scholarly journals Structure of the SANT domain from the Xenopus chromatin remodeling factor ISWI

2007 ◽  
Vol 67 (4) ◽  
pp. 1198-1202 ◽  
Author(s):  
John R. Horton ◽  
Stuart J. Elgar ◽  
Seema I. Khan ◽  
Xing Zhang ◽  
Paul A. Wade ◽  
...  
Keyword(s):  
Chromatin Remodeling ◽  
Sant Domain

scholarly journals Essential Role for the SANT Domain in the Functioning of Multiple Chromatin Remodeling Enzymes

2002 ◽  
Vol 10 (4) ◽  
pp. 935-942 ◽  
Author(s):  
Laurie A. Boyer ◽  
Michael R. Langer ◽  
Kimberly A. Crowley ◽  
Song Tan ◽  
John M. Denu ◽  
...  
Keyword(s):  
Chromatin Remodeling ◽  
Essential Role ◽  
Sant Domain

scholarly journals Multiple Mechanistically Distinct Functions of SAGA at the PHO5 Promoter

2003 ◽  
Vol 23 (10) ◽  
pp. 3468-3476 ◽  
Author(s):  
Slobodan Barbaric ◽  
Hans Reinke ◽  
Wolfram Hörz
Keyword(s):  
Chromatin Remodeling ◽  
Transcriptional Activation ◽  
Chromatin Immunoprecipitation ◽  
Promoter Activation ◽  
Sant Domain ◽  
Promoter Recruitment ◽  
Synthetic Phenotype ◽  
Pho5 Promoter ◽  
Histone Acetyltransferase Activity

ABSTRACT Our previous studies have shown that the rate of chromatin remodeling and consequently the rate of PHO5 activation are strongly decreased in the absence of Gcn5 histone acetyltransferase activity. Using chromatin immunoprecipitation, we demonstrate that SAGA is physically recruited to the PHO5 promoter. Recruitment is dependent on the specific activator Pho4 and occurs only under inducing conditions. Spt3, another subunit of SAGA, also plays a role in PHO5 activation but has a function that is completely different from that of Gcn5. An SPT3 deletion severely compromises the PHO5 promoter and reduces the extent of transcriptional activation by diminishing the binding of the TATA binding protein to the promoter without, however, affecting the rate or the extent of chromatin remodeling. A gcn5 spt3 double mutant shows a synthetic phenotype almost as severe as that observed for an spt7 or spt20 mutant. The latter two mutations are known to prevent the assembly of the complex and consequently lead to the loss of all SAGA functions. The absence of the Ada2 subunit causes a strong delay in chromatin remodeling and promoter activation that closely resembles the delay observed in the absence of Gcn5. A deletion of only the Ada2 SANT domain has exactly the same effect, strongly suggesting that Ada2 controls Gcn5 activity by virtue of its SANT domain. Finally, the Gcn5 bromodomain also contributes to but is not essential for Gcn5 function at the PHO5 promoter. Taken together, the results provide a detailed and differentiated description of the role of SAGA as a coactivator at the PHO5 promoter.

scholarly journals Nucleosome Remodeling and Transcriptional Repression Are Distinct Functions of Isw1 in Saccharomyces cerevisiae

2009 ◽  
Vol 29 (9) ◽  
pp. 2419-2430 ◽  
Author(s):  
Marina Pinskaya ◽  
Anitha Nair ◽  
David Clynes ◽  
Antonin Morillon ◽  
Jane Mellor
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Chromatin Remodeling ◽  
Transcriptional Repression ◽  
Transcription Initiation ◽  
Copy Number ◽  
Regulatory Proteins ◽  
Nucleosome Remodeling ◽  
Transcriptional Regulatory ◽  
Sant Domain

ABSTRACT The SANT domain is a nucleosome recognition module found in transcriptional regulatory proteins, including chromatin-modifying enzymes. It shows high functional degeneracy between species, varying in sequence and copy number. Here, we investigate functions in vivo associated with two SANT motifs, SANT and SLIDE, in the Saccharomyces cerevisiae Isw1 chromatin-remodeling ATPase. We show that differences in the primary structures of the SANT and SLIDE domains in yeast and Drosophila melanogaster reflect their different functions. In yeast, the SLIDE domain is required for histone interactions, while this is a function of the SANT domain in flies. In yeast, both motifs are required for optimal association with chromatin and for formation of the Isw1b complex (Isw1, Ioc2, and Ioc4). Moreover, nucleosome remodeling at the MET16 locus is defective in strains lacking the SANT or SLIDE domain. In contrast, the SANT domain is dispensable for the interaction between Isw1 and Ioc3 in the Isw1a complex. We show that, although defective in nucleosome remodeling, Isw1 lacking the SANT domain is able to repress transcription initiation at the MET16 promoter. Thus, chromatin remodeling and transcriptional repression are distinct activities of Isw1.

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