Long filaments of a protein known as actin run through every cell in the body, serving as a kind of railroad along which another protein called myosin transports vital materials to locations throughout the cell. Until now, scientists believed that the fifteen known variants of myosin all moved in only one direction on the actin filaments, towards the plus end of the polarized filaments. If a cell needed materials carried in two directions, it simply provided parallel actin filaments running in both directions - but the myosin itself could only go forward along the actin.
Now, in a finding likely to surprise many cell biologists, University of Pennsylvania Medical Center scientists have discovered that one of the myosin variants - myosin VI - moves backwards on actin, toward the minus end of the filaments. A report on the new study appears in the September 30 issue of Nature and is featured on the cover.
The observation suggests how, in the relatively few structures in the body in which the actin filaments are known to run in only one direction - notably the inner-ear projections responsible for sensing sound - the cells are able to assemble and maintain themselves. In fact, mice in whom myosin VI is defective are deaf, suggesting the critical importance of the variant motor protein to the so-called hair cells of the inner ear upon which hearing depends. Myosin VI may be similarly crucial in other parts of the body where actin filaments are aligned in only one direction.
"In many ways, the myosin protein moving along an actin filament is like a sure-footed gymnast able to walk only one direction on a balance beam," says H. Lee Sweeney, PhD, chairman of the department of physiology and senior author on the study. "What we've shown here is that, surprisingly, one form of myosin is able to walk backwards on the beam."
Sweeney and his team began their efforts to identify myosin VI's unique
capabilities by assumi
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Contact: Franklin Hoke
hokef@mail.med.upenn.edu
215-349-5659
University of Pennsylvania School of Medicine
30-Sep-1999