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Molecular and Cellular Biology, December 2007, p. 8522-8532, Vol. 27, No. 24
0270-7306/07/$08.00+0     doi:10.1128/MCB.01007-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Transcription Alters Chromosomal Locations of Cohesin in Saccharomyces cerevisiae{triangledown} ,{dagger}

Christoph Bausch,1,{ddagger} Seth Noone,1,§ Jill M. Henry,1 Karin Gaudenz,1 Brian Sanderson,1 Chris Seidel,1 and Jennifer L. Gerton1,2*

Stowers Institute for Medical Research, Kansas City, Missouri 64110,1 Department of Biochemistry and Molecular Biology, University of Kansas Medical Center, 4011 Wahl Hall East, 3901 Rainbow Blvd., Kansas City, Kansas 661602

Received 7 June 2007/ Returned for modification 25 July 2007/ Accepted 25 September 2007

In eukaryotic cells, cohesion between sister chromatids allows chromosomes to biorient on the metaphase plate and holds them together until they separate into daughter cells during mitosis. Cohesion is mediated by the cohesin protein complex. Although the association of this complex with particular regions of the genome is highly reproducible, it is unclear what distinguishes a chromosomal region for cohesin association. Since one of the primary locations of cohesin is intergenic regions between converging transcription units, we explored the relationship between transcription and cohesin localization. Chromatin immunoprecipitation followed by hybridization to a microarray (ChIP chip) indicated that transcript elongation into cohesin association sites results in the local disassociation of cohesin. Once transcription is halted, cohesin can reassociate with its original sites, independent of DNA replication and the cohesin loading factor Scc2, although cohesin association with chromosomes in G2/M is not functional for cohesion. A computer program was developed to systematically identify differences between two ChIP chip data sets. Our results are consistent with a model for cohesin association in which (i) a portion of cohesin can be dynamically loaded and unloaded to accommodate transcription and (ii) the cohesin complex has preferences for features of chromatin that are a reflection of the local transcriptional status. Taken together, our results suggest that cohesion may be degraded by transcription.


* Corresponding author. Mailing address: Stowers Institute for Medical Research, 1000 E. 50th St., Kansas City, MO 64110. Phone: (816) 926-4443. Fax: (816) 926-2094. E-mail: jeg{at}stowers-institute.org

{triangledown} Published ahead of print on 8 October 2007.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

{ddagger} Present address: SAFC Biosciences, Cell Sciences and Development, 2909 Laclede Ave., St. Louis, MO 63103.

§ Present address: Department of Biochemistry and Molecular Genetics, University of Colorado Health Sciences, Aurora, CO 80045.

Present address: School of Pharmacy, Creighton University, Omaha, NE 68178.


Molecular and Cellular Biology, December 2007, p. 8522-8532, Vol. 27, No. 24
0270-7306/07/$08.00+0     doi:10.1128/MCB.01007-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.




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