Conly L. Rieder
Biological Sciences Department
Education and Training
1972: B.S. in Biology, University of California, Irvine, CA
1975: M.S. in Biology (with Honors), University of Oregon, Eugene,OR
1977: Ph.D. in Biology, University of Oregon, Eugene, OR
1977-1980: Postdoctoral work in Zoology/Molecular Biology, University of Wisconsin, Madison, WI.
1980-2011: Research Scientist, Wadsworth Center, New York State Department of Health, Albany, New York 12201-0509
1988-1999: Director: Biological Microscopy and Image Reconstruction Resource Facility, Wadsworth Center, Albany, N.Y.
1980-2011: Adjunct Professor, Department of Biological Sciences, State University of New York, Albany, New York.
1985-2010: Professor, Department of Biomedical Sciences, State University of New York, Albany, New York.
Tel: (518) 477-7780
The process by which a cell divides to produce two genetically identical daughters is called mitosis. During this terminal stage of the cell cycle the replicated chromosomes bind in animals, via their associated sister kinetochores, to microtubules emanating from two replicated and separated centrosomes. This interaction leads to the formation of a transient bipolar apparatus termed the mitotic spindle which is responsible for producing and transmitting the forces for chromosome segregation (karyokinesis) and cleavage (cytokinesis).
Considering that ~ 2.5 X 108 cells are dividing in the human body at any given time, even if few errors occur, many genetically abnormal cells will be produced during the lifetime of an organism. Some of these will lose their ability to regulate the cell cycle, which is one of the attributes of cancer cells. An important goal of cancer research is, therefore, to define the molecular mechanisms that form the spindle and generate the forces to accurately distribute the chromosomes. A more recent focus is to understand how the cell regulates progression into and through the division process. Surprisingly these problems are intimately linked because chromosome motion and progression through mitosis are both governed by the formation of kinetochore fibers.
The Rieder lab develops and applies sophisticated computer-based three dimensional (3-D) light and electron microscopic (EM) approaches to study the behavior, structure, composition, and function of centrosomes and kinetochores, and how these two organelles interact to form the mitotic spindle and move the chromosomes in vertebrate somatic cells. We are also defining and exploring the cell cycle checkpoint controls that regulate progression through the mitosis portion of the cell cycle, and how these can be used to selectively kill cells.
Lee, K, A. Kenny and C.L. Rieder. 2011. Caspase activity is not required for a functional mitotic checkpoint or mitotic slippage in human cells. Mol. Biol. Cell 22:2470-2479.
Rieder, C.L. 2011. Mitosis in vertebrates: the G2/M and M/A transitions and their associated checkpoints. Chromosome Res., 19:291-306.
Lee, K., A. Kenny and C.L. Rieder. 2010. P38 MAP kinase activity is required during mitosis for timely satisfaction of the mitotic checkpoint but not for the fidelity of chromosome segregation. Mol. Biol. Cell 21:2150-2160.
Yang, Z., A.E. Kenny, D.A. Brito and C.L. Rieder. 2009. Cells satisfy the mitotic checkpoint in Taxol and do so faster in concentrations that stabilize syntelic attachments. J. Cell Biol., 186:675-684.
Rieder, C.L. 2009. “Mitosis”. In “Cells” (Chapter 10). B. Lewin, L. Cassimeris, V.R. Lingappa, and G. Plopper, Eds. 2nd Edition Jones and Bartlett, Boston. pp 621-671.
Khodjakov, A. and C.L. Rieder. 2009. The mitotic checkpoint: some facts and fallacies. Journal of Biology 8:88.1-88.5
Brito, D., Z. Yang and C.L. Rieder. 2008. Microtubules do not promote mitotic slippage when the spindle assembly checkpoint cannot be satisfied. J. Cell Biol., 182:623-629.
Yang, Z., J. Loncarek, A. Khodjakov and C.L. Rieder. 2008. Extra centrosomes and/or chromosomes prolong mitosis in human cells. Nature Cell Biol., 10:748-751
Mikhailov, A., D.J. McCance and C.L. Rieder. 2007. The G2 p38-mediates stress-activated checkpoint pathway becomes attenuated in transformed cells. Current Biol., 17:2162-2168.
Brito, D. and C.L. Rieder. 2006. Mitotic checkpoint slippage in vertebrates requires destruction of cyclin B but not of kinetochore-checkpoint proteins. Current Biol., 16: 1194-1200.
Maiato, H., A. Khodjakov and C.L. Rieder. 2005. Drosophila CLASP is required for microtubule subunit incorporation into fluxing kinetochore fibers. Nature Cell Biol., 7:42-47.