Correction of the ultraviolet light induced DNA-repair defect in xeroderma pigmentosum cells by electroporation of a normal human endonuclease

Gregory J. Tsongalis, W. Clark Lambert, Muriel W. Lambert

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Cell from patients with xeroderma pigmentosum, complementation group A (XPA), are known to be defective in repair of pyrimidine dimers and other forms of damage produced by 254-mm ultraviolet (UVC) radiation. We have isolated a DNA endonuclease, p1 7.6, from the chromatin of normal human lymphoblastoid cells which recognizes damage produced by UVC light, and have introduced this endonuclease into UVC-irradiated XPA cells in culture to determine whether it can restore their markedly deficient DNA repair-related unscheduled DNA synthesis (UDS). Introduction of the normal endonuclease, which recognizes predominantly pyrimidine dimers. but not the corresponding XPA endonuclease into UVC-irradiated XPA cells restored their levels of UDS to approximately 80% of normal values. Electroporation of both the normal and the XPA endonuclease into normal human cells increases UDS is normal cells to higher than normal values. These results indicate that the normal endonuclease can restore UDS in UVC-irradiated XPA cells. They also indicate that XPA cells have an endonuclease capable of increasing the efficiency of repair of UVC damage in normal cells.

Original languageEnglish (US)
Pages (from-to)257-263
Number of pages7
JournalMutation Research Letters
Volume244
Issue number3
DOIs
StatePublished - Jul 1990

Fingerprint

Xeroderma Pigmentosum
Electroporation
Endonucleases
Ultraviolet Rays
DNA Repair
Pyrimidine Dimers
DNA
Reference Values
DNA Repair-Deficiency Disorders
Deoxyribonuclease I
Chromatin
Cell Culture Techniques
Radiation
Light

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Keywords

  • DNA endonucleases
  • Electroporation
  • Ultraviolet light damage
  • Xeroderma pigmentosum

Cite this

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title = "Correction of the ultraviolet light induced DNA-repair defect in xeroderma pigmentosum cells by electroporation of a normal human endonuclease",
abstract = "Cell from patients with xeroderma pigmentosum, complementation group A (XPA), are known to be defective in repair of pyrimidine dimers and other forms of damage produced by 254-mm ultraviolet (UVC) radiation. We have isolated a DNA endonuclease, p1 7.6, from the chromatin of normal human lymphoblastoid cells which recognizes damage produced by UVC light, and have introduced this endonuclease into UVC-irradiated XPA cells in culture to determine whether it can restore their markedly deficient DNA repair-related unscheduled DNA synthesis (UDS). Introduction of the normal endonuclease, which recognizes predominantly pyrimidine dimers. but not the corresponding XPA endonuclease into UVC-irradiated XPA cells restored their levels of UDS to approximately 80{\%} of normal values. Electroporation of both the normal and the XPA endonuclease into normal human cells increases UDS is normal cells to higher than normal values. These results indicate that the normal endonuclease can restore UDS in UVC-irradiated XPA cells. They also indicate that XPA cells have an endonuclease capable of increasing the efficiency of repair of UVC damage in normal cells.",
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Correction of the ultraviolet light induced DNA-repair defect in xeroderma pigmentosum cells by electroporation of a normal human endonuclease. / Tsongalis, Gregory J.; Lambert, W. Clark; Lambert, Muriel W.

In: Mutation Research Letters, Vol. 244, No. 3, 07.1990, p. 257-263.

Research output: Contribution to journalArticle

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AB - Cell from patients with xeroderma pigmentosum, complementation group A (XPA), are known to be defective in repair of pyrimidine dimers and other forms of damage produced by 254-mm ultraviolet (UVC) radiation. We have isolated a DNA endonuclease, p1 7.6, from the chromatin of normal human lymphoblastoid cells which recognizes damage produced by UVC light, and have introduced this endonuclease into UVC-irradiated XPA cells in culture to determine whether it can restore their markedly deficient DNA repair-related unscheduled DNA synthesis (UDS). Introduction of the normal endonuclease, which recognizes predominantly pyrimidine dimers. but not the corresponding XPA endonuclease into UVC-irradiated XPA cells restored their levels of UDS to approximately 80% of normal values. Electroporation of both the normal and the XPA endonuclease into normal human cells increases UDS is normal cells to higher than normal values. These results indicate that the normal endonuclease can restore UDS in UVC-irradiated XPA cells. They also indicate that XPA cells have an endonuclease capable of increasing the efficiency of repair of UVC damage in normal cells.

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