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Originally published as Genetics Published Articles Ahead of Print on December 6, 2006.

Genetics, Vol. 175, 513-525, February 2007, Copyright © 2007
doi:10.1534/genetics.106.064410

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The Overexpression of a Saccharomyces cerevisiae Centromeric Histone H3 Variant Mutant Protein Leads to a Defect in Kinetochore Biorientation

Kimberly A. Collins*,{dagger},1, Raymond Camahort{ddagger},§, Chris Seidel{ddagger}, Jennifer L. Gerton{ddagger},§ and Sue Biggins*,2

* Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1042, {dagger} Molecular and Cellular Biology Program, University of Washington and Fred Hutchinson Cancer Research Center, Seattle, Washington 98195, {ddagger} The Stowers Institute for Medical Research, Kansas City, Missouri 64110 and § Department of Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, Kansas 66160

2 Corresponding author: Division of Basic Sciences, Fred Hutchinson Cancer Research Center, P.O. Box 19024, 1100 Fairview Ave. N., Seattle, WA 98109-1042. 
E-mail: sbiggins{at}fhcrc.org

Chromosomes segregate using their kinetochores, the specialized protein structures that are assembled on centromeric DNA and mediate attachment to the mitotic spindle. Because centromeric sequences are not conserved, centromere identity is propagated by an epigenetic mechanism. All eukaryotes contain an essential histone H3 variant (CenH3) that localizes exclusively to centromeres. Because CenH3 is required for kinetochore assembly and is likely to be the epigenetic mark that specifies centromere identity, it is critical to elucidate the mechanisms that assemble and maintain CenH3 exclusively at centromeres. To learn more about the functions and regulation of CenH3, we isolated mutants in the budding yeast CenH3 that are lethal when overexpressed. These CenH3 mutants fall into three unique classes: (I) those that localize to euchromatin but do not alter kinetochore function, (II) those that localize to the centromere and disrupt kinetochore function, and (III) those that no longer target to the centromere but still disrupt chromosome segregation. We found that a class III mutant is specifically defective in the ability of sister kinetochores to biorient and attach to microtubules from opposite spindle poles, indicating that CenH3 mutants defective in kinetochore biorientation can be obtained.


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Genetics 2007 175: NP. [Full Text]  



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