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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Groisman, R. et al.

Groisman, Kuraoka, Chevallier, Gaye, Magnaldo, Tanaka, Kisselev, Harel-Bellan, Nakatani,

CSA-dependent degradation of CSB by the ubiquitin-proteasome pathway establishes a link between complementation factors of the Cockayne syndrome.

Mutations in the CSA or CSB complementation genes cause the Cockayne syndrome, a severe genetic disorder that results in patients' death in early adulthood. CSA and CSB act in a transcription-coupled repair (TCR) pathway, but their functional relationship is not understood. We have previously shown that CSA is a subunit of an E3 ubiquitin ligase complex. Here we demonstrate that CSB is a substrate of this ligase: Following UV irradiation, CSB is degraded at a late stage of the repair process in a proteasome- and CSA-dependent manner. Moreover, we demonstrate the importance of CSB degradation for post-TCR recovery of transcription and for the Cockayne syndrome. Our results unravel for the first time the functional relationship between CSA and CSB.[1]

References

CSA-dependent degradation of CSB by the ubiquitin-proteasome pathway establishes a link between complementation factors of the Cockayne syndrome. Groisman, R., Kuraoka, I., Chevallier, O., Gaye, N., Magnaldo, T., Tanaka, K., Kisselev, A.F., Harel-Bellan, A., Nakatani, Y. Genes Dev. (2006) [Pubmed]

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