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

Rochard, Pierrick; Cassar-Malek, Isabelle; Marchal, Sophie; Wrutniak, Chantal; Cabello, Gérard

doi:10.1002/(sici)1097-4652(199608)168:2<239::aid-jcp2>3.0.co;2-q

Cited by 14 publications

(12 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This observation clearly suggests that mitochondrial activity affects an important pathway involved in myoblast withdrawal from the cell cycle, an essential prerequisite for terminal differentiation. This result also provides new insight on our previous observations indicating that a sharp rise in mitochondrial activity occurs just before the onset of terminal differentiation (17). As this rise does not occur in differentiation-deficient myoblasts, the present data suggest that this event could take part in the induction of terminal differentiation.…”

Section: Mitochondrial Activity Affects Myoblast Differentiation By Isupporting

confidence: 85%

“…In an earlier work, we demonstrated that important changes in mitochondrial activity occurred during avian myoblast differentiation (17). In particular, high mitochondrial activity appears to be associated with the preliminary steps of myogenic differentiation, and its rise just before the onset of terminal differentiation could characterize the irreversible engagement of myoblasts in terminal differentiation.…”

mentioning

confidence: 77%

“…In addition, we have shown that important changes in mitochondrial activity occur just before the onset of differentiation, and are not observed in differentiation-deficient myoblasts (17). Furthermore, expression of the v-erb A oncogene induces significant changes in this activity (17) before stimulating myoblast differentiation (29).…”

Section: Influence Of Chloramphenicol or P43mentioning

confidence: 99%

See 2 more Smart Citations

Mitochondrial Activity Is Involved in the Regulation of Myoblast Differentiation through Myogenin Expression and Activity of Myogenic Factors

Rochard¹,

Rodier²,

Casas³

et al. 2000

Journal of Biological Chemistry

Self Cite

186

163

View full text Add to dashboard Cite

To characterize the regulatory pathways involved in the inhibition of cell differentiation induced by the impairment of mitochondrial activity, we investigated the relationships occurring between organelle activity and myogenesis using an avian myoblast cell line (QM7). The inhibition of mitochondrial translation by chloramphenicol led to a potent block of myoblast differentiation. Carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone and oligomycin, which affect the organelle at different levels, exerted a similar influence. In addition, we provided evidence that this phenomenon was not the result of an alteration in cell viability. Conversely, overexpression of the mitochondrial T3 receptor (p43) stimulated organelle activity and strongly potentiated myoblast differentiation. The involvement of mitochondrial activity in an actual regulation of myogenesis is further supported by results demonstrating that the muscle regulatory gene myogenin, in contrast to CMD1 (chicken MyoD) and myf5, is a specific transcriptional target of mitochondrial activity. Whereas myogenin mRNA and protein levels were down-regulated by chloramphenicol treatment, they were up-regulated by p43 overexpression, in a positive relationship with the expression level of the transgene. We also found that myogenin or CMD1 overexpression in chloramphenicol-treated myoblasts did not restore differentiation, thus indicating that an alteration in mitochondrial activity interferes with the ability of myogenic factors to induce terminal differentiation.Recent studies emphasize that mitochondria, in addition to their well known involvement in the regulation of energy metabolism, are implicated in the regulation of cell growth and differentiation. In particular, mitochondrial events are involved in the preliminary steps of apoptosis (1), and inhibition of mitochondrial activity, either by deleting mtDNA (rho°cells) or by blocking translation in the organelle, has been shown to stop or decrease the proliferation of different cell lines (2-4). Furthermore, the general activity of the organelle, not restricted to energy production, is implicated in such regulation (5, 6). In addition, mitochondrial protein synthesis inhibition is associated with the impairment of differentiation of different cell lines, such as mouse erythroleukemia (7) and mastocytoma cells (8), neurons (9), and human (10), avian (11) or murine myoblasts (12). In agreement with these data, several pathologies are associated with mitochondrial disorders, even if the links between mitochondrial genome rearrangements or activity and pathological symptoms are not always clearly established. Despite these reports, little is known about the molecular mechanisms involved in these regulations. First, the exclusive use of inhibitors of mitochondrial function in previous reports was not fully adapted to demonstrating the occurrence of an actual regulatory pathway involving mitochondrial activity in the regulation of cell differentiation. Second, the nature of the molecular signals underlying the...

show abstract

Section: Mitochondrial Activity Affects Myoblast Differentiation By Isupporting

confidence: 85%

mentioning

confidence: 77%

Section: Influence Of Chloramphenicol or P43mentioning

confidence: 99%

See 1 more Smart Citation

Mitochondrial Activity Is Involved in the Regulation of Myoblast Differentiation through Myogenin Expression and Activity of Myogenic Factors

Rochard¹,

Rodier²,

Casas³

et al. 2000

Journal of Biological Chemistry

Self Cite

186

163

View full text Add to dashboard Cite

show abstract

“…It is reported that high mt activity appears to be associated with the preliminary steps of avian myoblast differentiation, and its induction just before the onset of terminal differentiation could characterize an irreversible engagement in terminal differentiation (47,48). In line with this, we observed that HL-60RG cells treated with thiamphenicol, a specific inhibitor of mt translation, were unable to differentiate to monocyte/macrophage-like cells in response to TPA.…”

Section: Synthesis Of Mt Translation Factors Is Not Regulated At the supporting

confidence: 85%

Down-regulation of the Mitochondrial Translation System during Terminal Differentiation of HL-60 cells by 12-O-Tetradecanoyl-1-phorbol-13-acetate

Takeuchi

Ueda

2003

Journal of Biological Chemistry

View full text Add to dashboard Cite

Mitochondrial (mt) biogenesis depends on both the nuclear and mt genomes, and a coordination of these two genetic systems is necessary for proper cell functioning. Little is known about the regulatory mechanisms of mt translation or about the expression of mt translation factors. Here, we studied the expression of mt translation factors during 12-O-tetradecanoyl-1-phorbol-13-acetate (TPA)-induced terminal differentiation of HL-60 cells. For all mt translation factors investigated, mRNA expression was markedly downregulated in a coordinate and specific manner, whereas mRNA levels for the cytoplasmic translation factors showed only a slight reduction. An actinomycin D chase study and nuclear run-on assay revealed that the TPAinduced decrease in mt elongation factor Tu (EF-Tumt) mRNA mainly results from decreased mRNA stability. Polysome analysis showed that there was no significant translational control of mt translation factor (EF-Tumt, ribosomal proteins L7/L12mt and S12mt) mRNA expression during differentiation. Thus, the decreased protein level of one of these mt translation factors (EF-Tumt) simply reflects its decreased mRNA level. It was also demonstrated by pulse labeling of mt translation products that the down-regulation of mt translational activity is actually associated with down-regulated mt translation factor expression during cellular differentiation. Our results illustrate that the regulatory mechanisms of mt translational activity upon terminal differentiation (in response to the growth arrest) is different to that of the cytoplasmic system, where the control of mRNA translational efficiency of major translation factors is the central mechanism for their down-regulation.Mitochondrial (mt) biogenesis depends on both the nuclear and mitochondrial genomes (1, 2). Mitochondrial DNA (mtDNA) 1 is present in 10 3 -10 4 copies per cell and encodes 13proteins, which are critical subunits of the respiratory chain complexes I, III, IV, and V, as well as 2 ribosomal RNAs and 22 transfer RNAs, which are necessary for mitochondrial protein synthesis (3). Nuclear genes encode the majority of the respiratory chain subunits and all protein components necessary for maintenance and expression of mtDNA. Mitochondria play pivotal roles in eukaryotic cells in producing cellular energy and essential metabolites as well as in controlling apoptosis by integrating numerous death signals (4). Recently, evidence has emerged that mitochondria are also implicated in the regulation of cell growth and differentiation. Inhibition of mitochondrial activity either by deleting mtDNA (rho°cells) or by blocking translation in the organelle has been shown to arrest or decrease proliferation in various cell lines (5-9). Mitochondrial protein synthesis inhibition is associated with the impairment of differentiation in different cell types, including mouse erythroleukemia (10) and mastocytoma cells (11), neurons (12), and human (13), avian (14), or murine myoblasts (15). The coordination of mitochondrial and nuclear genetic systems in t...

show abstract

“…These data shed new light on the sharp increase in mitochondrial activity spontaneously occurring just before myoblast differentiation, already proposed as a possible mechanism involved in the commitment of these cells in the differentiation programme (Rochard et al 1996). As we have recently observed a similar regulation of preadipocyte differentiation (A Fraysse, C WrutniakCabello, L Daury, A Rodier, F Casas, P Rochard, G Cabello & J Charrier, unpublished observations), this set of data demonstrates that, like the nuclear pathway, the direct mitochondrial T3 pathway is involved in the regulation of cell differentiation.…”

Section: Physiological Importance Of the Direct Mitochondrial T3 Pathwaymentioning

confidence: 56%

Thyroid hormone action in mitochondria

Wrutniak‐Cabello¹,

Casas²,

Cabello³

2001

Journal of Molecular Endocrinology

275

175

View full text Add to dashboard Cite

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.

show abstract

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

Cited by 14 publications

References 35 publications

Mitochondrial Activity Is Involved in the Regulation of Myoblast Differentiation through Myogenin Expression and Activity of Myogenic Factors

Mitochondrial Activity Is Involved in the Regulation of Myoblast Differentiation through Myogenin Expression and Activity of Myogenic Factors

Down-regulation of the Mitochondrial Translation System during Terminal Differentiation of HL-60 cells by 12-O-Tetradecanoyl-1-phorbol-13-acetate

Thyroid hormone action in mitochondria

Contact Info

Product

Resources

About