Pair wins Nobel for 'split-gene' finding.

Two men whose discoveries underlie today's burgeoning genetic-engineering industry will share this year's Nobel Prize for Physiology or Medicine, the Karolinska Institute and the Swedish Academy of Sciences announced this week. Phillip A. Sharp of the Massachusetts Institute of Technology and Richard J. Roberts of New England Bio-labs in Beverly, Mass., will split the $825,000 award.

In 1977, the researchers shook the genetics community with related reports based on their independent studies of a common cold virus. They found that contrary to the prevailing view -- which had been based on work with bacteria -- individual genes do not always reside as continuous brands of information along a strand of DNA. Rather, surplus "nonsense" segments of DNA can lie between the usual bits of each gene in nonbacterial organisms.

To activate a gene -- the process by which proteins are made -- a cell must copy each fragment of the gene that codes for the desired protein. Then the cell must splice them into a continuous band of RNA, which contains the information for making that protein.

Shortly after publication of Sharp's and Roberts' reports on adenovirus DNA, other researchers showed that "split genes" occur throughout higher organisms. These studies also showed that functional gene segments vary depending on the tissue in which the gene is activated or on the stage in an organism's development. In other words, the same DNA can be spliced into patterns that produce different proteins -- and perform different functions.

Such observations have given rise to a new theory about the nature of evolutionary change.

Previously, biologists suspected evolution occurred as a series of accumulated, small alterations in an organism's DNA. But the split-gene finding immediately suggested that each segment of a gene might correspond to a particular subfunction of a protein. By merely shuffling these relatively large segments of DNA into new combinations, or swapping segments between genes, proteins with new functions could emerge.

Understanding the role of gene splicing also has helped researchers identify the mechanisms responsible for many genetic disorders. Beta-thalassemia, a potentially life-threatening anemia, for instance, traces to inherited gene-splicing errors. The faulty protein produced by the errors shortens the lifespan of red blood cells.