Disease relevance of SPT6

• Functional interaction between pleiotropic transactivator pUL69 of human cytomegalovirus and the human homolog of yeast chromatin regulatory protein SPT6 [1].
• Furthermore, transcribed chromatin in the spt6 mutant is hypersensitive to micrococcal nuclease, and this hypersensitivity is suppressed by mutational inactivation of RNA polymerase II [2].

High impact information on SPT6

• Genetic analysis has implicated SPT6, an essential gene of Saccharomyces cerevisiae, in the control of chromatin structure [3].
• Finally, we show that Spt4 and Spt5 are tightly associated in a complex that does not contain Spt6 [4].
• In this work, we report new genetic and biochemical studies of Spt4, Spt5, and Spt6 that reveal a role for these factors in transcription elongation [4].
• Transcriptional activators are dispensable for transcription in the absence of Spt6-mediated chromatin reassembly of promoter regions [5].
• Lastly, Eaf3 inhibits internal initiation within mRNA coding regions in a manner similar to FACT and Spt6 [6].

Biological context of SPT6

• Therefore, having either too many or too few copies of SPT6 causes a mutant phenotype [7].
• SPT6, an essential gene that affects transcription in Saccharomyces cerevisiae, encodes a nuclear protein with an extremely acidic amino terminus [8].
• In addition, we observed interesting SPT6 gene dosage effects [7].
• SPT6 was mapped to the right arm of chromosome VII, 44 centimorgans (cM) from ADE6 and 9 cM from CLY8 [7].
• Haploid spores carrying the spt6 null allele were inviable, indicating that the SPT6 gene is essential for mitotic growth [7].

Associations of SPT6 with chemical compounds

• Also, the ability of CCR4 to activate transcription when fused to the LexA DNA binding domain was not specifically enhanced by defects in either SPT10 or SPT6 [9].
• Recessive mutations in two negative control elements, CRE1 and CRE2, have been obtained that allow the glucose-repressible alcohol dehydrogenase (ADHII) of yeast to escape repression by glucose [10].

Regulatory relationships of SPT6

• SSN20 is an essential gene with mutant alleles that suppress defects in SUC2 transcription in Saccharomyces cerevisiae [11].

Other interactions of SPT6

• The mechanism by which mutations in CCR4 suppress defects in SPT10 and SPT6 was examined [9].
• Finally, the results of coimmunoprecipitation experiments demonstrate that at least the SPT5 and SPT6 proteins interact physically [12].
• Multicopy SPT6 caused improper expression of chromosomal ADH2 [13].
• We have now analyzed interactions between SPT4, SPT5 and SPT6 [12].
• Finally, this study and that in the accompanying paper (L. Neigeborn, J. L. Celenza, and M. Carlson, Mol. Cell. Biol. 7:679-686, 1986) showed that spt6 and ssn20 mutations (isolated as suppressors of snf2 and snf5 [sucrose nonfermenting] mutations) identify the same gene [7].

Analytical, diagnostic and therapeutic context of SPT6

• By use of an epitope-tagged SPT6 protein, we have determined by indirect immunofluorescence that the SPT6 protein is located in the nucleus [8].

References