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

• Published in: DNA repair Vol. 24; pp. 57 - 62
• Main Authors: Babu, Vipin, Hofmann, Kay, Schumacher, Björn
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.12.2014
• Subjects: Animals; C. elegans; Caenorhabditis elegans; Caenorhabditis elegans - drug effects; Caenorhabditis elegans - genetics; Caenorhabditis elegans - growth & development; Caenorhabditis elegans - radiation effects; Caenorhabditis elegans Proteins - genetics; Caenorhabditis elegans Proteins - metabolism; Cockayne syndrome; DNA Damage - radiation effects; DNA Repair - genetics; DNA Repair - radiation effects; DNA Repair Enzymes - genetics; DNA Repair Enzymes - metabolism; Female; Mutation; Nematoda; Nucleotide excision repair; Polycyclic Sesquiterpenes; Sequence Homology, Amino Acid; Sesquiterpenes; Transcription Factors - genetics; Transcription Factors - metabolism; Ultraviolet Rays; Cockayne syndrome; TC-NER; UV; C. elegans; ORF; RNAP II; COFS; nt; UVSS; GG-NER; Nucleotide excision repair; cm; bp; CS; UTR; NGM; CPD; XP; 6–4PP; NER; mJ
• ISSN: 1568-7864; 1568-7856; 1568-7856
• DOI: 10.1016/j.dnarep.2014.09.011

•C. elegans possesses an orthologue for the Cockayne syndrome complementation group A (CSA) gene.•C. elegans csa-1 mutants are sensitive to UV-induced DNA damage during development.•Genetically csa-1 is epistatic to csb-1 and mutant csa-1 enhances UV-sensitivity of global-genome NER defective xpc-1 mutants. 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.