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Mitochondrial Retrograde Signaling: Triggers, Pathways, and Outcomes.

da Cunha FM, Torelli NQ, Kowaltowski AJ - Oxid Med Cell Longev (2015)

Bottom Line: Although these organelles possess their own DNA, the vast majority (>99%) of mitochondrial proteins are encoded in the nucleus.This situation makes systems that allow the communication between mitochondria and the nucleus a requirement not only to coordinate mitochondrial protein synthesis during biogenesis but also to communicate eventual mitochondrial malfunctions, triggering compensatory responses in the nucleus.Mitochondria-to-nucleus retrograde signaling has been described in various organisms, albeit with differences in effector pathways, molecules, and outcomes, as discussed in this review.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Bioquímica, Escola Paulista de Medicina, Universidade Federal de São Paulo, 04044-020 São Paulo, SP, Brazil.

ABSTRACT
Mitochondria are essential organelles for eukaryotic homeostasis. Although these organelles possess their own DNA, the vast majority (>99%) of mitochondrial proteins are encoded in the nucleus. This situation makes systems that allow the communication between mitochondria and the nucleus a requirement not only to coordinate mitochondrial protein synthesis during biogenesis but also to communicate eventual mitochondrial malfunctions, triggering compensatory responses in the nucleus. Mitochondria-to-nucleus retrograde signaling has been described in various organisms, albeit with differences in effector pathways, molecules, and outcomes, as discussed in this review.

No MeSH data available.


Scheme comparing the classical retrograde signaling pathways in yeast and mammals. In yeast, mitochondrial dysfunction leads to decreases in intracellular ATP concentration, which may favor Rtg2-Mks1 interaction [54] allowing Rtg1-Rtg3 activation. In mammals, mitochondrial dysfunction translates into drops in mitochondrial membrane potential, causing increments in intracellular calcium. Calcium-dependent kinases and phosphatases are then activated culminating with the activation of different transcription factors. Alternative retrograde signaling pathways in yeast, mammals, and other model organisms are discussed in the text.
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fig2: Scheme comparing the classical retrograde signaling pathways in yeast and mammals. In yeast, mitochondrial dysfunction leads to decreases in intracellular ATP concentration, which may favor Rtg2-Mks1 interaction [54] allowing Rtg1-Rtg3 activation. In mammals, mitochondrial dysfunction translates into drops in mitochondrial membrane potential, causing increments in intracellular calcium. Calcium-dependent kinases and phosphatases are then activated culminating with the activation of different transcription factors. Alternative retrograde signaling pathways in yeast, mammals, and other model organisms are discussed in the text.

Mentions: Saccharomyces cerevisiae's RTG-dependent retrograde signaling was the first retrograde pathway to be described and is extensively characterized [13, 14]. It depends on three cytosolic proteins: Rtg1p, Rtg2p, and Rtg3p. Rtg1p and Rtg3p are basic helix-loop-helix/leucine zipper (bHLH/LeuZip) transcription factors that bind as heterodimers to the GTCAC DNA binding site. When activated, the Rtg1/3p complex translocates from the cytoplasm to the nucleus [15], where it controls the expression of genes that encode mitochondrial proteins (Figures 1 and 2). Although only Rtg3p contains a transcription activation domain, Rtg1p and Rtg3p are both required for DNA binding [16].


Mitochondrial Retrograde Signaling: Triggers, Pathways, and Outcomes.

da Cunha FM, Torelli NQ, Kowaltowski AJ - Oxid Med Cell Longev (2015)

Scheme comparing the classical retrograde signaling pathways in yeast and mammals. In yeast, mitochondrial dysfunction leads to decreases in intracellular ATP concentration, which may favor Rtg2-Mks1 interaction [54] allowing Rtg1-Rtg3 activation. In mammals, mitochondrial dysfunction translates into drops in mitochondrial membrane potential, causing increments in intracellular calcium. Calcium-dependent kinases and phosphatases are then activated culminating with the activation of different transcription factors. Alternative retrograde signaling pathways in yeast, mammals, and other model organisms are discussed in the text.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4637108&req=5

fig2: Scheme comparing the classical retrograde signaling pathways in yeast and mammals. In yeast, mitochondrial dysfunction leads to decreases in intracellular ATP concentration, which may favor Rtg2-Mks1 interaction [54] allowing Rtg1-Rtg3 activation. In mammals, mitochondrial dysfunction translates into drops in mitochondrial membrane potential, causing increments in intracellular calcium. Calcium-dependent kinases and phosphatases are then activated culminating with the activation of different transcription factors. Alternative retrograde signaling pathways in yeast, mammals, and other model organisms are discussed in the text.
Mentions: Saccharomyces cerevisiae's RTG-dependent retrograde signaling was the first retrograde pathway to be described and is extensively characterized [13, 14]. It depends on three cytosolic proteins: Rtg1p, Rtg2p, and Rtg3p. Rtg1p and Rtg3p are basic helix-loop-helix/leucine zipper (bHLH/LeuZip) transcription factors that bind as heterodimers to the GTCAC DNA binding site. When activated, the Rtg1/3p complex translocates from the cytoplasm to the nucleus [15], where it controls the expression of genes that encode mitochondrial proteins (Figures 1 and 2). Although only Rtg3p contains a transcription activation domain, Rtg1p and Rtg3p are both required for DNA binding [16].

Bottom Line: Although these organelles possess their own DNA, the vast majority (>99%) of mitochondrial proteins are encoded in the nucleus.This situation makes systems that allow the communication between mitochondria and the nucleus a requirement not only to coordinate mitochondrial protein synthesis during biogenesis but also to communicate eventual mitochondrial malfunctions, triggering compensatory responses in the nucleus.Mitochondria-to-nucleus retrograde signaling has been described in various organisms, albeit with differences in effector pathways, molecules, and outcomes, as discussed in this review.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Bioquímica, Escola Paulista de Medicina, Universidade Federal de São Paulo, 04044-020 São Paulo, SP, Brazil.

ABSTRACT
Mitochondria are essential organelles for eukaryotic homeostasis. Although these organelles possess their own DNA, the vast majority (>99%) of mitochondrial proteins are encoded in the nucleus. This situation makes systems that allow the communication between mitochondria and the nucleus a requirement not only to coordinate mitochondrial protein synthesis during biogenesis but also to communicate eventual mitochondrial malfunctions, triggering compensatory responses in the nucleus. Mitochondria-to-nucleus retrograde signaling has been described in various organisms, albeit with differences in effector pathways, molecules, and outcomes, as discussed in this review.

No MeSH data available.