High impact information on SPT7

• The bromodomain in the Spt7 subunit of SAGA is dispensable for this activity but will anchor SAGA if it is swapped into Gcn5, indicating that specificity of bromodomain function is determined in part by the subunit it occupies [1].
• The locations of two histone fold-containing core subunits, Spt7 and Ada1, are consistent with their role in providing a SAGA-specific interface with the Tafs [2].
• Besides lacking Spt8, SALSA contains Spt7 subunit that is truncated [3].
• Examining the role of this subunit, we find that C-terminally truncated SPT7 resulted in derepressed HIS3 transcription [3].
• In addition, partial SAGA complexes containing Spt7 can be assembled in the absence of both Spt20 and Ada1 [4].

Biological context of SPT7

• The SPT7 protein contains a bromodomain sequence; a deletion that removes the bromodomain from the SPT7 protein causes no detectable mutant phenotype [5].
• We also found a weaker dependence for chromatin remodeling on SPT7 than on GCN5, indicating that GCN5 can function via pathways independent of the SAGA complex [6].
• Three ORFs, YBR0726, YBR0735 and YBR0740 are completely contained in YBR0727, YBR0734 and YBR0739 respectively, and thus probably do not represent real genes [7].

Anatomical context of SPT7

• Initial rate of nickel uptake by whole cells of a SPT7-negative mutant FY963 was nearly equal to that of the parent strain FY61, and FY963 accumulated nickel about 1.7-fold of the value of FY61 when cultured in medium containing 0.1 mM NiCl2; most of which was sequestered into vacuoles [8].

Associations of SPT7 with chemical compounds

• Two of the genes, ADA3 and SPT7, are general transcriptional regulators; the third, YMR034c, is a putative sterol transporter [9].

Other interactions of SPT7

• Our selection and screen has identified two additional genes, SPT7 and SPT8, that are also required for transcription initiation in delta sequences [10].
• Of the other SPT genes tested, mutants with mutations in SPT7 and, strikingly, SPT15 (encoding the TATA-binding protein) show resistance to GAL4-VP16 [11].
• Strains that contain an spt7 null mutation are viable but grow very slowly and have transcriptional defects at many loci including insertion mutations, Ty elements, the INO1 gene and the MFA1 gene [5].
• Mutations in the SPT7 gene of Saccharomyces cerevisiae originally were identified as suppressors of Ty and delta insertion mutations in the 5' regions of the HIS4 and LYS2 genes [5].
• A gcn5 spt3 double mutant shows a synthetic phenotype almost as severe as that observed for an spt7 or spt20 mutant [12].

References