| Summary: | Mitochondrial <i>RTG</i>-dependent retrograde signaling, whose regulators have been characterized in <i>Saccharomyces cerevisiae</i>, 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 <i>RTG</i> signaling in salt-induced osmotic stress and its interaction with <i>HOG1</i>. Wild-type and mutant cells, lacking <i>HOG1</i> and/or <i>RTG</i> 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 <i>RTG2,</i> the main upstream regulator of the <i>RTG</i> pathway, contributes to osmoadaptation in an <i>HOG1</i>-dependent manner and that, with <i>RTG3</i>, it is notably involved in a late phase of growth. Our data demonstrate that impairment of <i>RTG</i> signaling causes a decrease in mitochondrial respiratory capacity exclusively under osmostress. Overall, these results suggest that <i>HOG1</i> and the <i>RTG</i> pathway may interact sequentially in the stress signaling cascade and that the <i>RTG</i> pathway may play a role in inter-organellar metabolic communication for osmoadaptation.
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