Linked Life Data

21596311

Source:http://linkedlifedata.com/resource/pubmed/id/21596311

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2011-5-20
pubmed:abstractText
Nucleosome-depleted regions (NDRs) are ubiquitous on eukaryotic promoters. The formation of many NDRs cannot be readily explained by previously proposed mechanisms. Here, we carry out a focused study on a physiologically important NDR in the yeast CLN2 promoter (CLN2pr). We show that this NDR does not result from intrinsically unfavorable histone-DNA interaction. Instead, we identified eight conserved factor binding sites, including that of Reb1, Mcm1, and Rsc3, that cause the local nucleosome depletion. These nucleosome-depleting factors (NDFs) work redundantly, and simultaneously mutating all their binding sites eliminates CLN2pr NDR. The loss of the NDR induces unreliable "on/off" expression in individual cell cycles, but in the presence of the NDR, NDFs have little direct effect on transcription. We present bioinformatic evidence that the formation of many NDRs across the genome involves multiple NDFs. Our findings also provide significant insight into the composition and spatial organization of functional promoters.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1097-4164
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
20
pubmed:volume
42
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
465-76
pubmed:dateRevised
2011-9-26
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Multiple sequence-specific factors generate the nucleosome-depleted region on CLN2 promoter.
pubmed:affiliation
Laboratory of Cell Cycle Genetics, The Rockefeller University, New York, NY, 10065, USA. lbai01@rockefeller.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural