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Author Spotlight: Understanding DNA Damage Response in Mammalian Oocytes and Preimplantation Embryos
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Author Spotlight: Understanding DNA Damage Response in Mammalian Oocytes and Preimplantation Embryos

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Different fates of oocytes with DNA double-strand breaks in vitro and in vivo

Fei Lin1, Xue-Shan Ma, Zhen-Bo Wang

  • 1a State Key Laboratory of Reproductive Biology; Institute of Zoology; Chinese Academy of Sciences ; Beijing , China.

Cell Cycle (Georgetown, Tex.)
|December 9, 2014
PubMed

Insights

Severe DNA double-strand breaks (DSBs) in oocytes delay meiosis resumption and polar body extrusion by activating the spindle assembly checkpoint (SAC). DNA DSBs also lead to chromosome fragmentation and increased oocyte apoptosis in vivo.

Area of Science:

  • Reproductive Biology
  • Cell Biology
  • Genetics

Background:

  • Oocyte maturation involves complex cellular events, including meiosis resumption and chromosome segregation.
  • DNA double-strand breaks (DSBs) can trigger DNA damage checkpoints, affecting cell cycle progression.
  • The impact of severe DNA DSBs on the spindle assembly checkpoint (SAC) during oocyte maturation is not well understood.

Purpose of the Study:

  • To investigate the effects of severe DNA DSBs on oocyte maturation, focusing on the spindle assembly checkpoint (SAC).
  • To examine chromosome integrity and polar body extrusion following DNA damage during in vitro maturation (IVM).
  • To assess the in vivo consequences of DNA DSBs on oocyte yield and viability.

Main Methods:

  • In vitro maturation (IVM) of mouse oocytes with induced severe DNA DSBs.
  • Assessment of germinal vesicle breakdown (GVBD), polar body extrusion (PB1), and meiotic stages (MI, MII).
  • Chromosome spread analysis to evaluate chromosome fragmentation and alignment.
  • In vivo induction of DNA DSBs in superovulated mice to assess oocyte yield and apoptosis.

Main Results:

  • Severe DNA DSBs significantly delayed PB1 extrusion during IVM, with limited extrusion observed at telophase.
  • Approximately 60% of oocytes with DSBs reached the MII stage, but exhibited chromosome fragmentation after GVBD.
  • Delayed PB1 extrusion was attributed to disrupted microtubule-kinetochore attachment and SAC activation.
  • Misaligned chromosome fragments were observed at the first metaphase (MI) stage.
  • In vivo, DNA DSBs reduced oocyte yield and increased oocyte apoptosis.

Conclusions:

  • Severe DNA DSBs disrupt oocyte maturation by activating the SAC and causing chromosome fragmentation.
  • The inactivation of the SAC during the first meiotic metaphase-anaphase transition appears independent of chromosome integrity.
  • DNA DSBs in vivo negatively impact oocyte quantity and quality, potentially leading to apoptosis.
Keywords:
DDR, DNA damage responseDNA double-strand breaksDSBs, DNA double-strand breaksGVBD, germinal vesicle breakdownICL, interstrand crosslinksIVM, in vitro maturationMI, the first metaphaseMII, the second metaphasePB1, first polar bodyPBE, PB1 extrusionSAC, spindle assembly checkpointapoptosismeiosisoocytespindle assembly checkpoint

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