Radiation sensitivity of the gastrula-stage embryo: Chromosome aberrations and mutation induction in lacZ transgenic mice: The roles of DNA double-strand break repair systems.

@article{Jacquet2015RadiationSO,
  title={Radiation sensitivity of the gastrula-stage embryo: Chromosome aberrations and mutation induction in lacZ transgenic mice: The roles of DNA double-strand break repair systems.},
  author={Paul Jacquet and Paul P W van Buul and Annemarie van Duijn-Goedhart and Karine Reynaud and Jasmine Buset and Mieke Neefs and Arlette Michaux and Pieter Monsieurs and Peter de Boer and Sarah Baatout},
  journal={Mutation research. Genetic toxicology and environmental mutagenesis},
  year={2015},
  volume={792},
  pages={26-34}
}
At the gastrula phase of development, just after the onset of implantation, the embryo proper is characterized by extremely rapid cell proliferation. The importance of DNA repair is illustrated by embryonic lethality at this stage after ablation of the genes involved. Insight into mutation induction is called for by the fact that women often do not realize they are pregnant, shortly after implantation, a circumstance which may have important consequences when women are subjected to medical… CONTINUE READING

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The compromised developmental profile after doses up to 2.5Gy likely is caused by both apoptosis and later cell death due to large deletions .
The compromised developmental profile after doses up to 2.5Gy likely is caused by both apoptosis and later cell death due to large deletions .
Radiation sensitivity of the gastrula - stage embryo : Chromosome aberrations and mutation induction in lacZ transgenic mice : The roles of DNA double - strand break repair systems .
The compromised developmental profile after doses up to 2.5Gy likely is caused by both apoptosis and later cell death due to large deletions .
Gastrula embryos are unusual in that they are low in exchange induction , even after compromised HR .
Gastrula embryos were radiation sensitive in the pUR288 shuttle vector assay , giving the highest mutation induction ever reported for this genetic toxicology model .
At the gastrula phase of development , just after the onset of implantation , the embryo proper is characterized by extremely rapid cell proliferation .
Radiation sensitivity of the gastrula - stage embryo : Chromosome aberrations and mutation induction in lacZ transgenic mice : The roles of DNA double - strand break repair systems .
We screened gastrula embryos for DNA synthesis , nuclear morphology , growth , and chromosome aberrations ( CA ) shortly after irradiation with doses up to 2.5Gy .
Our data indicate a distinct radiation - sensitive profile of gastrula embryos , including some stage - specific aspects that are not as yet understood .
Radiation sensitivity of the gastrula - stage embryo : Chromosome aberrations and mutation induction in lacZ transgenic mice : The roles of DNA double - strand break repair systems .
Radiation sensitivity of the gastrula - stage embryo : Chromosome aberrations and mutation induction in lacZ transgenic mice : The roles of DNA double - strand break repair systems .
The compromised developmental profile after doses up to 2.5Gy likely is caused by both apoptosis and later cell death due to large deletions .
The compromised developmental profile after doses up to 2.5Gy likely is caused by both apoptosis and later cell death due to large deletions .
The compromised developmental profile after doses up to 2.5Gy likely is caused by both apoptosis and later cell death due to large deletions .
In order to obtain an insight into the importance of DNA repair for CA induction , we included mutants for the non - homologous end joining ( NHEJ ) and homologous recombination repair ( HRR ) pathways , as well as Parp1-/- and p53+/- embryos .
In order to obtain an insight into the importance of DNA repair for CA induction , we included mutants for the non - homologous end joining ( NHEJ ) and homologous recombination repair ( HRR ) pathways , as well as Parp1-/- and p53+/- embryos .
In order to obtain an insight into the importance of DNA repair for CA induction , we included mutants for the non - homologous end joining ( NHEJ ) and homologous recombination repair ( HRR ) pathways , as well as Parp1-/- and p53+/- embryos .
In order to obtain an insight into the importance of DNA repair for CA induction , we included mutants for the non - homologous end joining ( NHEJ ) and homologous recombination repair ( HRR ) pathways , as well as Parp1-/- and p53+/- embryos .
In order to obtain an insight into the importance of DNA repair for CA induction , we included mutants for the non - homologous end joining ( NHEJ ) and homologous recombination repair ( HRR ) pathways , as well as Parp1-/- and p53+/- embryos .
In order to obtain an insight into the importance of DNA repair for CA induction , we included mutants for the non - homologous end joining ( NHEJ ) and homologous recombination repair ( HRR ) pathways , as well as Parp1-/- and p53+/- embryos .
In order to obtain an insight into the importance of DNA repair for CA induction , we included mutants for the non - homologous end joining ( NHEJ ) and homologous recombination repair ( HRR ) pathways , as well as Parp1-/- and p53+/- embryos .
In order to obtain an insight into the importance of DNA repair for CA induction , we included mutants for the non - homologous end joining ( NHEJ ) and homologous recombination repair ( HRR ) pathways , as well as Parp1-/- and p53+/- embryos .
In order to obtain an insight into the importance of DNA repair for CA induction , we included mutants for the non - homologous end joining ( NHEJ ) and homologous recombination repair ( HRR ) pathways , as well as Parp1-/- and p53+/- embryos .
In order to obtain an insight into the importance of DNA repair for CA induction , we included mutants for the non - homologous end joining ( NHEJ ) and homologous recombination repair ( HRR ) pathways , as well as Parp1-/- and p53+/- embryos .
In order to obtain an insight into the importance of DNA repair for CA induction , we included mutants for the non - homologous end joining ( NHEJ ) and homologous recombination repair ( HRR ) pathways , as well as Parp1-/- and p53+/- embryos .
In order to obtain an insight into the importance of DNA repair for CA induction , we included mutants for the non - homologous end joining ( NHEJ ) and homologous recombination repair ( HRR ) pathways , as well as Parp1-/- and p53+/- embryos .
In order to obtain an insight into the importance of DNA repair for CA induction , we included mutants for the non - homologous end joining ( NHEJ ) and homologous recombination repair ( HRR ) pathways , as well as Parp1-/- and p53+/- embryos .
In order to obtain an insight into the importance of DNA repair for CA induction , we included mutants for the non - homologous end joining ( NHEJ ) and homologous recombination repair ( HRR ) pathways , as well as Parp1-/- and p53+/- embryos .
In order to obtain an insight into the importance of DNA repair for CA induction , we included mutants for the non - homologous end joining ( NHEJ ) and homologous recombination repair ( HRR ) pathways , as well as Parp1-/- and p53+/- embryos .
In order to obtain an insight into the importance of DNA repair for CA induction , we included mutants for the non - homologous end joining ( NHEJ ) and homologous recombination repair ( HRR ) pathways , as well as Parp1-/- and p53+/- embryos .
In order to obtain an insight into the importance of DNA repair for CA induction , we included mutants for the non - homologous end joining ( NHEJ ) and homologous recombination repair ( HRR ) pathways , as well as Parp1-/- and p53+/- embryos .
In order to obtain an insight into the importance of DNA repair for CA induction , we included mutants for the non - homologous end joining ( NHEJ ) and homologous recombination repair ( HRR ) pathways , as well as Parp1-/- and p53+/- embryos .
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