Role of vitamin A in mitochondrial gene expression

Berdanier, Carolyn D.; Everts, Helen B.; Hermoyian, Christina; Mathews, Clayton E.

doi:10.1016/s0168-8227(01)00331-x

Cited by 45 publications

(32 citation statements)

References 80 publications

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“…Therefore, mt gene expression may be regulated with a PPARγ -like mechanism, and by PPARα ligands in a nucleus-dependent manner. In primary hepatocytes cultured in a serum-free medium we found that protein expression of the mitochondrially encoded ATPase subunit a could be upregulated by either DHEA (a PPARα ligand) or RA alone, but not T 3 alone (8). Interestingly, T 3 synergistically enhanced the DHEA and RA effects.…”

Section: Direct Regulation Of Mt Gene Expression By Steroid Hormones mentioning

confidence: 87%

Regulation of Mitochondrial Gene Expression by Retinoids

Everts

Berdanier

2002

IUBMB Life

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SummarySeveral nuclear hormone receptors have been localized to the mitochondrial compartment. Evidence supports the hypothesis that these receptors directly regulate mitochondrial transcription. Retinoic acid has also been shown to regulate mitochondrial transcription and function. This review discusses mechanisms of mitochondrial transcription and how retinoic acid may either indirectly or directly regulate mitochondrial transcription. How retinoic acid may affect individual nutrient requirements is also discussed.

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Section: Direct Regulation Of Mt Gene Expression By Steroid Hormones mentioning

confidence: 87%

Regulation of Mitochondrial Gene Expression by Retinoids

Everts

Berdanier

2002

IUBMB Life

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“…Despite repeated demonstration of glucose intolerance, most recent research has focussed on liver metabolism [7,17,18], while the function of pancreatic β-cells has been little studied. Specifically, the reports of impaired GSIS and disrupted islet morphology of aged BHE/cdb rats [5] have not been followed by studies elucidating the mechanisms responsible.…”

Section: Discussionmentioning

confidence: 99%

Mutated ATP synthase induces oxidative stress and impaired insulin secretion in β‐cells of female BHE/cdb rats

Saleh

Fatehi‐Hassanabad

Wang

et al. 2008

Diabetes Metabolism Res

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“…RA has been previously reported to upregulate transcription of the mtDNAencoded NADH dehydrogenase subunit 5 (mt-Nd5), mt-Co1 and 16S rRNA (mt-Rnr2) (Li et al, 1994;Gaemers et al, 1998). Upregulation of the mtDNA transcripts is likely to result from a direct effect of RA on RARE in the mtDNA (Wrutniak et al, 1995;Demonacos et al, 1996) and RAR in the mitochondria (Berdanier et al, 2001). Given that POLG requires an RNA primer to replicate mtDNA (Chang and Clayton, 1985;Xu and Clayton, 1996), it is possible that the increase in mtDNA transcription also generated the observed increases in mtDNA replication.…”

Section: Pluripotency and Differentiationmentioning

confidence: 99%

“…Exposure of murine (m)ESCs to 10 -7 -10 -6 M of RA in the early days of in vitro differentiation has been shown to considerably enhance neurogenesis (Bain et al, 1995;Strübing et al, 1995). Similar to the effect of RA on nuclear genes regulating cell differentiation (Gottlieb and Huettner, 1999), RA can bind to the RA-specific receptors (RAR) present in the mitochondria (Berdanier et al, 2001), activating the RA response elements (RARE) in the regulatory region of the mtDNA (D-loop) (Wrutniak et al, 1995;Demonacos et al, 1996), which, in turn, initiates mtDNA transcription and replication during ESC differentiation.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial DNA replication during differentiation of murine embryonic stem cells

Facucho-Oliveira

Alderson

Spikings

et al. 2007

Journal of Cell Science

261

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Oxidative phosphorylation (OXPHOS), the intracellular process that generates the majority of the ATP of a cell through the electron-transfer chain, is highly dependent on proteins encoded by the mitochondrial genome (mtDNA). MtDNA replication is regulated by the nuclear-encoded mitochondrial transcription factor A (TFAM) and the mitochondrial-specific DNA polymerase gamma, which consists of a catalytic (POLG) and an accessory (POLG2) subunit. Differentiation of pluripotent embryonic stem cells (ESCs) into specific cell types requires expansion of discrete populations of mitochondria and mtDNA replication to meet the specific metabolic requirements of the cell. We determined by real-time PCR that expression of pluripotent markers is reduced before the upregulation of Polg, Polg2 and Tfam in spontaneously differentiating R1 murine (m)ESCs, along with transient increases in mtDNA copy number. In D3 mESCs, the initial transient increase did not take place. However, precursors of neuronal and cardiomyocyte differentiation were positive for both POLG and TFAM. Similar-stage ESCs also showed active mtDNA replication, identified by 5-bromo-2′-deoxy-uridine labelling, as mtDNA copy number increased. Retinoic-acid-induced differentiation resulted in more consistent patterns of replication and upregulation of Polg, Polg2 and Tfam, whereas siRNA knockdown demonstrated that steady-state expression of POLG is essential for maintaining pluripotency.

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Role of vitamin A in mitochondrial gene expression

Cited by 45 publications

References 80 publications

Regulation of Mitochondrial Gene Expression by Retinoids

Regulation of Mitochondrial Gene Expression by Retinoids

Mutated ATP synthase induces oxidative stress and impaired insulin secretion in β‐cells of female BHE/cdb rats

Mitochondrial DNA replication during differentiation of murine embryonic stem cells

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