NRF-2 transcription factor is required for human TOMM20 gene expression

Blesa, Rafael; Prieto-Ruiz, Jesús A.; Hernández, José Miguel Azañón; Hernández-Yago, José

doi:10.1016/j.gene.2006.12.024

Cited by 47 publications

(29 citation statements)

References 23 publications

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“…Expression of a substantial number of nDNA-encoded OXPHOS genes has been linked to NRF-1 activity [78]. Moreover, NRF-1 has been found to regulate expression of key components of the mitochondrial protein import machinery, cytochrome c, and the rate-limiting enzyme in heme biosynthesis, 5-aminolevuline [79][80][81]. NRF-1 also regulates transcription factor A, mitochondrial (TFAM) [72], involved in transcription regulation of mtDNA-encoded genes and mitochondrial genome replication [82].…”

Section: Mitochondrial Biogenesismentioning

confidence: 99%

Regulation and Quantification of Cellular Mitochondrial Morphology and Content

Tronstad¹,

Nooteboom²,

Nilsson³

et al. 2014

CPD

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Running title: Regulation and quantification of mitochondrial morphology and content. Word count: 15,454 (total)Characters: 107,091 (including spaces); 92,067 (excluding spaces) Keywords: mitochondrial biogenesis, mitochondrial dynamics, mitochondrial degradation, living cells, TMRM, microscopy, segmentation, image analysis.Page 2 of 37 ABSTRACTMitochondria play a key role in signal transduction, redox homeostasis and cell survival, which extends far beyond their classical functioning in ATP production and energy metabolism. In living cells, mitochondrial content ("mitochondrial mass") depends on the cell-controlled balance between mitochondrial biogenesis and degradation. These processes are intricately linked to changes in net mitochondrial morphology and spatiotemporal positioning ("mitochondrial dynamics"), which are governed by mitochondrial fusion, fission and motility. It is becoming increasingly clear that mitochondrial mass and dynamics, as well as its ultrastructure and volume, are mechanistically linked to mitochondrial function and the cell. This means that proper quantification of mitochondrial morphology and content is of prime importance in understanding mitochondrial and cellular physiology in health and disease. This review first presents how cellular mitochondrial content is regulated at the level of mitochondrial biogenesis, degradation and dynamics. Next we discuss how mitochondrial dynamics and content can be analyzed with a special emphasis on quantitative live-cell microscopy strategies.

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Section: Mitochondrial Biogenesismentioning

confidence: 99%

Regulation and Quantification of Cellular Mitochondrial Morphology and Content

Tronstad¹,

Nooteboom²,

Nilsson³

et al. 2014

CPD

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“…Similar control by both NRFs extend to three of the four human succinate dehydrogenase (complex II) subunit genes [54-56]. Like NRF-1, NRF-2 participates in the expression of the mitochondrial protein import machinery with functional recognition sites in TOMM70 [57,58] and TOMM20 [34] promoters. NRF-2 has also been linked to the expression of several mitochondrial translation initiation factors [59].…”

Section: Nuclear Transcription Factorsmentioning

confidence: 99%

Nucleus-encoded regulators of mitochondrial function: Integration of respiratory chain expression, nutrient sensing and metabolic stress

Scarpulla¹

2012

Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanism

138

102

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Nucleus-encoded regulatory factors are major contributors to mitochondrial biogenesis and function. Several act within the organelle to regulate mitochondrial transcription and translation while others direct the expression of nuclear genes encoding the respiratory chain and other oxidative functions. Loss-of-function studies for many of these factors reveal a wide spectrum of phenotypes. These range from embryonic lethality and severe respiratory chain deficiency to relatively mild mitochondrial defects seen only under conditions of physiological stress. The PGC-1 family of regulated coactivators (PGC-1α, PGC-1β and PRC) plays an important integrative role through their interactions with transcription factors (NRF-1, NRF-2, ERRα, CREB, YY1 and others) that control respiratory gene expression. In addition, recent evidence suggests that PGC-1 coactivators may balance the cellular response to oxidant stress by promoting a pro-oxidant environment or by orchestrating an inflammatory response to severe metabolic stress. These pathways may serve as essential links between the energy generating functions of mitochondria and the cellular REDOX environment associated with longevity, senescence and disease.

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“…However, the transcriptional activation is not restricted to oxidative phosphorylation polypeptides because it was shown to control also the expression of a variety of proteins, including enzymes (12), TOM complex receptors (13), complex IV assembly factors (14,15), and peroxiredoxin V (16).…”

mentioning

confidence: 99%

Nuclear Respiratory Factor 2 Induces the Expression of Many but Not All Human Proteins Acting in Mitochondrial DNA Transcription and Replication

Bruni

Polosa

Gadaleta

et al. 2010

Journal of Biological Chemistry

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In mammals, NRF-2 (nuclear respiratory factor 2), also named GA-binding protein, is an Ets family transcription factor that controls many genes involved in cell cycle progression and protein synthesis as well as in mitochondrial biogenesis. In this paper, we analyzed the role of NRF-2 in the regulation of human genes involved in mitochondrial DNA transcription and replication. By a combination of bioinformatic and biochemical approaches, we found that the factor binds in vitro and in vivo to the proximal promoter region of the genes coding for the transcription termination factor mTERF, the RNA polymerase POLRMT, the B subunit of the DNA polymerase-␥, the DNA helicase TWINKLE, and the singlestranded DNA-binding protein mtSSB. The role of NRF-2 in modulating the expression of those genes was further established by RNA interference and overexpression strategies. On the contrary, we found that NRF-2 does not control the genes for the subunit A of DNA polymerase-␥ and for the transcription repressor MTERF3; we suggest that these genes are under regulatory mechanisms that do not involve NRF proteins. Since NRFs are known to positively control the expression of transcription-activating proteins, the novelty emerging from our data is that proteins playing antithetical roles in mitochondrial DNA transcription, namely activators and repressors, are under different regulatory pathways. Finally, we developed a more stringent consensus with respect to the general consensus of NRF-2/GA-binding protein when searching for NRF-2 binding sites in the promoter of mitochondrial proteins.

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NRF-2 transcription factor is required for human TOMM20 gene expression

Cited by 47 publications

References 23 publications

Regulation and Quantification of Cellular Mitochondrial Morphology and Content

Regulation and Quantification of Cellular Mitochondrial Morphology and Content

Nucleus-encoded regulators of mitochondrial function: Integration of respiratory chain expression, nutrient sensing and metabolic stress

Nuclear Respiratory Factor 2 Induces the Expression of Many but Not All Human Proteins Acting in Mitochondrial DNA Transcription and Replication

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