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Regulation of ultraviolet light-induced gene expression by gene size

Bruce C McKay1, Lawton J Stubbert, Casey C Fowler

  • 1Centre for Cancer Therapeutics, Ottawa Regional Cancer Centre, Department of Radiology, University of Ottawa, 503 Smyth Road, Ottawa, ON, Canada K1C 5T5. bmckay@ohri.ca

Proceedings of the National Academy of Sciences of the United States of America
|April 17, 2004
PubMed

Insights

UV radiation damages DNA, impacting gene expression. Researchers found UV light shifts gene activation towards smaller genes, acting as a molecular dosimeter to eliminate damaged cells.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Ultraviolet (UV) light exposure causes DNA damage, triggering a complex cellular response involving gene expression changes.
  • The precise mechanisms by which cells sense DNA damage extent and modulate UV-induced gene expression remain incompletely understood.
  • Transcription-blocking DNA damage induced by UV light is more probable in larger gene loci and at higher UV doses.

Purpose of the Study:

  • To investigate how cells sense DNA damage and appropriately alter UV-induced gene expression.
  • To explore the relationship between UV dose, gene locus characteristics, and p53-mediated gene expression.
  • To elucidate the role of gene size and intron structure in UV-responsive gene regulation.

Main Methods:

  • Utilized colon carcinoma cells expressing a temperature-sensitive p53 variant.
  • Applied UV irradiation and analyzed gene expression changes using oligonucleotide microarray analysis.
  • Correlated UV dose with the number and characteristics of p53-induced genes.

Main Results:

  • The number of p53-induced genes decreased in a UV dose-dependent manner.
  • A significant shift in the spectrum of p53-induced genes was observed, favoring compact genes with fewer and smaller introns.
  • Compact p53 target genes included those encoding proapoptotic proteins, while larger genes encoded negative regulators of p53 and apoptosis.

Conclusions:

  • The observed shift in UV-responsive gene expression, influenced by UV lesions affecting transcription, functions as a molecular dosimeter.
  • This mechanism ensures the elimination of cells with irreparable, transcription-blocking DNA damage.
  • Gene locus size and intron structure play a critical role in cellular UV damage response and apoptosis.

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