Direct in vitro action of thyroid hormones on mitochondrial RNA-polymerase

Martino, G.; Covello, C.; Giovanni, R. De; Filippelli, R; Pitrelli, G.

doi:10.1007/bf00419598

Cited by 19 publications

(16 citation statements)

References 20 publications

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“…Last, in organello transcription experiments demonstrated that p43 strongly increases mitochondrial genome transcription, and, as a consequence, mitochondrial protein synthesis (Casas et al 1999). In agreement with Martino et al (1986), this influence was detected as soon as the hormone had been present for 5 min. Complementary studies were performed in cultured cells.…”

Section: Thyroid Hormone Influence On Mitochondrial Genome Expressionsupporting

confidence: 83%

“…However, studies using isolated mitochondria from hypothyroid or control rat liver led to the conclusion that this mechanism was not exclusive. First, Martino et al (1986) observed that in vitro addition of T3 stimulates mt-RNA polymerases in the absence of nuclear influence, with a latency period of less than 5 min. Secondly, Enriquez et al (1999) demonstrated that addition of minute amounts of the hormone to isolated mitochondria influenced mitochondrial transcription, and particularly the mRNA/rRNA ratio, in relation to changes in the pattern of protein binding to the mitochondrial genome.…”

Section: Thyroid Hormone Influence On Mitochondrial Genome Expressionmentioning

confidence: 99%

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Thyroid hormone action in mitochondria

Wrutniak‐Cabello¹,

Casas²,

Cabello³

2001

Journal of Molecular Endocrinology

275

175

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Triiodothyronine (T3) is considered a major regulator of mitochondrial activity. In this review, we show evidence of the existence of a direct T3 mitochondrial pathway, and try to clarify the respective importance of the nuclear and mitochondrial pathways for organelle activity. Numerous studies have reported short-term and delayed T3 stimulation of mitochondrial oxygen consumption. Convincing data indicate that an early influence occurs through an extra-nuclear mechanism insensitive to inhibitors of protein synthesis. Although it has been shown that diiodothyronines could actually be T3 mediators of this short-term influence, the detection of specific T3-binding sites, probably corresponding to a 28 kDa c-Erb A 1 protein of the inner membrane, also supports a direct T3 influence. The more delayed influence of thyroid hormone upon mitochondrial respiration probably results from mechanisms elicited at the nuclear level, including changes in phospholipid turnover and stimulation of uncoupling protein expression, leading to an increased inner membrane proton leak. However, the involvement of a direct mitochondrial T3 pathway leading to a rapid stimulation of mitochondrial protein synthesis has to be considered.Both pathways are obviously involved in the T3 stimulation of mitochondrial genome transcription. First, a 43 kDa c-Erb A 1 protein located in the mitochondrial matrix (p43), acting as a potent T3-dependent transcription factor of the mitochondrial genome, induces early stimulation of organelle transcription. In addition, T3 increases mitochondrial TFA expression, a mitochondrial transcription factor encoded by a nuclear gene. Similarly, the stimulation of mitochondriogenesis by thyroid hormone probably involves both pathways. In particular, the c-erb A gene simultaneously encodes a nuclear and a mitochondrial T3 receptor (p43), thus ensuring coordination of the expression of the mitochondrial genome and of nuclear genes encoding mitochondrial proteins.Recent studies concerning the physiological importance of the direct mitochondrial T3 pathway involving p43 led to the conclusion that it is not only involved in the regulation of fuel metabolism, but also in the regulation of cell differentiation. As the processes leading to or resulting from differentiation are energy-consuming, p43 coordination of metabolism and differentiation could be of significant importance in the regulation of development.

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Section: Thyroid Hormone Influence On Mitochondrial Genome Expressionsupporting

confidence: 83%

Section: Thyroid Hormone Influence On Mitochondrial Genome Expressionmentioning

confidence: 99%

Thyroid hormone action in mitochondria

Wrutniak‐Cabello¹,

Casas²,

Cabello³

2001

Journal of Molecular Endocrinology

275

175

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“…While the maximal influence requires several hours, this action is initiated after a latency period of several minutes in isolated mitochondria. 11 As T3 increases the steady‐state level of mt‐TFA mRNA, 12 a constitutive mitochondrial transcription factor 13 encoded by a nuclear gene, several investigators consider this action to be induced at the nuclear level. However, this hypothesis is not fully supported by the very short‐term effect recorded in isolated mitochondria.…”

Section: The Influence Of T3 Upon Mitochondrial Activitymentioning

confidence: 99%

“…However, this hypothesis is not fully supported by the very short‐term effect recorded in isolated mitochondria. 11…”

Section: The Influence Of T3 Upon Mitochondrial Activitymentioning

confidence: 99%

Physiological Importance of the T3 Mitochondrial Pathway

Wrutniak¹,

Rochard²,

Casas³

et al. 1998

Annals of the New York Academy of Sciences

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“…Moreover, T3 is considered as the major regulator of mitochondrial biogenesis (Mutvei et al, 1989). Its influence upon mitochondrial protein synthesis (Freeman et al, 1963), mitochondriogenesis (De Leo et al, 1976), oxydative phosphorylations (Sterling et al, 1977;, and mitochondrial gene expression (De Leo et al, 1976;Martino et al, 1986) is well established. The identification of a T3 mitochondrial receptor belonging to the c-erb A family in the mitochondrial matrix is probably a major key to understanding the T3 action at the mitochondrial level.…”

mentioning

confidence: 98%

Changes in mitochondrial activity during avian myoblast differentiation: Influence of triiodothyronine or v-erbA expression

Rochard¹,

Cassar-Malek

Marchal

et al. 1996

J. Cell. Physiol.

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Numerous data suggest that mitochondrial activity is involved in the regulation of cell growth and differentiation. Therefore, we have studied the changes in mitochondrial activity in avian myoblast cultures (QM7 line) undergoing differentiation or in BrdU-treated, differentiation-deficient cells. As we have previously shown that triiodothyronine and v-erb A expression stimulate myogenic differentiation, we have also observed their influence upon mitochondrial activity. Comparison of control and BrdU-treated myoblasts indicated that precocious differentiation events were associated with a stimulation of citrate synthase and cytochrome oxidase activities. They also induced a transient decrease in mitochondrial membrane potential assessed by rhodamine 123 uptake. In control myoblasts, a general stimulation of mitochondrial activity was recorded at cell confluence, prior to terminal differentiation. These events did not occur in BrdU-treated myoblasts, thus indicating that they were tightly linked to myoblast commitment. Whereas no significant triiodothyronine influence could be detected upon mitochondrial activity, we observed that v-erb A expression significantly depresses the mitochondrial membrane potential in control myoblasts. This action was not observed in BrdU-treated myoblasts, thus suggesting that it involves an indirect pathway linked to differentiation. Moreover, the oncoprotein abrogated the decrease in E2-PDH subunit level observed at cell confluence. These data underline that changes in mitochondrial activity occurred prior to myoblast terminal differentiation and could be involved in the processes regulating myogenesis. In addition, they provide the first evidence that the v-erb A oncoprotein influences mitochondrial activity.

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Direct in vitro action of thyroid hormones on mitochondrial RNA-polymerase

Cited by 19 publications

References 20 publications

Thyroid hormone action in mitochondria

Thyroid hormone action in mitochondria

Physiological Importance of the T3 Mitochondrial Pathway

Changes in mitochondrial activity during avian myoblast differentiation: Influence of triiodothyronine or v-erbA expression

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