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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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Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
Nucleosome remodeling complex
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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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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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Multilayered Reprogramming in Response to Persistent DNA Damage in C. elegans.

Diletta Edifizi1, Hendrik Nolte2, Vipin Babu1

  • 1Institute for Genome Stability in Aging and Disease, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, Cologne 50931, Germany; Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases and Systems Biology of Aging Cologne, University of Cologne, Joseph-Stelzmann-Str. 26, Cologne 50931, Germany.

Cell Reports
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PubMed
Summary
This summary is machine-generated.

DNA damage accelerates aging. This study reveals how DNA repair-deficient worms adapt via metabolic shifts and autophagy, highlighting key signaling pathways involved in organismal DNA damage response.

Keywords:
Caenorhabditis elegansDNA damage responseDNA repairaginglipidomicsnucleotide excision repairproteomics

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Area of Science:

  • Molecular Biology
  • Genetics
  • Aging Research

Background:

  • DNA damage is a key factor in aging and disease.
  • Defects in nucleotide excision repair (NER) cause syndromes with accelerated aging.
  • C. elegans models NER deficiency to study DNA damage impacts.

Purpose of the Study:

  • To comprehensively analyze physiological adaptations to unrepaired DNA damage.
  • To understand the organismal response to DNA damage using multi-omics.
  • To investigate the roles of signaling pathways in DNA damage adaptation.

Main Methods:

  • Proteome, lipidome, and phosphoproteome analysis in NER-deficient C. elegans.
  • UV treatment to induce DNA damage.
  • Comparative analysis of wild-type and NER-deficient models.

Main Results:

  • Identified metabolic changes suggesting a tissue maintenance program.
  • Demonstrated an autophagy-mediated proteostatic response to DNA damage.
  • Highlighted the involvement of insulin, EGF, and AMPK-like signaling pathways.

Conclusions:

  • NER deficiency triggers adaptive metabolic and proteostatic responses.
  • Signaling pathways are crucial for orchestrating organismal DNA damage response.
  • This study provides insights into DNA damage response in a whole-organism context.