Nucleotide Excision Repair (NER), which removes a variety of helix-distorting 
lesions from DNA, is initiated by two distinct DNA damage-sensing mechanisms. 
Transcription Coupled Repair (TCR) removes damage from the active strand of 
transcribed genes and depends on the SWI/SNF family protein CSB. Global Genome 
Repair (GGR) removes damage present elsewhere in the genome and depends on 
damage recognition by the XPC/RAD23/Centrin2 complex. Currently, it is not well 
understood to what extent both pathways contribute to genome maintenance and 
cell survival in a developing organism exposed to UV light. Here, we show that 
eukaryotic NER, initiated by two distinct subpathways, is well conserved in the 
nematode Caenorhabditis elegans. In C. elegans, involvement of TCR and GGR in 
the UV-induced DNA damage response changes during development. In germ cells and 
early embryos, we find that GGR is the major pathway contributing to normal 
development and survival after UV irradiation, whereas in later developmental 
stages TCR is predominantly engaged. Furthermore, we identify four ISWI/Cohesin 
and four SWI/SNF family chromatin remodeling factors that are implicated in the 
UV damage response in a developmental stage dependent manner. These in vivo 
studies strongly suggest that involvement of different repair pathways and 
chromatin remodeling proteins in UV-induced DNA repair depends on developmental 
stage of cells.