Distribution of mitochondria in reconstructed mouse oocytes

Fulka, Helena

doi:10.1530/rep.1.00093

Cited by 20 publications

(28 citation statements)

References 30 publications

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“…This may be solved eventually by mitochondria-free karyoplasts. In the present study, oocyte centrifugation before manipulation led to the isolation of karyoplasts with a negligible amount of mitochondria (4.3%), lower than that approximated in previous reports (11,34), therefore preventing the heteroplasmy which would result from the mixture of karyoplast and cytoplast mitochondria, as recently suggested (21,47). However, given the potential for following a clinical approach of ooplasm donation and GVT in humans (48,49), efforts still need to be made to evaluate such treatments for both efficacy and safety in an appropriate animal model.…”

Section: Figurecontrasting

confidence: 47%

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Developmental competence of gametes reconstructed by germinal vesicle transplantation from fresh and cryopreserved bovine oocytes

Franciosi

Perazzoli

Lodde

et al. 2010

Fertility and Sterility

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Section: Figurecontrasting

confidence: 47%

“…GVT has been indicated as a possible treatment to correct age-related aneuploidy caused by dysfunctional ooplasm (15,20) and as a therapeutic advancement which could help prevent the transmission of mutated mitochondrial DNA from mother to offspring (21)(22)(23).…”

mentioning

confidence: 99%

Developmental competence of gametes reconstructed by germinal vesicle transplantation from fresh and cryopreserved bovine oocytes

Franciosi

Perazzoli

Lodde

et al. 2010

Fertility and Sterility

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“…However, in a few embryos, some donor mtDNA was detected at considerably increased levels, clearly indicating the occurrence of premature mtDNA replication. While this could result from the close proximity of the somatic mtDNA to the nucleus , this is likely to have occurred only prior to the first cleavage stage, as the donor mtDNA will have dispersed to varying regions of the cytoplasm in the newly formed blastomeres (Fulka 2004). Consequently, in these exceptional cases, it is more likely that the nuclear-encoded replication factors interacted with their own mtDNA more efficiently and hence replicated it preferentially, especially as POLG was expressed throughout early development for both mtDNA 1 and mtDNA R embryos (see Figure 6).…”

Section: Discussionmentioning

confidence: 99%

Contrasting Effects of in Vitro Fertilization and Nuclear Transfer on the Expression of mtDNA Replication Factors

et al. 2007

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Mitochondrial DNA (mtDNA) is normally only inherited through the oocyte. However, nuclear transfer (NT), the fusion of a donor cell with an enucleated oocyte, can transmit both donor cell and recipient oocyte mtDNA. mtDNA replication is under the control of nuclear-encoded replication factors, such as polymerase gamma (POLG) and mitochondrial transcription factor A (TFAM). These are first expressed during late preimplantation embryo development. To account for the persistence of donor cell mtDNA, even when introduced at residual levels (mtDNA R ), we hypothesized that POLG and TFAM would be upregulated in intra-and interspecific (ovine-ovine) and intergeneric (caprine-ovine) NT embryos when compared to in vitro fertilized (IVF) embryos. For the intra-and interspecific crosses, PolGA (catalytic subunit), PolGB (accessory subunit), and TFAM mRNA were expressed at the 2-cell stage in both nondepleted (mtDNA 1 ) and mtDNA R embryos with protein being expressed up to the 16-cell stage for POLGA and TFAM. However, at the 16-cell stage, there was significantly more PolGA expression in the mtDNA R embryos compared to their mtDNA 1 counterparts. Expression for all three genes first matched IVF embryos at the blastocyst stage. In the intergeneric model, POLG was upregulated during preimplantation development. Although these embryos did not persist further than the 161-cell stage, significantly more mtDNA R embryos reached this stage. However, the vast majority of these embryos were homoplasmic for recipient oocyte mtDNA. The upreglation in mtDNA replication factors was most likely due to the donor cells still expressing these factors prior to NT.

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“…However, even in this case, it is necessary to know how the introduced mitochondria will be distributed in reconstructed cells [24,25]. It has been demonstrated that the speed of mitochondria distribution is cell-cycle dependent [14].…”

Section: Destruction Of Mutated Mitochondrial Dnamentioning

confidence: 99%

How to Repair the Oocyte and Zygote?

Fulka

Langerova

Barnetova

et al. 2009

Journal of Reproduction and Development

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Abstract. The supply of human oocytes is very limited. This restricts not only certain assisted reproduction procedures in IVF clinics where recipients wait for oocytes from donors, but also development of some promising approaches, like therapeutic nuclear transfer with subsequent derivation of patient compatible embryonic stem cells. Moreover, in some patients, collected oocytes exhibit certain specific defects, and logically, we can expect that after fertilization, the embryos arising from these defective oocytes may not develop or that their development might eventually be compromised. For this reason, an increased effort to determine how to repair oocytes is evident in the literature. In general, abnormalities (defects) can be detected in different oocyte components, the zona pellucida, cytoplasm, nucleus (chromosomes) and nucleolus. Whereas defects of a nuclear component are impossible (nuclear DNA) or very hard to repair (nucleolus), zona pellucida abnormalities and cytoplasm defects (for example, if containing mutated mitochondrial DNA, mtDNA) can be repaired in some cases with the help of micromanipulation schemes. In the present article, we will briefly outline the current methodological approaches that can be used to repair the oocyte or one-cell stage embryo. Oocytes and one-cell stage embryos are most commonly used in model animal experiments and are also considered to be the most convenient biological material for relevant therapies in humans. The reason for this is their large size (in mammals, typically about 100 μm) and the relative ease of access to this material. The important aspect is that if the oocyte or one-cell stage embryo is repaired, the resulting cell will be, in theory, normal. This will not be the case, if for example, two-cell stage embryos are manipulated. In this case, both blastomeres must be manipulated to obtain a normal embryo. Logically, this is more complicated from a technical point of view, and thus this approach is not used.The oocytes can be collected either as immature with a prominent nucleus containing one or more nucleoli (germinal vesicle, GV), maturing (with condensed chromosomes, metaphase I, anaphase I or telophase I) or mature (metaphase II). Oocytes are enclosed with a glycoprotein coat known as the zona pellucida. Here, we speculate that only so-called fully-grown oocytes can be used for manipulations because only these cells are able to undergo germinal vesicle breakdown (GVBD) and reach metaphase II (MII) stage. Less advanced oocytes (growing) do not normally undergo GVBD in culture, and if they do, they only reach the metaphase I (MI) stage [1]. Because, mature (metaphase II) oocytes are almost exclusively collected from ovaries in human assisted reproduction, one may expect that this stage would be most commonly used for manipulations. Moreover, use of these oocytes is also advantageous because they are fully developmentally competent due to maturation in their natural environment, follicles. It is well documented that developmental competence decreases ...

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Distribution of mitochondria in reconstructed mouse oocytes

Cited by 20 publications

References 30 publications

Developmental competence of gametes reconstructed by germinal vesicle transplantation from fresh and cryopreserved bovine oocytes

Developmental competence of gametes reconstructed by germinal vesicle transplantation from fresh and cryopreserved bovine oocytes

Contrasting Effects of in Vitro Fertilization and Nuclear Transfer on the Expression of mtDNA Replication Factors

How to Repair the Oocyte and Zygote?

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