The Saccharomyces cerevisiae SPT13/GAL11 gene has both positive and negative regulatory roles in transcription.

Abstract

To understand the function of SPT13, a gene encoding a trans-acting factor involved in regulation of Ty-mediated gene expression, we (13,17,50,60,66). Ty element insertion mutations often reduce adjacent-gene transcription, whereas solo 8 insertion mutations often alter adjacent-gene transcription qualitatively by providing an alternate and preferred site for transcription initiation (29,59,69). In both cases, the change in the pattern of transcription of the adjacent gene can lead to a mutant phenotype. For example, Ty and 8 insertion mutations at the HIS4 and LYS2 genes frequently cause respectively (50,59,60,67). By selection for unlinked suppressors of Ty and 8 insertion mutations, we have identified 15 different SPT (suppressor of Ty insertion mutation) genes, each of which is likely to encode a protein involved in the regulation of Ty-mediated transcription and possibly in the transcription of other yeast genes (19,67,68).The upstream activation site, TATA, and initiation site sequences for Ty transcription are located in the 8 sequences (14,40). However, control of Ty and adjacent-gene transcription is also mediated by sequences located within the Ty transcription unit (18, 51). At the nucleotide sequence level, the internal regulatory sequences in Ty elements show similarity to the simian virus 40 enhancer core sequence (18,51). Functional studies also suggest an enhancerlike activity, since these sequences, located downstream of the Ty promoter, contribute to activation of Ty transcription (12,18,24,40,51

Yeast GAL11 protein is a distinctive type transcription factor that enhances basal transcription in vitro.

“…We suggest therefore that GALli protein functions as a basal transcription factor of some genes and that the GAL1l dependency is determined by the promoter context of the genes. This is consistent with the observations that the function of GALlI is pleiotropic (15,16,21,22). Since GALli protein did not bind a specific DNA sequence as judged by footprint analysis (H.S., unpublished results), it may regulate the basal transcription by protein-protein interactions with the basal or general transcription factors.…”

“…They further find that GALII is required for normal functioning of PPR1, an activator for the URA3 gene. Puzzlingly, GALI is also involved in the transcriptional repression of genes, since a loss-of-function mutation of GALII, called sptl3, restores the transcription of genes inactivated by insertion of the yeast transposon Ty (22).…”

The Swi5 activator recruits the Mediator complex to theHOpromoter without RNA polymerase II

“…The Gal11 subcomplex contains the Gal11, Pgd1, Sin4, Med2, and Rgr1 proteins, and mutations in the genes encoding these proteins can affect either transcriptional activation or repression, depending on the promoter . For example, a gal11 mutation results in reduced expression of SUC2, CTS1, and mating type genes, and increased expression of GAL1 and Ty1 genes (Fassler and Winston 1989;Vallier and Carlson 1991;Chen et al 1993;Sakurai and Fukasawa 1997). Gal11 functions as a strong activator when artificially recruited to DNA (Barberis et al 1995), and Gal11 interacts with TFIIE (Sakurai and Fukasawa 1997).…”

MCM1 binds to a transcriptional control element in Ty1.

“…For example, SPT13 (GAL11) is a negative regulator of Tyl transcriptional activity but a positive regulator of some mating-specific genes such as MFal (14). (The SPT13 and GALII genes were identified by different mutational screens but are the same gene [14].)…”

“…For example, SPT13 (GAL11) is a negative regulator of Tyl transcriptional activity but a positive regulator of some mating-specific genes such as MFal (14). (The SPT13 and GALII genes were identified by different mutational screens but are the same gene [14].) Although it is not known how SPT13 (GAL11) acts to modulate transcriptional activation, studies by Yu and Fassler reported in the accompanying article (37) show that SPT13 exerts its negative effects through the regulatory sequence in Tyl that binds to MCM1.…”