Jaap Brouwer

TL;DR: The data suggest that RNAPII stalled at a DNA lesion triggers a coordinated rescue mechanism that requires the Rad26–Def1 complex, and that Def1 enables ubiquitination and proteolysis of RNAP II when the lesion cannot be rapidly removed by Rad26-promoted DNA repair.

TL;DR: The phenotype of rad7 and rad16 mutants closely resembles that of human xeroderma pigmentosum complementation group C (XP-C) cells, suggesting that RAD7 and RAD16 in S. cerevisiae function in the same pathway as the XPC gene in human cells.

TL;DR: The experiments show that detoxification by GSH is an effective resistance mechanism against dinuclear platinum compounds, however, the dinuclear complexes are less sensitive towards detoxification compared to cisplatin.

TL;DR: Analysis of yeast double mutants of RAD26 with the global genome repair determinants RAD7 and RAD16 appeared more UV sensitive than the single rad7 or rad16 mutants but not as sensitive as completely NER-deficient mutants, and indicates locus heterogeneity for the dependence of transcription-coupled repair on RAD26.

TL;DR: The cloned RAD16 gene of Saccharomyces cerevisiae complements the UV sensitivity of a rad16 mutant and restores the ability to repair the transcriptionally inactive HML alpha locus that is absent in this mutant.