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Stalled Pol II: search and rescue, or search and destroy?

Damage to DNA can block transcription of essential genes: RNA polymerase II (Pol II) encounters the lesion and simply stalls. To get round this problem, cells have developed an efficient form of transcription-coupled DNA repair (TCR). The mammalian protein Cockayne syndrome B (CSB) and its yeast counterpart Rad26 are thought to be central to TCR; however, its molecular details have remained obscure. In a Hypothesis on p. 447, Jesper Svejstrup discusses recent work that has shed light on the TCR mechanism, proposing that a stalled Pol II can be dealt with in several different ways. Studies of CSB/Rad26 relatives, for example, suggest that these enzymes are DNA translocases that can move proteins along DNA. Other experiments indicate that Pol II is ubiquity lated and degraded in response to DNA damage and implicate Rad26 and a novel protein, Def1, in this process. Svejstrup therefore proposes a model for TCR in which CSB/Rad26 initially tries to push Pol II past a roadblock such as DNA damage but, if this fails, induces Def1-dependent ubiquitylation and degradation of Pol II so that the repair machinery can access the lesion.

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Rescue of arrested RNA polymerase II complexes

Jesper Q. Svejstrup
JCS 2003 116: 447-451. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?