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Significant decrease of maternal mitochondria carryover using optimized spindle-chromosomal complex transfer.

Xiaoyu Liao1, Wenzhi Li1, Kaibo Lin1

  • 1Department of Assisted Reproduction, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, People's Republic of China.

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|October 5, 2023
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Summary
This summary is machine-generated.

This study introduces a new method, spindle-chromosomal complex transfer with maximal residue removal (SCCT-MRR), to prevent the inheritance of mitochondrial DNA (mtDNA) diseases by removing mutant mtDNA from oocytes.

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Area of Science:

  • Reproductive Biology
  • Genetics
  • Mitochondrial Diseases

Background:

  • Mitochondrial DNA (mtDNA) mutations cause severe inherited human diseases.
  • Current treatments are limited, and mitochondrial replacement (MR) therapy faces challenges like mitochondrial genetic drift.
  • Preventing transmission of mtDNA diseases is a critical unmet medical need.

Purpose of the Study:

  • To develop and validate a novel technique, spindle-chromosomal complex transfer with maximal residue removal (SCCT-MRR), for preventing the transmission of mtDNA diseases.
  • To assess the efficacy of MRR in eliminating mutant mtDNA and the safety of SCCT-MRR in oocytes.
  • To evaluate the developmental competence of oocytes reconstructed using SCCT-MRR and its potential as a clinical treatment.

Main Methods:

  • Investigated mtDNA copy number proportions in karyoplasts and oocytes using the MRR procedure.
  • Performed spindle-chromosomal complex transfer (SCCT) with maximal residue removal (MRR) on metaphase II (MII) oocytes.
  • Optimized the order of intracytoplasmic sperm injection (ICSI) and SCCT, and assessed embryo development in mouse and human oocytes.

Main Results:

  • MRR effectively removed the majority of mtDNA, with minimal residue in reconstructed oocytes.
  • SCCT-MRR demonstrated safety, maintaining normal spindle-chromosomal morphology and chromosomal copy numbers.
  • Reconstructed oocytes developed into blastocysts, and resulting mice showed stable mtDNA carryover without genetic drift.
  • Successful application in human MII oocytes resulted in minimal mtDNA residue and excellent embryo development.

Conclusions:

  • The MRR-SCCT strategy efficiently removes mutant mtDNA and is compatible with normal embryo development.
  • This preclinical approach shows promise as a feasible clinical treatment to prevent the inheritance of mitochondrial diseases.
  • Further research and validation in human models support its potential for clinical application.