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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 order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
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Tolerance thresholds underlie responses to DNA damage during germline development.

Gloria Jansen1,2, Daniel Gebert1,2, Tharini Ravindra Kumar1

  • 1Department of Genetics, University of Cambridge, Cambridge CB2 3EH, United Kingdom.

Genes & Development
|July 25, 2024
PubMed
Summary

Germ cells unexpectedly tolerate DNA damage from transposable elements (TEs) by developing resistance thresholds. This protects genome integrity during germline development, even with significant DNA double-strand breaks (DSBs).

Keywords:
CRISPR–Cas9DNA damageDrosophila melanogasterP-elementdouble-strand breakgenome integritygermline developmenthybrid dysgenesismeiosistransposable element

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Area of Science:

  • Developmental Biology
  • Genetics
  • Molecular Biology

Background:

  • Transposable elements (TEs) are active in the germline, potentially disrupting genes and impairing germ cell viability.
  • P-M hybrid dysgenesis in Drosophila, caused by P-element transposons, leads to sterility but shows few new TE insertions in germ cells despite DNA damage.

Purpose of the Study:

  • To investigate why germ cells accumulate DNA double-strand breaks (DSBs) without new transposable element (TE) insertions during P-M hybrid dysgenesis.
  • To determine the impact of DSBs on germ cell viability and the role of DNA damage tolerance thresholds in germline development.

Main Methods:

  • Utilized an engineered CRISPR-Cas9 system to induce DNA double-strand breaks (DSBs) at silenced P-elements and noncoding sequences in Drosophila.
  • Assessed germ cell loss and viability in response to induced DSBs at different developmental stages (mitotic vs. meiotic transition).

Main Results:

  • Generating DSBs in silenced P-elements or noncoding DNA induced germ cell loss, independent of gene disruption.
  • Mitotic germ cells exhibited dosage-dependent sensitivity to DSBs, leading to cell cycle arrest and loss.
  • Germ cells became more tolerant to DSBs after the mitotic-to-meiotic transition, allowing oogenesis to proceed despite accumulated genome damage.

Conclusions:

  • DNA damage tolerance thresholds are critical for safeguarding genome integrity during germline development.
  • Germ cell sensitivity to DSBs varies with developmental stage, with post-mitotic cells showing increased tolerance.