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EVIDENCE THAT SNF2/SWI2 AND SNF5 ACTIVATE TRANSCRIPTION IN YEAST BY ALTERING CHROMATIN STRUCTURE
Author(s): HIRSCHHORN JN, BROWN SA, CLARK CD, WINSTON F
Source: GENES & DEVELOPMENT    Volume: 6    Issue: 12A    Pages: 2288-2298    Published: DEC 1992  
Times Cited: 356     References: 68     
Abstract: Changes in chromatin structure have frequently been correlated with changes in transcription. However, the cause-and-effect relationship between chromatin structure and transcription has been hard to determine. In addition, identifying the proteins that regulate chromatin structure has been difficult. Recent evidence suggests that a functionally related set of yeast transcriptional activators (SNF2/SWI2, SNF5, SNF6, SWI1, and SWI3), required for transcription of a diverse set of genes, may affect chromatin structure. We now present genetic and molecular evidence that at least two of these transcriptional activators, SNF2/SWI2 and SNF5, function by antagonizing repression mediated by nucleosomes. First, the transcriptional defects in strains lacking these SNF genes are suppressed by a deletion of one of the two sets of genes encoding histones H2A and H2B, (hta1-htb1)DELTA. Second, at one affected promoter (SUC2), chromatin structure is altered in snf2/swi2 and snf5 mutants, and this chromatin defect is suppressed by (hta1-htb1)DELTA. Finally, analysis of chromatin structure at a mutant SUC2 promoter, in which the TATA box has been destroyed, demonstrates that the differences in SUC2 chromatin structure between SNF5+ and snf5 mutant strains are not simply an effect of different levels of SUC2 transcription. Thus, these results strongly suggest that SNF2/SWI2 and SNF5 cause changes in chromatin structure and that these changes allow transcriptional activation.
Document Type: Article
Language: English
Addresses:
1. HARVARD UNIV, SCH MED, DEPT GENET, BOSTON, MA 02115 USA
Publisher: COLD SPRING HARBOR LAB PRESS, 1 BUNGTOWN RD, PLAINVIEW, NY 11724
Subject Category: Cell Biology; Developmental Biology; Genetics & Heredity
IDS Number: KB977
ISSN: 0890-9369
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