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Nucleic Acids Research Advance Access originally published online on May 30, 2007
Nucleic Acids Research 2007 35(12):3893-3906; doi:10.1093/nar/gkm373
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Nucleic Acids Research, 2007, Vol. 35, No. 12 3893-3906
© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

A new connection of mRNP biogenesis and export with transcription-coupled repair

Hélène Gaillard, Ralf Erik Wellinger and Andrés Aguilera*

Departamento de Genética, Facultad de Biología, Universidad de Sevilla, and Departamento de Biología Molecular, CABIMER, CSIC-Universidad de Sevilla, Avenida Américo Vespucio s/n, 41092 Sevilla, Spain

*To whom correspondence should be addressed. Tel: +34-954-468-372; Fax: +34-954-461-664; Email: aguilo{at}us.es

Received March 5, 2007. Revised April 27, 2007. Accepted April 27, 2007.

Although DNA repair is faster in the transcribed strand of active genes, little is known about the possible contribution of mRNP biogenesis and export in transcription-coupled repair (TCR). Interestingly, mutants of THO, a transcription complex involved in maintenance of genome integrity, mRNP biogenesis and export, were recently found to be deficient in nucleotide excision repair. In this study we show by molecular DNA repair analysis, that Sub2-Yra1 and Thp1-Sac3, two main mRNA export complexes, are required for efficient TCR in yeast. Careful analysis revealed that THO mutants are also specifically affected in TCR. Ribozyme-mediated mRNA self-cleavage between two hot spots for UV damage showed that efficient TCR does not depend on the nascent mRNA, neither in wild-type nor in mutant cells. Along with severe UV damage-dependent loss in processivity, RNAPII was found binding to chromatin upon UV irradiation in THO mutants, suggesting that RNAPII remains stalled at DNA lesions. Furthermore, Def1, a factor responsible for the degradation of stalled RNAPII, appears essential for the viability of THO mutants subjected to DNA damage. Our results indicate that RNAPII is not proficient for TCR in mRNP biogenesis and export mutants, opening new perspectives on our knowledge of TCR in eukaryotic cells.


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