Dysfunctional mitochondria modulate cAMP-PKA signaling and filamentous and invasive growth of Saccharomyces cerevisiae

Mitochondrial metabolism is targeted by conserved signaling pathways that mediate external information to the cell. However, less is known about whether mitochondrial dysfunction interferes with signaling and thereby modulates the cellular response to environmental changes. In this study, we analyze...

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Bibliographic Details
Published in:Genetics (Austin) 2013-02, Vol.193 (2), p.467-481
Main Authors: Aun, Anu, Tamm, Tiina, Sedman, Juhan
Format: Article
Language:English
Subjects:
Cyclic AMP - metabolism
Cyclic AMP-Dependent Protein Kinases - metabolism
DNA Polymerase I - genetics
DNA-Directed RNA Polymerases - genetics
Down-Regulation
Investigations
MAP Kinase Signaling System
Membrane Glycoproteins - genetics
Membrane Glycoproteins - metabolism
Membranes
Metabolism
Mitochondria - genetics
Mitochondria - metabolism
Mitochondrial Proteins - genetics
Mutation
Phosphorylation
Saccharomyces cerevisiae - genetics
Saccharomyces cerevisiae - growth & development
Saccharomyces cerevisiae - metabolism
Saccharomyces cerevisiae Proteins - genetics
Saccharomyces cerevisiae Proteins - metabolism
Studies
Transcription, Genetic
Yeast
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Summary:Mitochondrial metabolism is targeted by conserved signaling pathways that mediate external information to the cell. However, less is known about whether mitochondrial dysfunction interferes with signaling and thereby modulates the cellular response to environmental changes. In this study, we analyzed defective filamentous and invasive growth of the yeast Saccharomyces cerevisiae strains that have a dysfunctional mitochondrial genome (rho mutants). We found that the morphogenetic defect of rho mutants was caused by specific downregulation of FLO11, the adhesin essential for invasive and filamentous growth, and did not result from general metabolic changes brought about by interorganellar retrograde signaling. Transcription of FLO11 is known to be regulated by several signaling pathways, including the filamentous-growth-specific MAPK and cAMP-activated protein kinase A (cAMP-PKA) pathways. Our analysis showed that the filamentous-growth-specific MAPK pathway retained functionality in respiratory-deficient yeast cells. In contrast, the cAMP-PKA pathway was downregulated, explaining also various phenotypic traits observed in rho mutants. Thus, our results indicate that dysfunctional mitochondria modulate the output of the conserved cAMP-PKA signaling pathway.
ISSN:1943-2631
0016-6731
1943-2631
DOI:10.1534/genetics.112.147389