[en] The pathway of nucleotide excision repair (NER) consists of two sub pathways i.e. global genome repair (GGR) and transcription coupled repair (TCR). GGR removes DNA damage from the genome overall while TCR is responsible for the accelerated removal of lesions from the transcribed strand of expressed genes. We have analysed the assembly of the GGR complex in normal and DNA repair-deficient (xeroderma pigmentosum) human cells, employing a technique of local UV-irradiation and immuno staining. Local exposure of small parts of the nucleus of normal human cells causes rapid accumulation of NER factors to sites of local damage. This accumulation disappears after about 2 to 3 hours, a time frame which is similar to that observed for the repair of 6-4 photo products. Comparison of cells from various xeroderma pigmentosum complementation groups showed that XPC is essential for NER complex formation at sites of local damage. Furthermore, DDB2 which is deficient in XP-E cells, binds to DNA damage before XPC and facilitates NER complex formation. Recognition of UV-induced DNA damage during TCR does not need the presence of XPC and is probably mediated by RNA polymerase II (RNAPII) stalled at the site of a lesion. Upon removal of the lesion transcription is resumed. This is in line with the observation that Cockayne syndrome cells are unable to carry out TCR and are also defective in restart of transcription following inhibition after UV-exposure. Since it has been shown that TCR is also observed after introduction of base damage by exposure to ionising radiation, we investigated the frequency of base damage as a function of dose following X-rays. Subsequently, we determined the inhibition of RNA synthesis at a dose of X-rays causing equal frequency of base damage as found after exposure to 10 J/m2 UV-radiation. The results show that inhibition of transcription following exposure to X-rays is very limited and much less than observed after exposure to UV-radiation when compared at equal levels of DNA base damage. Furthermore, CS cells behave in this respect in the same way as normal cells or cells defective in Ligase 4. Analysis of cell free extracts showed that the unphosphorylated form of RNAPII disappears after UV-radiation but not following exposure to X-rays. These data suggest that TCR of base damage induced by X-rays is not dependent on stalling of RNAPII at the site of a lesion