Selective removal of transcription-blocking DNA damage from the transcribed strand of the mammalian DHFR gene

Isabel Mellon; Graciela Spivak; Philip C. Hanawalt

doi:10.1016/0092-8674(87)90151-6

Selective removal of transcription-blocking DNA damage from the transcribed strand of the mammalian DHFR gene

Isabel Mellon
, Graciela Spivak
, Philip C. Hanawalt

Producción científica: Article › revisión exhaustiva

1125 Citas (Scopus)

Resumen

We find a dramatic difference in the efficiency of removal of UV-induced pyrimidine dimers from the transcribed and nontranscribed strands of the dihydrofolate reductase (DHFR) gene in cultured hamster and human cells. In hamster cells, 80% of the dimers are removed from the transcribed strand in 4 hr, but little repair occurs in the nontranscribed strand even after 24 hr. In human cells, repair is significantly faster in the transcribed strand than in the other strand. Furthermore, in the 5' flanking region of the human DHFR gene, selective rapid repair occurs in the opposite DNA strand relative to the transcribed strand of the DHFR gene. This strand is thought to serve as a template for transcription of a divergent transcript. These results have important implications for excision repair pathways and mutagenesis in mammalian cells.

Idioma original	English
Páginas (desde-hasta)	241-249
Número de páginas	9
Publicación	Cell
Volumen	51
N.º	2
DOI	https://doi.org/10.1016/0092-8674(87)90151-6
Estado	Published - oct 23 1987

Nota bibliográfica

Funding Information:
We thank C. A. Smith and A. K. Ganesan for many helpful discussions and critical readings of the manuscript, E. Wauthier for preparation of T4 endonuclease V, G. Attardi for 6A3 cells and human DHFR plasmids, R. T. Schimke for Bll cells and methotrexate, and L. Chasin for the CHO DHFR plasmid. This work was supported by a grant from the National Cancer Institute (CA35744) and an American Cancer Society Postdoctoral Fellowship (PF-2730) to I. Mellon.

Financiación

We thank C. A. Smith and A. K. Ganesan for many helpful discussions and critical readings of the manuscript, E. Wauthier for preparation of T4 endonuclease V, G. Attardi for 6A3 cells and human DHFR plasmids, R. T. Schimke for Bll cells and methotrexate, and L. Chasin for the CHO DHFR plasmid. This work was supported by a grant from the National Cancer Institute (CA35744) and an American Cancer Society Postdoctoral Fellowship (PF-2730) to I. Mellon.

Financiadores	Número del financiador
American Cancer Society	PF-2730
National Childhood Cancer Registry – National Cancer Institute	R01CA035744

ASJC Scopus subject areas

General Biochemistry, Genetics and Molecular Biology

Acceder al documento

10.1016/0092-8674(87)90151-6

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@article{bc77e7eb24f940f99c9e62efb6be22c6,

title = "Selective removal of transcription-blocking DNA damage from the transcribed strand of the mammalian DHFR gene",

abstract = "We find a dramatic difference in the efficiency of removal of UV-induced pyrimidine dimers from the transcribed and nontranscribed strands of the dihydrofolate reductase (DHFR) gene in cultured hamster and human cells. In hamster cells, 80\% of the dimers are removed from the transcribed strand in 4 hr, but little repair occurs in the nontranscribed strand even after 24 hr. In human cells, repair is significantly faster in the transcribed strand than in the other strand. Furthermore, in the 5' flanking region of the human DHFR gene, selective rapid repair occurs in the opposite DNA strand relative to the transcribed strand of the DHFR gene. This strand is thought to serve as a template for transcription of a divergent transcript. These results have important implications for excision repair pathways and mutagenesis in mammalian cells.",

author = "Isabel Mellon and Graciela Spivak and Hanawalt, \{Philip C.\}",

note = "Funding Information: We thank C. A. Smith and A. K. Ganesan for many helpful discussions and critical readings of the manuscript, E. Wauthier for preparation of T4 endonuclease V, G. Attardi for 6A3 cells and human DHFR plasmids, R. T. Schimke for Bll cells and methotrexate, and L. Chasin for the CHO DHFR plasmid. This work was supported by a grant from the National Cancer Institute (CA35744) and an American Cancer Society Postdoctoral Fellowship (PF-2730) to I. Mellon.",

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doi = "10.1016/0092-8674(87)90151-6",

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AU - Mellon, Isabel

AU - Spivak, Graciela

AU - Hanawalt, Philip C.

N1 - Funding Information: We thank C. A. Smith and A. K. Ganesan for many helpful discussions and critical readings of the manuscript, E. Wauthier for preparation of T4 endonuclease V, G. Attardi for 6A3 cells and human DHFR plasmids, R. T. Schimke for Bll cells and methotrexate, and L. Chasin for the CHO DHFR plasmid. This work was supported by a grant from the National Cancer Institute (CA35744) and an American Cancer Society Postdoctoral Fellowship (PF-2730) to I. Mellon.

PY - 1987/10/23

Y1 - 1987/10/23

N2 - We find a dramatic difference in the efficiency of removal of UV-induced pyrimidine dimers from the transcribed and nontranscribed strands of the dihydrofolate reductase (DHFR) gene in cultured hamster and human cells. In hamster cells, 80% of the dimers are removed from the transcribed strand in 4 hr, but little repair occurs in the nontranscribed strand even after 24 hr. In human cells, repair is significantly faster in the transcribed strand than in the other strand. Furthermore, in the 5' flanking region of the human DHFR gene, selective rapid repair occurs in the opposite DNA strand relative to the transcribed strand of the DHFR gene. This strand is thought to serve as a template for transcription of a divergent transcript. These results have important implications for excision repair pathways and mutagenesis in mammalian cells.

AB - We find a dramatic difference in the efficiency of removal of UV-induced pyrimidine dimers from the transcribed and nontranscribed strands of the dihydrofolate reductase (DHFR) gene in cultured hamster and human cells. In hamster cells, 80% of the dimers are removed from the transcribed strand in 4 hr, but little repair occurs in the nontranscribed strand even after 24 hr. In human cells, repair is significantly faster in the transcribed strand than in the other strand. Furthermore, in the 5' flanking region of the human DHFR gene, selective rapid repair occurs in the opposite DNA strand relative to the transcribed strand of the DHFR gene. This strand is thought to serve as a template for transcription of a divergent transcript. These results have important implications for excision repair pathways and mutagenesis in mammalian cells.

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JF - Cell

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Selective removal of transcription-blocking DNA damage from the transcribed strand of the mammalian DHFR gene

Resumen

Nota bibliográfica

Financiación

ASJC Scopus subject areas

Acceder al documento

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Huella

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