High impact information on GIS1

• Here, we show that the zinc finger protein Gis1 acts as a dosage-dependent suppressor of the rim15Delta defect in nutrient limitation-induced transcriptional derepression of SSA3 [1].
• Tests of epistasis as well as transcriptional analyses of Gis1-dependent expression indicate that Gis1 acts in this pathway downstream of Rim15 to mediate transcription from the previously identified post-diauxic shift (PDS) element [1].
• Saccharomyces cerevisiae Ras/cAMP pathway controls post-diauxic shift element-dependent transcription through the zinc finger protein Gis1 [1].
• Both proteins contain two putative zinc fingers that are identical throughout the DNA binding region, and deletion of both RPH1 and GIS1 is required to fully derepress PHR1 in the absence of damage [2].
• RPH1 and GIS1 are damage-responsive repressors of PHR1 [2].

Biological context of GIS1

• In vitro footprinting and binding competition studies indicate that the sequence AG(4) (C(4)T) within URS(PHR1) is the binding site for Rph1p and Gis1p and suggests that at least one additional DNA binding component is present in the PRP complex [2].
• The jmjN and jmjC domains of the yeast zinc finger protein Gis1 interact with 19 proteins involved in transcription, sumoylation and DNA repair [3].

Associations of GIS1 with chemical compounds

• Phospholipid composition analysis of the gis1 Delta mutant showed that Gis1p played a role in regulating the cellular level of diacylglycerol pyrophosphate, as well as the levels of the major phospholipids phosphatidylethanolamine and phosphatidylcholine [4].

Other interactions of GIS1

• Repression of DPP1 expression is mediated by the transcription factor Gis1p, which binds to three post-diauxic shift elements in the promoter [5].

Analytical, diagnostic and therapeutic context of GIS1

• Direct interaction between Gis1p and DPP1 promoter elements was demonstrated by electrophoretic mobility shift assays [4].

References