Expression Data Set 44 details

Information Item Value
Dataset Name snf/swi mutant expression analysis
Dataset Number 44
Short Description microarray analysis of knockout mutants of snf and swi, two
components of the Snf/Swi complex
Source URL http://genome-www.stanford.edu/swisnf/
Reference Sudarsanam, P; Iyer, VR; Brown, PO; and Winston, F,
Whole-genome expression analysis of snf/swi mutants of Saccharomyces
cerevisiae, Proc. Natl. Acad. Sci. USA 2000, 97(7):3364-3369
Strains Strains isogenic to S288C: FY2 (MATalpha ura3-52),
FY31 (MATalpha ura3-52 his3delta200 snfdelta10:2000:HIS3),
FY1882 (MATalpha ura3-52 leu2delta1 swidelta10:2000:LEU2)
Conditions Grown to cell density of 1-2 x 10**7 cells/ml in rich
medium (yeast extract/peptone/dextrose containing 2% glucose) or in
synthetic minimal medium (yeast nitrogen base without amino acids plus
ammonium sulfate), supplemented with uracil and 2% glucose.
Date Added to ExpressDB Sep 22 2000 4:01:28:613PM
Number of Measures on ExpressDB 14 (here to download dataset and view measure details)
Long Description Abstract - The Saccharomyces cerevisiae Snf/Swi
complex has been previously demonstrated to control transcription and
chromatin structure of particular genes in vivo and to remodel
nucleosomes in vitro. We have performed whole-genome expression
analysis, using DNA microarrays, to study mutants deleted for a gene
encoding one conserved (Snf2) or one unconserved (Swi1) Snf/Swi
component. This analysis was performed on cells grown in both rich and
minimal media. The microarray results, combined with Northern blot,
computational, and genetic analyses, show that snf2Delta and swi1Delta
mutations cause similar effects on mRNA levels, that Snf/Swi controls
some genes differently in rich and minimal media, and that Snf/Swi
control is exerted at the level of individual genes rather than over
larger chromosomal domains. In addition, this work shows that Snf/Swi
controls mRNA levels of MATalpha-specific genes, likely via
controlling transcription of the regulators MATalpha1 and
MCM1. Finally, we provide evidence that Snf/Swi acts both as an
activator and as a repressor of transcription, and that neither mode
of control is an indirect effect of the other.

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Copyright (c) 2006 by Wayne Rindone and the President and Fellows of Harvard University