The ENA1 gene is a mayor component in the Na+ and Li+ efflux system. ENA1 is induced by salt stress. Induction is mediated at low salt concentrations by the HOG pathway and at high salt by calcineurin. (Marquez and Serrano (1996), FEBS Lett. 382, 89-92). We have found that ENA1 is also regulated by glucose repression, as shown the increased expression of an ENA1-lacZ gene fusion observed in non-repressing carbon sources. Like other glucose repressed genes, transcription of ENA1 depends on SNF1 pathway. The level of ENA1 expression is reduced in a snf1 mutant, although salt induction is still observed, being the induction factor similar to wild type. According to this, Na+ and Li+ tolerance is impaired in snf1 and snf4 mutants. By other hand, mig1 mutants exhibit a dramatic increase in both basal and salt induced ENA1 expression, again without changes in the ratio of activation. Mig1p could directly regulated ENA1 expression, since two putative Mig-binding sites are found in the ENA1 promoter. Additionally, we addressed the functionality of a STRE-like sequence found in the ENA1 promoter. Our results argue against the functionality of this sequence. First, ENA1 is not induced by stresses which has been shown to activate STRE-containing genes. Second, induction of ENA1 expression is independent of Msn2p and Msn4p , two transcriptional factors that are required for stress-induced activation trough STRE (Martinez-Pastor et al., 1996, EMBO J. in press).