DNA repair decline during mouse spermiogenesis results in the accumulation of heritable DNA damage.

@article{Marchetti2008DNARD,
  title={DNA repair decline during mouse spermiogenesis results in the accumulation of heritable DNA damage.},
  author={Francesco Marchetti and Andrew J Wyrobek},
  journal={DNA repair},
  year={2008},
  volume={7 4},
  pages={
          572-81
        }
}

DNA repair efficiency in germ cells and early mouse embryos and consequences for radiation-induced transgenerational genomic damage

There is growing evidence that implicates DNA damage carried by the fertilizing gamete as a mediator of postfertilization processes that contribute to genomic instability in subsequent generations.

Paternal DNA damage resulting from various sperm treatments persists after fertilization and is similar before and after DNA replication.

Evidence is provided that subjecting sperm to DNA damage-inducing treatments results in degradation of highly condensed sperm chromatin when it is still packed within the sperm head, and that this DNA damage persists after fertilization.

Oxidative stress in sperm affects the epigenetic reprogramming in early embryonic development

It is shown that fertilization using sperm exposed to oxidative stress caused a major developmental arrest at the time of embryonic genome activation and the recruitment of XRCC1 to damaged paternal pronuclei indicates that oxidative DNA lesions drive BER to repair DNA at the expense of DNA demethylation.

Direct and delayed X‐ray‐induced DNA damage in male mouse germ cells

The results suggest that proliferating spermatogonia retain a memory of the radiation insult that is recognized at a later developmental stage and activates a process leading to DNA fragmentation.

DNA Double Strand Break Response and Limited Repair Capacity in Mouse Elongated Spermatids

The genetic mutant analysis suggests that an incomplete or defective meiotic recombinational repair of Spo11-induced DSBs may lead to a carry-over of the DSB damage or induce a delayed nuclear fragmentation during the sensitive programmed chromatin remodeling occurring in elongated spermatids.

Meiotic interstrand DNA damage escapes paternal repair and causes chromosomal aberrations in the zygote by maternal misrepair

Treatment of male mice with melphalan, a bifunctional alkylating agent widely used in chemotherapy, induces DNA lesions during male mouse meiosis that persist unrepaired as germ cells progress through DNA repair-competent phases of spermatogenic development, highlighting the importance of both pre- and post-fertilization DNA repair in assuring the genomic integrity of the conceptus.

Assessment of Sperm DNA Integrity and Implications for the Outcome of ICSI Treatments

Damage to sperm DNA is likely to result in poor implantation rates or miscarriage, and therefore leads to a reduction in clinical pregnancy rates and the repair by the oocyte may result in malformations or diseases in the offspring.

Rad54/Rad54B deficiency is associated to increased chromosome breakage in mouse spermatocytes

The results provide the first evidence of the role of Rad54/Rad54B in the maintenance of a stable karyotype during male meiosis, and suggest that Rad54-deficient animals may impact on the DNA integrity of developing mouse gametes.

Genetic Instability and Chromatin Remodeling in Spermatids

It is proposed that the chromatin remodeling in spermatids offers a proper context for the induction of de novo polymorphism and structural variations that can be transmitted to the next generation.

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