Animal mitochondrial biogenesis and function: a regulatory cross-talk between two genomes

Garesse, Rafael; Vallejo, Carmen G.

doi:10.1016/s0378-1119(00)00582-5

Cited by 262 publications

(173 citation statements)

References 150 publications

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“…In addition, nuclear and mitochondrial genes involved in OXPHOS were upregulated in the type 2 diabetes library. Subunits of respiratory complexes in the mitochondria were encoded by both nuclear and mitochondrial DNA [22]. However, the limited coding capacity of mitochondrial DNA means that nuclear genes make a major contribution to OXPHOS.…”

Section: Discussionmentioning

confidence: 99%

Genes involved in oxidative phosphorylation are coordinately upregulated with fasting hyperglycaemia in livers of patients with type 2 diabetes

et al. 2006

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Aims/hypothesis Mitochondrial oxidative phosphorylation (OXPHOS) plays an important role in the pathophysiology of type 2 diabetes. Genes involved in OXPHOS have been reported to be down-regulated in skeletal muscle from patients with type 2 diabetes; however, hepatic regulation is unknown. Materials and methods We analysed expression of genes involved in OXPHOS from the livers of 14 patients with type 2 diabetes and 14 subjects with NGT using serial analysis of gene expression (SAGE) and DNA chip analysis. We evaluated the correlation between expression levels of genes involved in OXPHOS and the clinical parameters of individuals with type 2 diabetes and NGT. Results Both gene analyses showed that genes involved in OXPHOS were significantly upregulated in the type 2 diabetic liver. In the SAGE analysis, tag count comparisons of mitochondrial transcripts showed that ribosomal RNAs (rRNA) were 3.5-fold over-expressed, and mRNAs were 1.2-fold over-expressed in the type 2 diabetes library. DNA chip analysis revealed that expression of genes involved in OXPHOS, which correlated with several nuclear factors, including estrogen-related receptor-α or peroxisome proliferator-activated receptor-γ, was a predictor of fasting plasma glucose levels, independently of age, BMI, insulin resistance and fasting insulin levels (p=0.04). Surprisingly, genes involved in OXPHOS did not correlate with peroxisome proliferator-activated receptor-γ coactivator-1α or nuclear respiratory factor 1. Conclusions/interpretation Our results indicate that upregulation of genes involved in OXPHOS in the liver, which are regulated by different mechanisms from genes in the skeletal muscle, is associated with fasting hyperglycaemia in patients with type 2 diabetes.

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Section: Discussionmentioning

confidence: 99%

Genes involved in oxidative phosphorylation are coordinately upregulated with fasting hyperglycaemia in livers of patients with type 2 diabetes

et al. 2006

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“…In fact, mitochondrial genome only encodes 13 genes of the mitochondrial oxidative phosphorylation system, with all others encoded by nuclear genome. Therefore, the biogenesis of mitochondria depends on the coordinated expression of two genomes, nuclear and mitochondrial (Garesse and Vallejo, 2001). The structure of ERβ could enable it to track between nucleus and mitochondria, hence orchestra the function of mitochondria through its genomic action.…”

Section: Erβ As a Mitochondrial Transcriptional Factormentioning

confidence: 99%

Estrogen actions on mitochondria—Physiological and pathological implications

Simpkins

Yang

Sarkar

et al. 2008

Molecular and Cellular Endocrinology

135

105

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Estrogens are potent neuroprotective hormones and mitochondria are the site of cellular life-death decisions. As such, it is not surprising that we and other have shown that estrogens have remarkable effects on mitochondrial function. Herein we provide evidence for a primary effect of estrogens on mitochondrial function, achieved in part by the import of estrogen receptor β (ERβ) into the mitochondria where it mediates a number of estrogen actions on this vital organelle. ERβ is imported into the mitochondria, through tethering to cytosolic chaperone protein and/or through direct interaction with mitochondrial import proteins. In the mitochondria, ERβ can affect transcription of critical mitochondrial genes through the interaction with estrogen response elements (ERE) or through protein-protein interactions with mitochondrially imported transcription factors. The potent effects of estrogens on mitochondrial function, particularly during mitochondrial stress, argues for a role of estrogens in the treatment of mitochondrial defects in chronic neurodegenerative diseases like Alzheimer's disease (AD) and Parkinson's disease (PD) and more acute conditions of mitochondrial compromise, like cerebral ischemia and traumatic brain injury.

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“…Mitochondria possess their own genomic apparatus, mtDNA, a 16.5 kb closed-circular double stranded DNA, which codes for some of their proteins. Consequently, mitochondrial biogenesis is highly orchestrated by the transcriptional regulatory circuits between this mtDNA and nuclear genes encoding mitochondrial proteins (Garesse and Vallejo, 2001;Kelly and Scarpulla, 2004). Transcription of mtDNA requires, in addition to the mitochondrial specific DNA polymerase gamma (POLG), a small number of nucleus-encoded proteins comprising the mitochondrial transcription factor A (TFAM) (Clayton, 1998;Scarpulla, 2002).…”

Section: Introductionmentioning

confidence: 99%

An active mitochondrial biogenesis occurs during dendritic cell differentiation

Zaccagnino

Saltarella

Maiorano

et al. 2012

The International Journal of Biochemistry & Cell Biology

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This article appeared in a journal published by Elsevier. The attached copy is furnished to the author for internal non-commercial research and education use, including for instruction at the authors institution and sharing with colleagues.Other uses, including reproduction and distribution, or selling or licensing copies, or posting to personal, institutional or third party websites are prohibited. b s t r a c tDendritic cells (DC) are sentinels of the immune system deriving from circulating monocyte precursors recruited to sites of inflammation. In a previous report (Del Prete et al., 2008) we showed that, after differentiation, DC exhibited increased number of condensed mitochondria and dynamic changes in their energy metabolism. A study is presented here showing that the DC differentiation process is characterized by increased expression level and activity of mitochondrial respiratory complexes, as well as by an increased mitochondrial DNA (mtDNA) copy number. Moreover, DC are equipped with more efficient antioxidant protection systems, over expressed most likely to detoxify increased ROS production, as a consequence of the much higher mitochondrial activity. Kinetic analysis of the three main mitochondrial biogenesis-associated genes revealed that the peak in PPAR␥ coactivator-1alpha (PGC-1␣) gene expression was suddenly reached few hours after the onset of the differentiation. While PGC-1␣ expression rapidly declines, the mitochondrial transcription factor A (TFAM) and nuclear respiratory factor-1 (NRF-1) expression gradually increased. These findings demonstrate that an active mitochondrial biogenesis occurs during DC differentiation and further suggest that an early input by the master regulator of mitochondrial biogenesis PGC-1␣ is needed to trigger the subsequent activation of the downstream transcription factors, NRF-1 and TFAM in this process.

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Animal mitochondrial biogenesis and function: a regulatory cross-talk between two genomes

Cited by 262 publications

References 150 publications

Genes involved in oxidative phosphorylation are coordinately upregulated with fasting hyperglycaemia in livers of patients with type 2 diabetes

Genes involved in oxidative phosphorylation are coordinately upregulated with fasting hyperglycaemia in livers of patients with type 2 diabetes

Estrogen actions on mitochondria—Physiological and pathological implications

An active mitochondrial biogenesis occurs during dendritic cell differentiation

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