Effects of UV Damage on Apoptosis and Cell Growth Arrest in XPv Cell Lines
Number: 00S13. Issue: Spring 2000
Author[s]:
Aubrey Chung Yan Lau
Integrative Biology Major, College of Letters and Science, University of California, Berkeley
James C. Bartholomew
Physical Biosciences Division, Lawrence Berkeley National Laboratory
Keywords:
Xeroderma pigmentosum variant (XPv) cells, apoptosis, cell growth arrest, annexin-V assay, flow cytometry, cell cycle analysis
Abstract:
Xeroderma pigmentosum (XP) is a disease that results from a genetic defect in one of many genes. Patients with this condition are ultrasensitive to UV light and are more susceptible to getting skin cancer. Previous studies have shown that many of the genetic lesions that result in XP are in genes that code for components of the DNA repair pathway. One group of patients called XP variants (XPv) has lesions in a gene that does not alter DNA repair capacity. Upon UV damage, XPv cells go into apoptosis, even though they are equipped with a functional DNA repair system. The purpose of this study is to examine differences in response to UV damage between XPv cells and normal cells that may explain the mutant conditions in XPv individuals. We analyzed the effect of UV irradiation on the growth of XPv and normal cells in culture. Using an assay specific for apoptosis (annexin V) we also looked at how the two types of cells entered programmed cell death after UV irradiation. Results from these analyses support the notion that the reasons for XPv cells? tendency to go into apoptosis instead of initiating DNA repair may be caused by the loss of their ability to stop cell proliferation at the G1 phase following UV damage. This defect leads to fatal DNA lesions that eventually cause the cells to go into apoptosis.
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