Model of regulation of the translation elongation factor eIF5A expression by nutrient availability through different signalling pathways. Under nutrient availability conditions, glucose signalling via TOR up-regulates eIF5A expression to facilitate cytoplasmic translation, and glycolysis predominates over mitochondrial respiration. Under low glucose and/or non-fermentative carbon sources, TOR positive eIF5A regulation is inhibited, but eIF5A expression is up-regulated by the increase in heme levels and subsequent Hap1 activation. In these conditions, eIF5A promotes, additionally to cytoplasmic translation, not-well known functions in mitochondrial respiration.