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Nucleic Acids Research Advance Access published online on December 7, 2006

Nucleic Acids Research, doi:10.1093/nar/gkl1059
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© 2006 The Author(s).
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.


Genomics

Genome-wide analysis of transcriptional dependence and probable target sites for Abf1 and Rap1 in Saccharomyces cerevisiae

Arunadevi Yarragudi1, Laura Wegener Parfrey1 and Randall H. Morse1,2,*

1 Laboratory of Developmental Genetics, Wadsworth Center, New York State Department of Health Albany, NY 12201-2002, USA 2 Department of Biomedical Sciences, State University of New York at Albany School of Public Health Albany, NY 12201-2002, USA

*To whom correspondence should be addressed. Tel: +1 518 486 3116; Fax: +1 518 474 3181; Email: Randall.Morse{at}wadsworth.org

Received September 25, 2006. Revised October 19, 2006. Accepted November 7, 2006.

Abf1 and Rap1 are general regulatory factors (GRFs) that contribute to transcriptional activation of a large number of genes, as well as to replication, silencing and telomere structure in yeast. In spite of their widespread roles in transcription, the scope of their functional targets genome-wide has not been previously determined. Here, we use microarrays to examine the contribution of these essential GRFs to transcription genome-wide, by using ts mutants that dissociate from their binding sites at 37°C. We then combine this data with published ChIP-chip studies and motif analysis to identify probable direct targets for Abf1 and Rap1. We also identify a substantial number of genes likely to bind Rap1 or Abf1, but not affected by loss of GRF binding. Interestingly, the results strongly suggest that Rap1 can contribute to gene activation from farther upstream than can Abf1. Also, consistent with previous work, more genes that bind Abf1 are unaffected by loss of binding than those that bind Rap1. Finally, we show for several such genes that the Abf1 C-terminal region, which contains the putative activation domain, is not needed to confer this peculiar ‘memory effect’ that allows continued transcription after loss of Abf1 binding.


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