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Nerve Cells On The Go

the proper places, or the rogue travels of metastatic cancer cells.

Van Vactor started this research as a postdoctoral fellow in the lab of Corey Goodman at the University of California, Berkeley, who is a co-author on the first paper.

Using the fruit fly, Van Vactor analyzed two types of mutant phenotypes with derailed motor nerve development. In one set of mutants--dubbed stop short--a motor nerve called intersegmental nerve b (ISNb) arrested its growth before reaching its target muscles, suggesting the disrupted genes were essential for the growth cones to proceed. In mutants dubbed bypass, ISNb neurons miss their exit, growing straight past the muscle instead of turning sharply toward it.

When he cloned the genes underlying stop short and bypass, Van Vactor expected the genes would operate in different contexts. But once he analyzed them a puzzle fell into place, and the genes turned out to belong to the same pathway. The story starts at the bottom of the pathway.

The first gene he cloned caused the stop short phenotype. It turned out to be profilin, a much-studied protein actin known bind and control actin. That made sense but was not really surprising, Van Vactor says.

Unexpected, however, was his finding that the stop short phenotype also arose in embryos lacking the gene for the protein kinase Abl. (Protein kinases are enzymes that tack phosphate groups onto other kinds of proteins.) When analyzing mutant embryos that lacked both profilin genes and one copy of the Abl gene, the scientists found that cutting the amount of Abl protein in half dramatically worsened the embryos' stunted nerve growth.

This genetic way of asking whether one protein is sensitive to the dose of another helps scientists find out whether two proteins cooperate in the same pathway. Profilin and Abl clearly seemed to do so.

Abl provided an intriguing step up the pathway, since its substrate--a prote
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Contact: Peta Gillyatt
gillyatt@hms.harvard.edu
617-432-0443
Harvard Medical School
26-Feb-1999


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