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Acid stress causes resistance to acetic acid-induced regulated cell death (AA-RCD) in budding yeast, resulting in catalase activation. In order to explore the molecular determinants of evasion of AA-RCD triggered by acid stress adaptation, we studied the involvement and the possible interplay of the master regulator of transcription high-osmolarity glycerol 1 ( HOG1 ) and  RTG2 , a positive regulator of the  RTG -dependent mitochondrial retrograde signaling. Viability, DNA fragmentation, and ROS accumulation have been analyzed in wild-type and mutant cells lacking  HOG1  and/or  RTG2 . Catalase activity and transcription of  CTT1  and  CTA1 , coding the cytosolic and peroxisomal/mitochondrial catalase, respectively, as well as  Hog1  phosphorylation, were also analyzed. Our results show that  HOG1  is essential for resistance to AA-RCD and its activation results in the upregulation of  CTT1 , but not  CTA1 , transcription during acid stress adaptation.  RTG2  is required for  Hog1 -dependent  CTT1  upregulation upon acid stress, despite failure of  RTG  pathway activation. We give evidence that  Rtg2  has a cytoprotective role and can act as a general cell stress sensor independent of Rtg1/3-dependent transcription.

Acid Stress Triggers Resistance to Acetic Acid-Induced Regulated Cell Death throughHog1Activation Which RequiresRTG2in Yeast