WORCESTER, Mass. Researchers at the University of Massachusetts Medical School have described a previously unknown role for the cilia protein IFT88 in mitosis, the process by which a dividing cell separates its chromosomes containing the cell's DNA into two identical sets of new daughter cells. Published in advance online by Nature Cell Biology, this newly discovered function for IFT88 suggests a possible alternative or contributory cause for cilia-related diseases such as primary ciliary dyskinesia, and polycystic kidney disease.
Famous for its ability to build cilia, a slender protrusion responsible for motility and sensory input, IFT88 is part of a family of transport proteins and cellular machinery that is responsible for moving materials from the cell body to the cilia. These cellular materials are necessary for the proper formation and maintenance of cilia and in the absence of IFT88 cilia are either unable to form or are defective. Over the last several years, scientists have linked cilia dysfunction to a number of diseases now known as ciliopathies. In particular, the loss of IFT88, one of the best-studied cilia proteins, has been associated with polycystic kidney disease (PKD). PKD is characterized by the presence of multiple cysts in the kidneys and is believed to be caused by cilia dysfunction in kidney cells.
Stephen J. Doxsey, PhD, professor of molecular medicine and biochemistry & molecular pharmacology and cell biology and lead author of the study, shows that IFT88 also plays an important role in mitosis. Doxsey and colleagues at UMass Medical School observed that the IFT88 protein is present at the poles of the mitotic spindle, structures which form during mitosis and are required to guide chromosome sets as the cell divides in two and to orient the plane of cell division. He hypothesized that the cilia protein played a transport function during mitosis that was similar to that in cilia.
"We knew that IFT88 a
|Contact: Jim Fessenden|
University of Massachusetts Medical School