A novel gene called rumi regulates Notch signaling by adding a glucose molecule to the part of the Notch protein that extends outside a cell, said researchers from Baylor College of Medicine in Houston and Stony Brook University in New York in a report that appears in the journal Cell.
Cellular signaling governed by the Notch protein determines cell fate determination and differentiation. The complete loss of rumi causes a temperature-dependent defect in Notch signaling, an unusual phenomenon said Dr. Hugo Bellen, professor of molecular and human genetics at BCM and director of the program in developmental biology. He is also a Howard Hughes Medical Institute investigator.
Bellen and his colleagues discovered the gene’s effect on bristles in the fruit fly. These bristles are external sensory organs that can be easily screened for changes involved in Notch signaling. Indeed, loss of Notch signaling causes loss of these external sensory organs. Fruit flies that lack the rumi protein have a higher than normal density of bristles on the thorax, indicating a subtle loss of Notch activity. However, at 25 degrees C, the bristles are lost, which suggests a severe loss of Notch signaling.
Release date: January 25, 2008
Source: Baylor College of Medicine
Filed Under: Genomics/Proteomics