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Molecular and Cellular Biology Volume 10, 1990 - Issue 9
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Cell Growth and Development

Differential Repair of UV Damage in rad Mutants of Saccharomyces cerevisiae: a Possible Function of G2 Arrest upon UV Irradiation

Carrol Terleth1 Laboratory of Molecular Genetics, Department of Biochemistry, Gorlaeus Laboratories, Leiden University, P.O. Box 9502, 2300 RALeiden, The Netherlands
,
Paul Schenk1 Laboratory of Molecular Genetics, Department of Biochemistry, Gorlaeus Laboratories, Leiden University, P.O. Box 9502, 2300 RALeiden, The Netherlands
,
Raymond Poot1 Laboratory of Molecular Genetics, Department of Biochemistry, Gorlaeus Laboratories, Leiden University, P.O. Box 9502, 2300 RALeiden, The Netherlands
,
Jaap Brouwer1 Laboratory of Molecular Genetics, Department of Biochemistry, Gorlaeus Laboratories, Leiden University, P.O. Box 9502, 2300 RALeiden, The Netherlands
&
Pieter Van De Putte1 Laboratory of Molecular Genetics, Department of Biochemistry, Gorlaeus Laboratories, Leiden University, P.O. Box 9502, 2300 RALeiden, The Netherlands
Pages 4678-4684 | Received 09 Jan 1990, Accepted 23 Apr 1990, Published online: 31 Mar 2023
 
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Abstract

After UV irradiation, the transcriptionally active MATα locus in Saccharomyces cerevisiae is preferentially repaired compared with the inactive HMLα locus. The effect of rad mutations from three different epistasis groups on differential repair was investigated. Three mutants, rad9, radio, and rad24, were impaired in the removal of UV dimers from the inactive HMLα locus, whereas they had generally normal repair of the active MATol locus. Since RAD9 is necessary for G2 arrest after UV irradiation, we propose that the G2 stage plays a role in making the dimers accessible for repair, at least in the repressed HMLol locus.

View correction statement:
Differential Repair of UV Damage in rad Mutants of Saccharomyces cerevisiae: a Possible Function of G2 Arrest upon UV Irradiation

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