Mitochondrial Transcription Factor A (TFAM) is Increased in Rat Embryo During Placentation and Associated with Mitochondrial Differentiation

Alcolea, Maria P.; Colom, Bartomeu; Lladó, Isabel; Gianotti, Magdalena; García-Palmer, Francisco J.

doi:10.1159/000091466

Cited by 12 publications

(12 citation statements)

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“…Thus, the aforementioned increase in the nuclear-encoded proteins, such as TFAM, would lead to an activation of the mtDNA transcription and all together would help the embryo mitochondria to reach a more differentiated stage through a coordinate regulation of both nuclear and mitochondrial-encoded proteins. This idea corroborates the activation of the mitochondrial differentiation process in rat embryo during the placentation period that we have previously suggested (Alcolea et al 2006). …”

Section: Discussionsupporting

confidence: 91%

“…In middle pregnancy, rat embryo mitochondria undergo considerable morphofunctional changes (Mackler et al 1973, Shepard et al 1998, Yang et al 1998 coinciding with the switch from glycolytic to oxidative metabolism that takes place on gestational day 12 (Akazawa et al 1994, Shepard et al 1997, just when the placentary circulation is established and oxygen becomes more available to the embryo (Jollie 1986, Akazawa 2005. In addition, a previous study in our laboratory reported the activation of mitochondrial gene expression throughout the placentation period, suggesting that mitochondrial biogenesis is an active process in rat embryo during this developmental stage (Alcolea et al 2006). Therefore, embryo development during the placentation period is a suitable model to further understand the mitochondrial proliferation and differentiation processes (Justo et al 2002).…”

Section: Introductionmentioning

confidence: 83%

“…Finally, a basic local alignment search tool (NCBI BLAST) revealed that the primer sequence homology was obtained only for the target genes. Real-time PCR was performed as previously described (Alcolea et al 2006). The amplification programme consisted of a preincubation step for denaturation of the template cDNA (10 min at 95 8C), followed by 40 cycles consisting of a denaturation step (10 s at 95 8C), an annealing step (12 s at 60 8C for PGC-1a and 62 8C for 18S, 10 s at 58 8C for mtSSB and COX IV at 60 8C for TFAM and at 64 8C for NRF-2a, 8 s at 55 8C for COX I, 5 s at 56 8C for NRF-1) and an extension step (12 s at 72 8C for all, except for NRF-1 and COX I, which were 8 s at 72 8C and 26 s at 72 8C respectively).…”

Section: Mitochondrial Biogenesis In Rat Embryomentioning

confidence: 99%

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Mitochondrial differentiation and oxidative phosphorylation system capacity in rat embryo during placentation period

Alcolea

Colom²,

Lladó³

et al. 2007

Reproduction

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Mitochondrial biogenesis and function are essential for proper embryo development; however, these processes have not been further studied during the placentation period, when important oxidative metabolism activation is taking place. Thus, the aim of the present study was to investigate the oxidative phosphorylation system (OXPHOS) enzymatic activities as well as the expression of genes involved in the coordinated regulation of both mitochondrial and nuclear genomes (peroxisome proliferatoractivated receptor-g coactivator-1a, nuclear respiratory factors 1 and 2, mitochondrial single-strand DNA-binding protein, mitochondrial transcription factor A), and mitochondrial function (cytochrome c oxidase subunit IV, cytochrome c oxidase subunit I and b-ATP phosphohydrolase) in rat embryo throughout the placentation period (gestational days 11, 12 and 13). Our results reflect that embryo mitochondria were enhancing their OXPHOS potential capacities, pointing out that embryo mitochondria become more differentiated during the placentation period. Besides, the current findings show that the mRNAs of the nuclear genes involved in mitochondrial biogenesis were downregulated, whereas their protein content together with the mitochondrial DNA expression were upregulated throughout the period studied. These data indicate that the molecular regulation of the mitochondrial differentiation process during placentation involves a post-transcriptional activation of the nuclear-encoded genes that would lead to an increase in both the nuclear-and mitochondrial-encoded proteins responsible for the mitochondrial biogenic process. As a result, embryo mitochondria would reach a more differentiated stage with a more efficient oxidative metabolism that would facilitate the important embryo growth during the second half of the pregnancy. Reproduction (2007) 134 147-154

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 83%

Section: Mitochondrial Biogenesis In Rat Embryomentioning

confidence: 99%

See 1 more Smart Citation

Mitochondrial differentiation and oxidative phosphorylation system capacity in rat embryo during placentation period

Alcolea

Colom²,

Lladó³

et al. 2007

Reproduction

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“…This metabolic onset entails a mitochondrial biogenic process that implies important changes in mitochondrial function, morphology, and expression, which leads to embryo mitochondria reaching a more differentiated stage (4,28,43,51).…”

mentioning

confidence: 99%

“…In this sense, diabetes-induced oxidative stress is known to cause defects in the expression, function, and structure of mitochondria (23,33,41,42), which in turn might further increase reactive oxygen species production and, thus, the diabetic complications. However, despite the fact that mitochondrial biogenesis is a critical process in embryo development (4,30,48), nothing is known about the effect of maternal diabetes on this process and about its relationship to the embryopathies associated with this pathology.…”

mentioning

confidence: 99%

Responses of mitochondrial biogenesis and function to maternal diabetes in rat embryo during the placentation period

Alcolea¹,

Lladó²,

García-Palmer³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Alcolea MP, Lladó I, García-Palmer FJ, Gianotti M. Responses of mitochondrial biogenesis and function to maternal diabetes in rat embryo during the placentation period. Am J Physiol Endocrinol Metab 293: E636-E644, 2007; doi:10.1152/ajpendo.00120.2007.-Mitochondria are cellular organelles that have been reported to be altered in diabetes, being closely related to its associated complications. Moreover, mitochondrial biogenesis and function are essential for proper embryo development throughout the placentation period, occurring during organogenesis, when a great rate of congenital malformations have been associated with diabetic pregnancy. Thus, the aim of the current work was to investigate the effect of the diabetic environment on mitochondrial function and biogenesis during the placentation period. For this purpose, we studied the oxidative phosphorylation system (OXPHOS) enzymatic activities as well as the expression of genes involved in the coordinated regulation of both mitochondrial and nuclear genome (PGC-1␣, NRF-1, NRF-2␣, mtSSB, and TFAM) and mitochondrial function (COX-IV, COX-I, and ␤-ATPase) in rat embryos from control and streptozotocininduced diabetic mothers. Our results reflected that diabetic pregnancy retarded and altered embryo growth. The embryos from diabetic mothers showing normal morphology presented a reduced content of proteins regulated through the PGC-1␣ mitochondriogenic pathway on gestational day 12. This fact was accompanied by several responses that entailed the activation of OXPHOS activities on the same day and the recovery of the content of the studied proteins to control levels on day 13. As a result, the mitochondria of these embryos would reach a situation close to control on day 13 that could allow them to follow the normal mitochondriogenic schedule throughout a gestational period in which the mitochondrial differentiation process is critical. Nevertheless, malformed embryos from diabetic mothers seemed to show a lower adaptation capability, which could exacerbate their maldevelopment.peroxisome proliferator-activated receptor-␥ coactivator-1␣; nuclear respiratory factors; mitochondrial transcription factor A; oxidative phosphorylation system THE ALTERED EMBRYO-FETAL DEVELOPMENT induced by the oxida-

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Expression of mitochondrial transcription factor A (TFAM) during porcine gametogenesis and preimplantation embryo development

Antelman

Manandhar

et al. 2008

Journal Cellular Physiology

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Mitochondrial transcription factor A (TFAM) is responsible for stability, maintenance, and transcriptional control of mitochondrial DNA (mtDNA). We have studied the expression and distribution of TFAM in the gametes and preimplantation embryos of the domestic pig (Sus scrofa). We hypothesized that TFAM is not present in the boar sperm mitochondria to reduce the possibility of paternal mtDNA propagation in the progeny. In contrast, we anticipated that Tfam gene is expressed in a developmental stage-dependent manner in porcine oocytes and embryos. The appropriate TFAM band of 25 kDa was detected by Western blotting in ejaculated boar spermatozoa, as well as in porcine oocytes and zygotes. Boar sperm extracts also displayed several bands >25 kDa suggestive of post-translational modification by ubiquitination, confirmed by affinity purification of ubiquitinated proteins. TFAM immunoreactivity was relegated to the sperm tail principal piece and sperm head in fully differentiated spermatozoa. The content of Tfam mRNA increased considerably from the germinal vesicle to blastocyst stage and also between in vitro fertilized and cultured blastocysts compared to in vivo-derived blastocysts. TFAM protein accumulated in the oocytes during maturation and was reduced by proteolysis after fertilization. This pattern was not mirrored in parthenogenetically activated oocytes and zygotes reconstructed by SCNT, suggesting deviant processing of TFAM protein and transcript after oocyte/embryo manipulation. Thus, TFAM may exert a critical role in porcine gametogenesis and preimplantation embryo development. Altogether, our data on the role of TFAM in mitochondrial function and inheritance have broad implications for cell physiology and evolutionary biology.

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Mitochondrial Transcription Factor A (TFAM) is Increased in Rat Embryo During Placentation and Associated with Mitochondrial Differentiation

Cited by 12 publications

References 57 publications

Mitochondrial differentiation and oxidative phosphorylation system capacity in rat embryo during placentation period

Mitochondrial differentiation and oxidative phosphorylation system capacity in rat embryo during placentation period

Responses of mitochondrial biogenesis and function to maternal diabetes in rat embryo during the placentation period

Expression of mitochondrial transcription factor A (TFAM) during porcine gametogenesis and preimplantation embryo development

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