Abstract
Mitochondrial RTG-dependent retrograde signaling, whose regulators have been characterized in Saccharomyces cerevisiae, plays a recognized role under various environmental stresses. Of special significance, the activity of the transcriptional complex Rtg1/3 has been shown to be modulated by Hog1, the master regulator of the high osmolarity glycerol pathway, in response to osmotic stress. The present work focuses on the role of RTG signaling in salt-induced osmotic stress and its interaction with HOG1. Wild-type and mutant cells, lacking HOG1 and/or RTG genes, are compared with respect to cell growth features, retrograde signaling activation and mitochondrial function in the presence and in the absence of high osmostress. We show that RTG2, the main upstream regulator of the RTG pathway, contributes to osmoadaptation in an HOG1-dependent manner and that, with RTG3, it is notably involved in a late phase of growth. Our data demonstrate that impairment of RTG signaling causes a decrease in mitochondrial respiratory capacity exclusively under osmostress. Overall, these results suggest that HOG1 and the RTG pathway may interact sequentially in the stress signaling cascade and that the RTG pathway may play a role in inter-organellar metabolic communication for osmoadaptation.
Highlights
Mitochondrial retrograde signaling is an evolutionarily conserved pro-survival pathway sustaining metabolic adaptation especially, but not exclusively, in the case of mitochondrial dysfunction
We demonstrated that RTG-dependent retrograde signaling sustains mitochondrial function in a late phase of yeast osmoadaptation still de4
This work highlights the relevance of the interplay between signaling and metabolism its interaction with HOG1 were investigated in wild-type and mutant cells on solid and in cellular stress response
Summary
Mitochondrial retrograde signaling is an evolutionarily conserved pro-survival pathway sustaining metabolic adaptation especially, but not exclusively, in the case of mitochondrial dysfunction. This pathway has been characterized in its molecular details in Saccharomyces cerevisiae yeast cells lacking mitochondrial DNA. Up-regulation of the peroxisomal isoform of citrate synthase (CIT2) serves to replenish the tricarboxylic acid cycle (TCA) cycle and is considered the hallmark of RTG pathway activation [2,3]. The contribution of mitochondrial retrograde signaling to yeast stress response and cellular adaptation has been described in several cases, including acid stress, endoplasmic reticulum stress, as well as oxidative and osmotic stress [4,5,6,7,8,9].
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