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Telomeres and genomic instability during early development.

David L Keefe1

  • 1Department of Ob/Gyn, NYU Langone Medical Center, 550 First Avenue, NBV 9N1A, New York, 10012, New York, USA.

European Journal of Medical Genetics
|March 14, 2019
PubMed
Summary
This summary is machine-generated.

Genomic instability, including aneuploidy and copy number variants (CNVs), is common in early human embryos. Telomere attrition in oocytes and inefficient repair mechanisms in embryos contribute to this instability, impacting development.

Keywords:
EmbryosGenomic instabilityOocytesReproductive agingTelomeres

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Area of Science:

  • Reproductive Biology
  • Genetics
  • Developmental Biology

Background:

  • Genomic instability is prevalent in early human embryo development, manifesting as aneuploidy, mosaicism, and copy number variants (CNVs).
  • Both age-dependent meiotic and age-independent mitotic errors contribute to genomic instability in embryos.
  • Telomere attrition, a known factor in somatic cell genomic instability, may also affect preimplantation embryos.

Purpose of the Study:

  • To investigate the role of telomere dynamics and repair mechanisms in early embryo genomic instability.
  • To understand the dimorphic telomere dynamics between male and female gametes and their impact on embryonic development.
  • To explore how inefficient telomere reconstitution in cleavage stage embryos contributes to genomic alterations.

Main Methods:

  • Analysis of telomere dynamics during gametogenesis in males and females.
  • Assessment of telomerase activity in oocytes and early embryos.
  • Investigation of DNA repair pathways, such as Non-Homologous End Joining (NHEJ) and Alternative Lengthening of Telomeres (ALT), in cleavage stage embryos.

Main Results:

  • Sperm telomeres lengthen with paternal age, while oocyte telomeres are short.
  • Oocytes and early embryos exhibit low telomerase activity.
  • Telomere attrition in oocytes leads to meiotic dysfunction.
  • Cleavage stage embryos utilize NHEJ and ALT for telomere reconstitution, but these processes are linked to genomic instability, including mosaicism and CNVs.

Conclusions:

  • Telomere attrition and inefficient repair mechanisms are key drivers of genomic instability in early human embryos.
  • The distinct telomere dynamics in male and female gametes, coupled with low telomerase activity in oocytes and embryos, create a predisposition to genomic errors.
  • While ALT can reconstitute telomeres, it also increases the risk of genomic instability during crucial early developmental stages.