Increased UV light sensitivity in transgenic Drosophila expressing the antisense XPD homolog.
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.
Sandoval
M T
MT
Department of Genetics and Molecular Physiology, Institute of Biotechnology, Universidad Nacional Autónoma de México, Cuernavaca, Morelos.
Zurita
M
M
D000818:Animals; D030801:Animals, Genetically Modified; D004265:DNA Helicases; D004268:DNA-Binding Proteins; D004331:Drosophila melanogaster / Q000235:genetics / Q000528:radiation effects*; D011506:Proteins / Q000235:genetics*; D016372:RNA, Antisense / Q000096:biosynthesis*; D011836:Radiation Tolerance / Q000235:genetics*; D014157:Transcription Factors; D014466:Ultraviolet Rays / Q000009:adverse effects*; D051759:Xeroderma Pigmentosum Group D Protein
D004268:DNA-Binding Proteins; D011506:Proteins; D016372:RNA, Antisense; D014157:Transcription Factors; D004265:DNA Helicases; D051759:Xeroderma Pigmentosum Group D Protein