Number of mitochondria and some properties of mitochondrial DNA in the mouse egg

Pikó, Lajos; Matsumoto, Lloyd

doi:10.1016/0012-1606(76)90253-0

Cited by 208 publications

(93 citation statements)

References 25 publications

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“…Gene expression analysis showed that nuclear-and mitochondrial-encoded gene transcripts (Tfam, Polg and Polg2, mt-Cox1 and mt-Cox2) were significantly downregulated in cytoplasmic hybrids. Although mtDNA replication does not occur until at least blastocyst stage (Thundathil et al 2005), nuclear-encoded mitochondrial transcription and replication factors are significantly increased (Piko & Taylor 1987, Thundathil et al 2005 and mitochondria undergo significant morphological changes from simple spherical mitochondria observed in MII oocytes to become elongated with numerous cristae from eightcell to blastocyst stages (Piko & Matsumoto 1976). It was suggested that such an increase in abundance of mitochondrial gene transcripts and mitochondrial morphological changes are required for an increased level of mitochondrial metabolism in morula and blastocyst stage embryos (Thundathil et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Nuclear–cytoplasmic incompatibility and inefficient development of pig–mouse cytoplasmic hybrid embryos

Amarnath

Choi²,

Moawad³

et al. 2011

Reproduction

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Inter-species somatic cell nuclear transfer (iSCNT) embryos usually fail to develop to the blastocyst stage and beyond due to incomplete reprogramming of donor cell. We evaluated whether using a karyoplast that would require less extensive reprogramming such as an embryonic blastomere or the meiotic spindle from metaphase II oocytes would provide additional insight into the development of iSCNT embryos. Our results showed that karyoplasts of embryonic or oocyte origin are no different from somatic cells; all iSCNT embryos, irrespective of karyoplast origin, were arrested during early development. We hypothesized that nuclear-cytoplasmic incompatibility could be another reason for failure of embryonic development from iSCNT. We used pig-mouse cytoplasmic hybrids as a model to address nuclear-cytoplasmic incompatibility in iSCNT embryos. Fertilized murine zygotes were reconstructed by fusing with porcine cytoplasts of varying cytoplasmic volumes (1/10 (small) and 1/5 (large) total volume of mouse zygote). The presence of pig cytoplasm significantly reduced the development of mouse zygotes to the blastocyst stage compared with control embryos at 120 h post-human chorionic gondotropin (41 vs 6 vs 94%, P!0.05; 1/10, 1/5, control respectively). While mitochondrial DNA copy numbers remained relatively unchanged, expression of several important genes namely Tfam, Polg, Polg2, Mfn2, Slc2a3 (Glut3), Slc2a1 (Glut1), Bcl2, Hspb1, Pou5f1 (Oct4), Nanog, Cdx2, Gata3, Tcfap2c, mt-Cox1 and mt-Cox2 was significantly reduced in cytoplasmic hybrids compared with control embryos. These results demonstrate that the presence of even a small amount of porcine cytoplasm is detrimental to murine embryo development and suggest that a range of factors are likely to contribute to the failure of inter-species nuclear transfer embryos.

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Section: Discussionmentioning

confidence: 99%

Nuclear–cytoplasmic incompatibility and inefficient development of pig–mouse cytoplasmic hybrid embryos

Amarnath

Choi²,

Moawad³

et al. 2011

Reproduction

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“…On the other hand, we observed a significant increase in mtDNA copy number in in vitroproduced expanding and hatching blastocysts in bovines . Increasing mtDNA copy number in in vitro embryos can be interpreted as the following two possibilities: (1) accelerated mtDNA replication, which should occur after implantation; in mice, mtDNA replication is known to resume after the egg cylinder stage (Piko & Matsumoto 1976, Ebert et al 1988; (2) failure of mtDNA turnover immediately after fertilization. Recently, it was reported that there is a very short period of mtDNA synthesis from the 1-cell to 2-cell stage, which can be affected by environmental stress in mice (McConnell & Petrie 2004).…”

Section: Discussionmentioning

confidence: 99%

“…Mitochondrial RNA polymerase carries out the central activity of mitochondrial gene expression and, by providing RNA primers for replication, is also implicated in the maintenance and propagation of the mitochondrial genome (Tiranti et al 1997). With in vivo embryos, a slight increase of Polrmt mRNA at the late 2-cell stage might be related to increased transcription of mt-Nd4 and further slight increase at the blastocyst stage might trigger mitochondrial replication after the egg cylinder stage (Piko & Matsumoto 1976, Ebert et al 1988. A subtle difference in the amount of Polrmt mRNA between in vivo and in vitro at the late 2-cell stage might cause a difference in the mtDNA copy number at morula and blastocyst stages.…”

Section: Discussionmentioning

confidence: 99%

Characterization of mitochondrial replication and transcription control during rat early development in vivo and in vitro

Kameyama

Yoo²,

Smith

2007

Reproduction

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In vitro culture (IVC), used in assisted reproductive technologies, is a major environmental stress on the embryo. To evaluate the effect of IVC on mitochondrial transcription and the control of mtDNA replication, we measured the mtDNA copy number and relative amount of mRNA for mitochondrial-related genes in individual rat oocytes, zygotes and embryos using real-time PCR. The average mtDNA copy number was 147 600 (G3000) in metaphase II oocytes. The mtDNA copy number was stable throughout in vivo early development and IVC induced an increase in mtDNA copy number from the 8-cell stage onwards. Gapd mRNA levels vary during early development and IVC did not change the patterns of these housekeeping gene transcripts. Polrmt mRNA levels did not vary during early development up to the morula stage but increased at the blastocyst stage. IVC induced the up-regulation of Polrmt mRNA, one of the key genes regulating mtDNA transcription and replication, at the blastocyst stage. An increase in mt-Nd4 mRNA preceded the blastocyst-related event observed in nuclear-encoded Gapd and Polrmt, suggesting that the expression of mitochondrial encoded genes is controlled differently from nuclear encoded genes. We conclude that the IVC system can perturb mitochondrial transcription and the control of mtDNA replication in rat embryos. This perturbation of mtDNA regulation may be responsible for the abnormal physiology, metabolism and viability of in vitro-derived embryos.

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“…Mature mouse and human oocytes contain somewhere between 50,000 and 550,000 mtDNA copies, with considerable degree of variability between samples (Pikó & Taylor, 1987; Steuerwald et al., 2000). In an interesting manner, despite drastic changes in mitochondria morphology observed during early pre‐implantation embryo development, total number of mitochondria and mtDNA copy number seem to remain unchanged during cleavage divisions, making the oocyte the primary source of mitochondria for pre‐implantation embryos (Piko & Matsumoto, 1976). Mitochondrial DNA replication resumes around the time of blastocyst formation and is first observed in trophectoderm (TE) cells (reviewed in St John, 2014), consistent with the significant increase in the energy needs of the embryo associated with rapid cell proliferation and implantation (Van Blerkom, 2011).…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial unfolded protein response gene Clpp is required to maintain ovarian follicular reserve during aging, for oocyte competence, and development of pre‐implantation embryos

et al. 2018

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SummaryCaseinolytic peptidase P mediates degradation of unfolded mitochondrial proteins and activates mitochondrial unfolded protein response (mtUPR) to maintain protein homeostasis. Clpp −/− female mice generate a lower number of mature oocytes and two‐cell embryos, and no blastocysts. Clpp −/− oocytes have smaller mitochondria, with lower aspect ratio (length/width), and decreased expression of genes that promote fusion. A 4‐fold increase in atretic follicles at 3 months, and reduced number of primordial follicles at 6–12 months are observed in Clpp −/− ovaries. This is associated with upregulation of p‐S6, p‐S6K, p‐4EBP1 and p‐AKT473, p‐mTOR2481 consistent with mTORC1 and mTORC2 activation, respectively, and Clpp −/− oocyte competence is partially rescued by mTOR inhibitor rapamycin. Our findings demonstrate that CLPP is required for oocyte and embryo development and oocyte mitochondrial function and dynamics. Absence of CLPP results in mTOR pathway activation, and accelerated depletion of ovarian follicular reserve.

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Number of mitochondria and some properties of mitochondrial DNA in the mouse egg

Cited by 208 publications

References 25 publications

Nuclear–cytoplasmic incompatibility and inefficient development of pig–mouse cytoplasmic hybrid embryos

Nuclear–cytoplasmic incompatibility and inefficient development of pig–mouse cytoplasmic hybrid embryos

Characterization of mitochondrial replication and transcription control during rat early development in vivo and in vitro

Mitochondrial unfolded protein response gene Clpp is required to maintain ovarian follicular reserve during aging, for oocyte competence, and development of pre‐implantation embryos

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