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

Authors
  • Babu, Vipin
  • Hofmann, Kay
  • Schumacher, Björn
Type
Published Article
Journal
DNA repair
Publication Date
Dec 01, 2014
Volume
24
Pages
57–62
Identifiers
DOI: 10.1016/j.dnarep.2014.09.011
PMID: 25453470
Source
Medline
Keywords
License
Unknown

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.

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