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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...
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The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...
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Replication protein A1 is essential for DNA damage repair during mammalian oogenesis.

Xiaosu Miao1, Rui Guo2,3, Andrea Williams1

  • 1Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, MA, USA.

Biology of Reproduction
|February 27, 2026
PubMed
Summary
This summary is machine-generated.

Replication protein A (RPA) is crucial for DNA repair in developing oocytes. Its absence causes DNA damage, chromosomal issues, and infertility in female mammals.

Keywords:
DNA damagechromosome alignmentfemale fertilityfolliculogenesisoocyte-specific conditional knockout

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Area of Science:

  • Reproductive biology
  • Molecular genetics
  • Cellular biology

Background:

  • Unrepaired DNA damage in oocytes can lead to genetic abnormalities, miscarriage, and infertility.
  • Replication protein A (RPA) is a vital single-stranded DNA-binding complex involved in DNA processes.

Purpose of the Study:

  • To investigate the novel role of RPA in DNA damage repair during postnatal oocyte development.
  • To understand the consequences of RPA deficiency in oocytes.

Main Methods:

  • Inactivation of RPA1 (replication protein A1) in oocytes using germline-specific Cre drivers (Ddx4-Cre and Zp3-Cre).
  • Assessed RPA complex disassembly, DNA damage, DNA damage response activation, chromosome alignment, and folliculogenesis.
  • Analyzed transcript levels of genes involved in cytoskeleton organization.

Main Results:

  • RPA1 depletion led to RPA complex disassembly and severe DNA damage in GV-stage oocytes.
  • RPA deficiency activated canonical DNA damage response pathways (ATM, ATR, DNA-PK, p53).
  • Chromosome misalignment and impaired folliculogenesis were observed, resulting in reduced oocyte number and female infertility.

Conclusions:

  • RPA plays a critical, previously unrecognized role in DNA damage repair during mammalian oogenesis.
  • RPA is essential for maintaining oocyte genetic integrity and female fertility.