Abstract

The severe hereditary progeroid disorder Cockayne syndrome is a consequence of a defective transcription‐coupled repair (TCR) pathway. This special mode of DNA repair aids a RNA polymerase that is stalled by a DNA lesion in the template and ensures efficient DNA repair to permit resumption of transcription and prevent cell death. Although some key players in TCR, such as the Cockayne syndrome A (CSA) and B (CSB) proteins have been identified, the exact molecular mechanism still remains illusive. A recent report provides new unexpected insights into TCR in yeast.1 The identification and characterisation of a novel protein co‐purifying with the yeast homologue of CSB (Rad26) imposes reassessment of our current understanding of TCR in yeast. What about humans? BioEssays 24:780–784, 2002. © 2002 Wiley Periodicals, Inc.