scholarly journals Enhanced osteoclastogenesis by mitochondrial retrograde signaling through transcriptional activation of the cathepsin K gene

2015 ◽  
Vol 1364 (1) ◽  
pp. 52-61 ◽  
Author(s):  
Manti Guha ◽  
Satish Srinivasan ◽  
Alexander Koenigstein ◽  
Mone Zaidi ◽  
Narayan G. Avadhani
Keyword(s):  
Transcriptional Activation ◽  
Cathepsin K ◽  
Retrograde Signaling ◽  
Mitochondrial Retrograde Signaling

scholarly journals GPS2 regulates mitochondria biogenesis via mitochondrial retrograde signaling and chromatin remodeling of nuclear-encoded mitochondrial genes

2017 ◽  
Author(s):  
Maria Dafne Cardamone ◽  
Bogdan Tanasa ◽  
Carly Cederquist ◽  
Jiawen Huang ◽  
Kiana Mahdaviani ◽  
...  
Keyword(s):  
Rna Polymerase Ii ◽  
Transcriptional Activation ◽  
Mitochondrial Gene ◽  
Nuclear Gene ◽  
Mitochondrial Genes ◽  
Retrograde Signaling ◽  
Gene Promoters ◽  
Brown Adipose ◽  
Mitochondrial Functions ◽  
Mitochondrial Retrograde Signaling

SummaryAs most of the mitochondrial proteome is encoded in the nucleus, mitochondrial functions critically depend on nuclear gene expression and bidirectional mito-nuclear communication. However, mitochondria-to-nucleus communication pathways are incompletely understood. Here, we identify G-Protein Pathway Suppressor 2 (GPS2) as a mediator of mitochondrial retrograde signaling and a key transcriptional activator of nuclear-encoded mitochondrial genes in mammals. GPS2 regulated translocation from mitochondria to nucleus is essential for the transcriptional activation of the nuclear stress response to mitochondrial depolarization and for supporting basal mitochondrial biogenesis in differentiating adipocytes and in brown adipose tissue from mice. In the nucleus, GPS2 recruitment to target gene promoters regulates histone H3K9 demethylation and RNA Polymerase II (POL2) activation through inhibition of Ubc13-mediated ubiquitination. Together, these findings reveal an unexpected layer of regulation of mitochondrial gene transcription as they uncover a novel mitochondria-nuclear communication pathway.

The biochemistry and cell biology of aging: metabolic regulation through mitochondrial signaling

2014 ◽  
Vol 306 (6) ◽  
pp. E581-E591 ◽  
Author(s):  
Yun Chau Long ◽  
Theresa May Chin Tan ◽  
Inoue Takao ◽  
Bor Luen Tang
Keyword(s):  
Cell Biology ◽  
Metabolic Regulation ◽  
Nutrient Sensing ◽  
Cellular Aging ◽  
Retrograde Signaling ◽  
Unfolded Protein ◽  
Mitochondrial Retrograde Signaling ◽  
Long Time ◽  
Biology Of Aging ◽  
Protein Response

Cellular and organ metabolism affects organismal lifespan. Aging is characterized by increased risks for metabolic disorders, with age-associated degenerative diseases exhibiting varying degrees of mitochondrial dysfunction. The traditional view of the role of mitochondria generated reactive oxygen species (ROS) in cellular aging, assumed to be causative and simply detrimental for a long time now, is in need of reassessment. While there is little doubt that high levels of ROS are detrimental, mounting evidence points toward a lifespan extension effect exerted by mild to moderate ROS elevation. Dietary caloric restriction, inhibition of insulin-like growth factor-I signaling, and inhibition of the nutrient-sensing mechanistic target of rapamycin are robust longevity-promoting interventions. All of these appear to elicit mitochondrial retrograde signaling processes (defined as signaling from the mitochondria to the rest of the cell, for example, the mitochondrial unfolded protein response, or UPRmt). The effects of mitochondrial retrograde signaling may even spread to other cells/tissues in a noncell autonomous manner by yet unidentified signaling mediators. Multiple recent publications support the notion that an evolutionarily conserved, mitochondria-initiated signaling is central to the genetic and epigenetic regulation of cellular aging and organismal lifespan.

scholarly journals Rewiring AMPK and Mitochondrial Retrograde Signaling for Metabolic Control of Aging and Histone Acetylation in Respiratory-Defective Cells

Cell Reports ◽  
2014 ◽  
Vol 7 (2) ◽  
pp. 565-574 ◽  
Author(s):  
R. Magnus N. Friis ◽  
John Paul Glaves ◽  
Tao Huan ◽  
Liang Li ◽  
Brian D. Sykes ◽  
...  
Keyword(s):  
Histone Acetylation ◽  
Metabolic Control ◽  
Retrograde Signaling ◽  
Mitochondrial Retrograde Signaling

scholarly journals Mitochondrial retrograde signaling connects respiratory capacity to thermogenic gene expression

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Minwoo Nam ◽  
Thomas E. Akie ◽  
Masato Sanosaka ◽  
Siobhan M. Craige ◽  
Shashi Kant ◽  
...  
Keyword(s):  
Gene Expression ◽  
Retrograde Signaling ◽  
Respiratory Capacity ◽  
Mitochondrial Retrograde Signaling

scholarly journals Mathematical Model for the Study of Mitochondrial Retrograde Signaling Dynamics

2021 ◽  
Author(s):  
Shao-Ting Chiu ◽  
Wen-Wei Tseng ◽  
An-Chi Wei
Keyword(s):  
Mathematical Model ◽  
Quality Control ◽  
Signal Propagation ◽  
Boolean Model ◽  
Retrograde Signaling ◽  
Specific Gene ◽  
Signaling Dynamics ◽  
Model Response ◽  
Mitochondrial Retrograde Signaling ◽  
Model Dynamics

SummaryMitochondria are semi-autonomous eukaryotic organelles, that participate in energy production and metabolism, making mitochondrial quality control crucial. As most mitochondrial proteins are encoded by nuclear genes, quality control depends on proper mitochondria-nucleus communication, designated mitochondrial retrograde signaling. Early studies focused on retrograde signaling participants and specific gene knockouts. However, mitochondrial signal modulation remains elusive. Using yeast, we simulated signal propagation following mitochondrial damage and proposed a mathematical model based on enzyme kinetics and ordinary differential equations. Mitochondrial retrograde signaling decisions were described by a Boolean model. Dynamics were analyzed through an ordinary differential equation-based model and extended to evaluate the model response to noisy damage signals. Simulation revealed localized protein concentration dynamics, including waveforms, frequency response, and robustness under noise. Retrograde signaling is bistable with three localized steady states, while increased damage compromises robustness. We elucidated mitochondrial retrograde signaling, providing a basis for drug design against yeast and fungi.

scholarly journals SDHA gain-of-function engages inflammatory mitochondrial retrograde signaling via KEAP1–Nrf2

2019 ◽  
Vol 20 (10) ◽  
pp. 1311-1321 ◽  
Author(s):  
Anne-Valérie Burgener ◽  
Glenn R. Bantug ◽  
Benedikt J. Meyer ◽  
Rebecca Higgins ◽  
Adhideb Ghosh ◽  
...  
Keyword(s):  
Retrograde Signaling ◽  
Gain Of Function ◽  
Mitochondrial Retrograde Signaling
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