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Related Concept Videos

Resonance and Hybrid Structures02:16

Resonance and Hybrid Structures

According to the theory of resonance, if two or more Lewis structures with the same arrangement of atoms can be written for a molecule, ion, or radical, the actual distribution of electrons is an average of that shown by the various Lewis structures.
Resonance Structures and Resonance Hybrids
The Lewis structure of a nitrite anion (NO2−) may actually be drawn in two different ways, distinguished by the locations of the N–O and N=O bonds.
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Related Experiment Video

Updated: May 24, 2026

Dendrochronological Dating and Provenancing of String Instruments
10:26

Dendrochronological Dating and Provenancing of String Instruments

Published on: October 6, 2022

NER and DDR: classical music with new instruments.

Sarah Sertic1, Sara Pizzi, Federico Lazzaro

  • 1Dipartimento di Scienze Biomolecolari e Biotecnologie, Università degli Studi di Milano, Milano, Italy.

Cell Cycle (Georgetown, Tex.)
|March 1, 2012
PubMed
Summary

UV-induced DNA damage triggers the DNA damage response (DDR) and checkpoint activation. Nucleotide excision repair (NER) processing of UV lesions is essential for generating single-stranded DNA (ssDNA) required for checkpoint signaling.

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Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Genetics

Background:

  • Genomic insults activate the DNA damage response (DDR), involving DNA repair and checkpoint surveillance.
  • UV light causes DNA lesions like 6,4 photoproducts (6-4PP) and cyclobutane pyrimidine dimers (CPD), which are repaired by nucleotide excision repair (NER).
  • The mechanism linking NER and DDR activation following UV irradiation is under investigation.

Purpose of the Study:

  • To elucidate how UV-induced DNA damage activates checkpoint kinases.
  • To understand the generation of single-stranded DNA (ssDNA) at UV lesions.
  • To review the connections between NER processing of UV lesions and checkpoint activation.

Main Methods:

  • Review of recent reports on DNA repair and checkpoint activation.
  • Analysis of yeast and human cell models with defects in NER.
  • Investigation of the role of exonuclease 1 in generating ssDNA during NER.

Main Results:

  • Persistent UV lesions block replication fork progression, leading to ssDNA generation.
  • Defects in NER impair checkpoint cascade activation in non-replicating cells.
  • Exonuclease 1 is crucial for generating long ssDNA tracts from NER intermediates.

Conclusions:

  • Processing of UV lesions by NER is a prerequisite for DNA damage checkpoint activation.
  • NER intermediates and exonuclease 1 activity are critical for generating ssDNA that triggers checkpoint signaling.
  • Recent findings highlight novel players in the NER-DDR pathway following UV damage.