic defects, the mice did not develop full-blown prostate cancer. Mice with only one copy of the Rb gene in their prostate developed a condition characterized by precancerous growths. "This suggests to us that loss of a single copy of Rb can initiate this excess cell growth but is not sufficient for cancer to develop," the researchers wrote. The next goal is to identify the additional mutations that collaborate with Rb to drive the benign growths into cancer. This study was published in the Sept. 1 issue of Cancer Research.
GENE LINKED TO SKIN CANCER INITIATION, PROMOTION
For the first time, a protein called Stat3 has been shown to be necessary for the initiation of one form of skin cancer. Researchers at The University of Texas MD Anderson Cancer Center used a two-stage chemical skin cancer mouse model to investigate whether or not Stat3 was involved in skin cancer, finding that mice deficient in Stat3 were completely resistant to skin tumor development. The researchers were further able to block growth of already transformed skin cells if they inhibited Stat3 function using a functional inhibitor. The injection of the inhibitor into developed tumors also impaired tumor growth. Stat3 has already come under focus as a possible target for cancer therapy, and these results suggest it also may be important for developing cancer prevention strategies. These results were published in the Sept. 1 issue of the Journal of Clinical Investigation.
NEW SUPPORT OF GENETIC LINK FOR SCHIZOPHRENIA
Mice with specific genetic mutations exhibit behaviors similar to those seen in human psychosis. University of Texas Southwestern Medical Center scientists genetically engineered mice with a mutation in the gene NPAS3, a mutation in the gene NPAS1, or a mutation in both genes. "These mice display certain deficits that are potentially consistent with schizophrenia," the researchers wrote. The mice avoided interaction with their normal siblings, darted about wildly, and had an abnormal startle response. "It's too early to tell whether the abnormal behavior we observed in these mutated mice can be directly connected with human disease. On the other hand, we find it intriguing that members of a Canadian family carrying a mutation in the human NPAS3 gene have been reported to suffer from schizophrenia," the researchers explained. NPAS1 and NPAS3 are transcription factors that work to activate or deactivate other genes, though it is unclear at this time which genes they control. This research appeared in the September online edition of the Proceedings of the National Academy of Sciences.
(EDITORS: For SMELL, contact Lynn Love at (212) 327-8977 or [email protected]. For CONTROL, contact David Cameron at (617) 324-0460 or [email protected]. For PROSTATE, contact Dean Forbes at (206) 667-2896 or [email protected]. For SKIN, contact Laurie Goodman at (212) 342-4159 or [email protected]. For SCHIZOPHRENIA, contact Amanda Siegfried at (214) 648-3404 or [email protected])
