Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Selective DNA repair in active genes.

P C Hanawalt1

  • 1Department of Biological Sciences, Stanford University, CA 94305-5020.

Acta Biologica Hungarica
|January 1, 1990
PubMed
Summary

Mammalian cells show varied DNA repair efficiency based on DNA sequence location. Active genes like DHFR are repaired faster, especially on transcribed strands, ensuring cell survival and UV resistance.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Regulation of nucleotide excision repair in bacteria and mammalian cells.

Cold Spring Harbor symposia on quantitative biology·2003
Same author

Revisiting the rodent repairadox.

Environmental and molecular mutagenesis·2001
Same author

The SOS-dependent upregulation of uvrD is not required for efficient nucleotide excision repair of ultraviolet light induced DNA photoproducts in Escherichia coli.

Mutation research·2001
Same author

Spatially localized generation of nucleotide sequence-specific DNA damage.

Proceedings of the National Academy of Sciences of the United States of America·2001
Same author

Effect of thymine glycol on transcription elongation by T7 RNA polymerase and mammalian RNA polymerase II.

The Journal of biological chemistry·2001
Same author

Participation of recombination proteins in rescue of arrested replication forks in UV-irradiated Escherichia coli need not involve recombination.

Proceedings of the National Academy of Sciences of the United States of America·2001

Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • DNA damage consequences depend on location relative to genes.
  • Understanding DNA sequence accessibility in chromatin to damage and repair is crucial.
  • Mammalian cells exhibit intragenomic heterogeneity in DNA repair.

Purpose of the Study:

  • To investigate the rules governing DNA sequence accessibility to damage and repair in mammalian chromatin.
  • To map the efficiency of pyrimidine dimer removal in the active dihydrofolate reductase (DHFR) gene.
  • To compare DNA repair efficiency in active versus silent genes and transcribed versus non-transcribed DNA strands.

Main Methods:

  • Mapping pyrimidine dimer removal efficiency in the DHFR gene in Chinese hamster ovary (CHO) and human cells.
  • Comparing repair rates in active genes (DHFR, c-abl) versus silent sequences (alpha DNA, c-mos).
  • Assessing replicative bypass of psoralen monoadducts and interstrand crosslinks in the human DHFR gene.

Main Results:

  • Repair is significantly more efficient within the active DHFR gene than in flanking silent sequences or the overall genome.
  • Pyrimidine dimer removal is higher in transcribed DNA strands compared to non-transcribed strands in the DHFR gene (both CHO and human cells).
  • Active protooncogenes (c-abl) are repaired more efficiently than inactive ones (c-mos).
  • Replicative bypass of psoralen monoadducts is efficient, but not of interstrand crosslinks.

Conclusions:

  • Preferential repair of active and essential genes like DHFR may explain higher UV resistance in rodent cells despite lower overall repair efficiency.
  • A potential coupling of excision-repair complexes to transcription machinery ensures rapid removal of transcription-blocking lesions in active genes.
  • Cell-specific differences in DNA repair and protooncogene regulation may influence carcinogenic responses.
  • Most DNA lesions, except crosslinks, can be bypassed during replication, but removal from essential transcribed sequences is vital for cell viability.

Related Experiment Videos