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. 1996 Aug;143(4):1533–1542. doi: 10.1093/genetics/143.4.1533

Mutations in the Yeast Srb2 General Transcription Factor Suppress Hpr1-Induced Recombination and Show Defects in DNA Repair

J L Piruat 1, A Aguilera 1
PMCID: PMC1207418  PMID: 8844143

Abstract

We have obtained genetic and molecular evidence that the hrs2-1 mutation, isolated as a suppressor of the hyperrecombination phenotype of hpr1Δ, is in the SRB2 gene, which encodes a component of the RNA polII holoenzyme. A newly constructed srb2Δ allele restores the wild-type levels of deletions in hpr1Δ cells, indicating that the lack of a functional SRB2 transcription factor suppresses recombination between direct repeats. These results suggest a direct connection between transcription and recombination between DNA repeats. On the other hand, the hrs2-1 mutation (renamed srb2-101), in which Gly(150) has been changed to Asp, makes cells sensitive to long MMS treatments, a phenotype observed for the srb2Δ null allele only in a hpr1Δ background. This indicates that mutations in the basal transcription factor SRB2 impair DNA repair of MMS-induced damage, which adds a new connection between transcription and DNA repair. We discuss the possibility that hpr1-induced deletions occurred as a consequence of a SRB2-dependent stalled or blocked transcription complex.

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Selected References

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