High impact information on SNF5

• Transcription of HO also requires SNF5 and SNF6 [1].
• Evidence that SNF2/SWI2 and SNF5 activate transcription in yeast by altering chromatin structure [2].
• Thus, these results strongly suggest that SNF2/SWI2 and SNF5 cause changes in chromatin structure and that these changes allow transcriptional activation [2].
• Here, we present evidence that SNF6 has a more direct role in stimulating transcription than SNF2 and SNF5 [3].
• Here we show that the N-terminal domain of Snf5 and the second quarter of Swi1 are sites of activation domain contact [4].

Biological context of SNF5

• Polymorphism for a suppressor gene was observed: in snf5-bearing strains, one allele of this suppressor gene resulted in elevated levels of PrB and the other allele resulted in wild-type levels of PrB; neither allele suppressed the Suc- phenotype of the snf5 mutant [5].
• We report the nucleotide sequence, which predicts that SNF5 encodes a 102,536-dalton protein [6].
• Mutations in other genes known to regulate gene expression in response to changes in glucose concentration, including SNF3, RGT2, and SNF5, also affect cell growth under ion stress conditions [7].
• Essential roles of Snf5p in Snf-Swi chromatin remodeling in vivo [8].
• SPT10 is also required for cell-cycle-specific K56 acetylation at histone genes, allowing the recruitment of the nucleosome remodeling factor Snf5 and subsequent regulation of gene transcription [9].

Associations of SNF5 with chemical compounds

• Neither was regulated by glucose repression, and the level of SNF2 RNA was not dependent on SNF5 function or vice versa [10].
• The SNF5 protein of Saccharomyces cerevisiae is a glutamine- and proline-rich transcriptional activator that affects expression of a broad spectrum of genes [6].
• The snf2, snf4, and snf5 mutants produced little or no secreted invertase under derepressing conditions and were pleiotropically defective in galactose and glycerol utilization, which are both regulated by glucose repression [11].

Physical interactions of SNF5

• TFG3 interacted with the SNF5 component of the SWI/SNF complex in protein interaction blots [12].
• A human protein with homology to Saccharomyces cerevisiae SNF5 interacts with the potential helicase hbrm [13].

Other interactions of SNF5

• In addition to mutations in STA2, five other recessive mutations were identified which fell into four complementation groups designated haf1 through haf4 [14].
• In addition, a ccr4 mutation had little effect on an ADH2 promoter alteration in contrast to the large effects displayed by mutations in SNF2 and SNF5 [15].
• The SNF2 and SNF5 functions were required for derepression of SUC2 mRNA [10].
• The non-derepressible mutants snf1, snf2 and snf5 present a chromatin structure characteristic of the repressed state, irrespective of the presence or absence of glucose [16].
• Snf5p was not recruited as an isolated subunit but was required with Snf6p and Swi3p for optimal recruitment of other SWI/SNF subunits [17].

Analytical, diagnostic and therapeutic context of SNF5

• A bifunctional SNF5-beta-galactosidase fusion protein was localized in the nucleus by immunofluorescence [6].

References