Abstract
The XPD gene is required for excision repair of UV-damaged DNA and is an important component of nucleotide excision repair (NER). Mutations in the XPD gene generate the cancer-prone syndrome xeroderma pigmentosum, Cockayne's syndrome, and trichothiodystrophy. XPD is a component of the TFIIH transcription factor, which is essential for RNA polymerase II elongation. In this work, we report the construction of transgenic flies overexpressing the antisense RNA of the Drosophila melanogaster XPD homolog (DmXPD). These flies show an increased sensitivity to UV radiation compared with the wild-type. This is an expected phenotype if the XPD function is affected and indicates that the antisense approach may be an alternative in the study of TFIIH functions in Drosophila.
