{
  "id": 3275766,
  "title": "XRCC1 Enables the Efficient Local Search for DNA Damage by DNA Polymerase Beta",
  "url": "https://urgent.news/2026/08/25/xrcc1-enables-the-efficient-local-search-for-dna-damage-by-dna",
  "topic": "science",
  "section": "Science",
  "published": "2026-08-25T00:00:00.000Z",
  "source": {
    "name": "bioRxiv",
    "slug": "biorxiv",
    "url": "https://www.biorxiv.org/content/10.64898/2026.08.24.746741v1?rss=1"
  },
  "original_language": "en",
  "account": "Oxidative DNA damage can threaten the stability of an organism's genome, as it may lead to mutations and instability. Cells combat this issue through base excision repair (BER), a complex process that involves several proteins working together. DNA polymerase beta (pol ) plays a key role in BER, locating single-nucleotide gaps and adding the correct nucleotide, while x-ray repair cross-complementing 1 (XRCC1) acts as a scaffold protein that helps coordinate BER factors at DNA damage sites. Despite XRCC1 enhancing BER efficiency, the exact mechanism remains unclear. Researchers have previously thought that pol {beta} recruits to DNA damage through scanning interactions with undamaged DNA, but this has not been directly observed. The impact of other BER proteins, especially XRCC1, on pol recruitment is also not fully understood. To better understand these processes, researchers used a technique called correlative optical tweezers-fluorescence microscopy to directly observe pol and XRCC1 as they searched for DNA damage. The study reveals that pol locates damage through 3D-diffusion, while XRCC1 displays both 3D- and 1D-diffusion. When the two proteins work together, they change pol's search behavior, enabling it to explore non-damaged DNA using both search mechanisms. The findings show that XRCC1 alters pol {beta}'s search behavior to enhance local damage recognition, offering a possible explanation for how BER factors coordinate lesion detection and processing to maintain genomic stability.",
  "summary": "Oxidative DNA damage is a common threat to genomic integrity, arising from endogenous metabolic processes and environmental exposures. If unrepaired, such oxidative DNA damage promotes mutagenesis and genomic instability. Cells counter this through base excision repair (BER), a multi-step pathway requiring the coordinated action of several proteins. Central to BER, DNA polymerase beta (pol )…",
  "key_points": [],
  "editors_take": null,
  "illustration": null,
  "coverage": {
    "outlets": 1,
    "also_reported_by": []
  },
  "ai_generated": true,
  "disclaimer": "Summaries, key points and the editor’s take are written by software from other outlets’ reporting and may contain errors — always check the linked original."
}