Birth of infant after transfer of anucleate donor oocyte cytoplasm into recipient eggs

Cohen, Jacques; Scott, Richard T.; Schimmel, Tim; Levron, Jacob; Willadsen, S. M.

doi:10.1016/s0140-6736(05)62353-7

Cited by 368 publications

(217 citation statements)

References 5 publications

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“…The transfer of the cytoplasm from a donor oocyte into a recipient oocyte by injection has been successfully used in assisted human reproduction to rescue those oocytes that had repeatedly failed to develop after fertilization (Cohen et al 1997, Barritt et al 2001a. Observations of injected mitochondria indicate their gradual dispersion from the site of injection but these observations also show that they are not evenly distributed in the oocyte cytoplasm even after a relatively long culture ( Van Blerkom et al 1998, Barritt et al 2001b.…”

Section: Discussionmentioning

confidence: 99%

Distribution of mitochondria in reconstructed mouse oocytes

Fulka¹

2004

Reproduction

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It has been suggested that nucleus replacement (transfer) may be used as an efficient oocyte therapy in order to prevent transmission of mutated mitochondrial DNA from mother to offspring in humans. The essential and not yet answered question is how mitochondria surrounding the karyoplast will be distributed in the newly reconstructed oocytes. In our model experiments, we have evaluated the distribution of mitochondria in reconstructed immature mouse oocytes when germinal vesicle karyoplasts, with labeled mitochondria, were fused to unlabeled cytoplasts. The penetration of mitochondria from karyoplasts into cytoplasts can be detected almost immediately after the beginning of fusion. In immature reconstructed oocytes, mitochondria are first located in the oocyte center but they are homogenously distributed within the whole cytoplasm before the completion of maturation. Fusion of oocytes at different stages of maturation suggests that the speed of mitochondria distribution is cell cycle dependent.

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Section: Discussionmentioning

confidence: 99%

Distribution of mitochondria in reconstructed mouse oocytes

Fulka¹

2004

Reproduction

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“…In particular, study of their stage-specific reorganization and association with other cytoplasmic components such as the SER should determine whether they are (a) directly involved in the focal or global cytoplasmic activities that determine normal competence or result in demise and (b) which of their many nonrespiratory functions in somatic cells also pertain to the oocyte and preimplantation-stage embryo. Continued research will also yield the type of basic scientific information that will be necessary to demonstrate that controversial procedures applied to certain infertile women, such as donor ooplasmic transfusion (Cohen et al 1997), actually treat mitochondrial defect(s) that have been assumed to occur in the recipient oocyte and are associated with cleavagestage demise , Brenner 2004). Clinicians and patients need to know whether these or other similar manipulations (e.g.…”

Section: Concluding Commentsmentioning

confidence: 99%

“…Because the normalcy of critical nuclear and cytoplasmic activities may be determined by mitochondria, it is not surprising that their role in early human development as related to outcome in IVF treatments has become a subject of clinical and basic research interest (Christodoulou 2000, Howell et al 2000, Jansen 2000a,b, Cummins 2002, Brenner 2004, Chinnery 2004, Eichenlaub-Ritter et al 2004. From a basic science viewpoint, the extent to which mitochondria contribute to or actually determine oocyte and embryo competence must be better understood if proactive clinical therapies such as oocyte mitochondrial donation/replacement (Cohen et al 1997) are to be considered acceptable treatments for certain types of infertility in which a mitochondrial association has been clearly identified (Brenner 2004, St John et al 2004.…”

Section: Introductionmentioning

confidence: 99%

Mitochondria in human oogenesis and preimplantation embryogenesis: engines of metabolism, ionic regulation and developmental competence

2004

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Mitochondria are the most abundant organelles in the mammalian oocyte and early embryo. While their role in ATP production has long been known, only recently has their contribution to oocyte and embryo competence been investigated in the human. This review considers whether such factors as mitochondrial complement size, mitochondrial DNA copy numbers and defects, levels of respiration, and stage-specific spatial distribution, influence the developmental normality and viability of human oocytes and preimplantation-stage embryos. The finding that mitochondrial polarity can differ within and between oocytes and embryos and that these organelles may participate in the regulation of intracellular Ca 21 homeostasis are discussed in the context of how focal domains of differential respiration and intracellular-free Ca 21 regulation may arise in early development and what functional implications this may have for preimplantation embryogenesis and developmental competence after implantation.

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“…Cytoplasmic transfer between human oocytes has been previously used to improve the success rate of assisted reproduction, 90 and might lead to a decrease in the rate of mutant mitochondria. However, because of the inherent uncertainty and the low effectiveness of this method, it is not likely to become practicable.…”

Section: Cytoplasmic Transfermentioning

confidence: 99%

How Can We Treat Mitochondrial Encephalomyopathies? Approaches to Therapy

2008

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Summary:Mitochondrial disorders are a heterogeneous group of diseases affecting different organs (brain, muscle, liver, and heart), and the severity of the disease is highly variable. The chronicity and heterogeneity, both clinically and genetically, means that many patients require surveillance follow-up over their lifetime, often involving multiple disciplines. Although our understanding of the genetic defects and their pathological impact underlying mitochondrial diseases has increased over the past decade, this has not been paralleled with regards to treatment. Currently, no definitive pharmacological treatment exists for patients with mitochondrial dysfunction, except for patients with primary deficiency of coenzyme Q10. Pharmacological and nonpharmacological treatments increasingly being investigated include ketogenic diet, exercise, and gene therapy. Management is aimed primarily at minimizing disability, preventing complications, and providing prognostic information and genetic counseling based on current best practice. Here, we evaluate therapies used previously and review current and future treatment modalities for both adults and children with mitochondrial disease.

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Birth of infant after transfer of anucleate donor oocyte cytoplasm into recipient eggs

Cited by 368 publications

References 5 publications

Distribution of mitochondria in reconstructed mouse oocytes

Distribution of mitochondria in reconstructed mouse oocytes

Mitochondria in human oogenesis and preimplantation embryogenesis: engines of metabolism, ionic regulation and developmental competence

How Can We Treat Mitochondrial Encephalomyopathies? Approaches to Therapy

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