A C. elegans homolog of the Cockayne syndrome complementation group A gene

DNA Repair (Amst). 2014 Dec:24:57-62. doi: 10.1016/j.dnarep.2014.09.011. Epub 2014 Nov 8.


Cockayne syndrome (CS) is a debilitating and complex disorder that results from inherited mutations in the CS complementation genes A and B, CSA and CSB. The links between the molecular functions of the CS genes and the complex pathophysiology of CS are as of yet poorly understood and are the subject of intense debate. While mouse models reflect the complexity of CS, studies on simpler genetic models might shed new light on the consequences of CS mutations. Here we describe a functional homolog of the human CSA gene in Caenorhabditis elegans. Similar to its human counterpart, mutations in the nematode csa-1 gene lead to developmental growth defects as a consequence of DNA lesions.

Keywords: C. elegans; Cockayne syndrome; Nucleotide excision repair.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Caenorhabditis elegans / drug effects
  • Caenorhabditis elegans / genetics*
  • Caenorhabditis elegans / growth & development
  • Caenorhabditis elegans / radiation effects
  • Caenorhabditis elegans Proteins / genetics*
  • Caenorhabditis elegans Proteins / metabolism
  • DNA Damage / radiation effects
  • DNA Repair / genetics
  • DNA Repair / radiation effects
  • DNA Repair Enzymes / genetics*
  • DNA Repair Enzymes / metabolism
  • Female
  • Mutation
  • Polycyclic Sesquiterpenes
  • Sequence Homology, Amino Acid
  • Sesquiterpenes
  • Transcription Factors / genetics*
  • Transcription Factors / metabolism
  • Ultraviolet Rays


  • Caenorhabditis elegans Proteins
  • ERCC8 protein, human
  • Polycyclic Sesquiterpenes
  • Sesquiterpenes
  • Transcription Factors
  • illudin M
  • DNA Repair Enzymes