The description of Xeroderma pigmentosum in 1874 introduced the first abnormality associated with XPB/D mutations. The discovery that all the gene mutations in trichothiodystrophy (TTD)had a relationship with the TFIIH complex paved the way for the identification of the relationship between DNA repair and transcription and the genotype-phenotype relationships attributed to XPB and XPD defects. The discovery led to the conclusion that mutations in the human helicase contribute to diverse genetic disorders that exhibit through chromosomal instability, which initiates age-related diseases and cancer. Genetic engineering can significantly enhance the study of the effects of XPD mutations on the functions of the TFIIH complex by allowing researchers to circumvent the XPD defects by overriding the lock-in repair mode to open the promoter. Researchers can develop cell lines supplemented with fetal bovine serum and appropriate antibiotics to study the functioning of the DNA damaged by UV. Genetic engineering is essential in the isolation of genomic DNA from cells exposed to radiation and control cells. Controlled growth of cells would allow the creation of different helicase domains and the cloning of mutant genes to allow the study of the manifestation of the Cockayne syndrome in different environments. Genetic engineering allows the incubation of DNA and incorporation of elements such as geneticin to create a collection of cells that can resist alterations evident in the gene transcription process.
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