Abstract: NC2 has been described as an essential and evolutionarily-conserved transcriptional repressor, although in vitro and in vivo experiments suggest that it can function as both a positive or negative effector of transcription. NC2 operates by interacting with the core promoter and components of the basal transcription machinery, like the TATA-binding protein (TBP). In this work, we have isolated mutations that suppress the growth defect caused by the depletion of NC2. We have identified mutations affecting components of three different complexes involved in the control of basal transcription: the mediator, TFIIH and RNA pol II itself. Mutations in RNA pol II include both overexpression of truncated forms of the two largest subunits (Rpb1 and Rpb2) and reduced levels of these proteins. Suppression of NC2 depletion was also observed by reducing the amounts of the mediator essential components Nut2 and Med7, as well as by deleting any of the non-essential mediator components, except Med2, Med3 and Gal11 subunits. Interestingly, the Med2/Med3/Gal11 triad form a submodule within the mediator tail. Our results support the existence of different components within the basic transcription complexes that antagonistically interact with the NC2 repressor, and suggest that the correct balance between the activities of specific positive and negative components is essential for cell growth.