Hal2p Functions in Bdf1p-Involved Salt Stress Response in Saccharomyces cerevisiae

The Saccharomyces cerevisiae Bdf1p associates with the basal transcription complexes TFIID and acts as a transcriptional regulator. Lack of Bdf1p is salt sensitive and displays abnormal mitochondrial function. The nucleotidase Hal2p detoxifies the toxic compound 3' -phosphoadenosine-5'-phosphate (pAp), which blocks the biosynthesis of methionine. Hal2p is also a target of high concentration of Na+. Here, we reported that HAL2 overexpression recovered the salt stress sensitivity of bdf1 Delta. Further evidence demonstrated that HAL2 expression was regulated indirectly by Bdf1p. The salt stress response mechanisms mediated by Bdf1p and Hal2p were different. Unlike hal2 Delta, high Na+ or Li+ stress did not cause pAp accumulation in bdf1 Delta and methionine supplementation did not recover its salt sensitivity. HAL2 overexpression in bdf1 Delta reduced ROS level and improved mitochondrial function, but not respiration. Further analyses suggested that autophagy was apparently defective in bdf1 Delta, and autophagy stimulated by Hal2p may play an important role in recovering mitochondrial functions and Na+ sensitivity of bdf1 Delta. Our findings shed new light towards our understanding about the molecular mechanism of Bdf1p-involved salt stress response in budding yeast.