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

Vipin Babu, Kay Hofmann, Björn Schumacher*

*Corresponding author for this work

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)57-62
JournalDNA Repair
Volume24
Early online date08 Nov 2014
DOIs
Publication statusPublished - 01 Dec 2014

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Keywords

  • C. elegans
  • Cockayne syndrome
  • Nucleotide excision repair

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