BY SHRUSHTI JOSHI 164551 NUCLEOTIDE EXCISION REPAIR
Nucleotide excision repair (NER) is a particularly important excision mechanism that removes DNA damage induced by ultraviolet light (UV). Discovered by Philip Courtland Hanawalt , in 1964 INTRODUCTION
NER can be divided into two subpathways : global genomic NER (GG-NER or GGR) Xeroderma pigmentosum (XP) transcription coupled NER (TC-NER or TCR) Cockayne syndrome (CS) TYPES
PROKARYOTIC NER
EUKARYOTIC NER
Xeroderma pigmentosum ( XP ) is a rare autosomal recessive genetic disorder of DNA repair in which the ability to repair damage caused by ultraviolet (UV) light is deficient. Those affected with XP are extremely sensitive to UV light produced by the sun and even with a short exposure to it causes dry, flaking skin and pigmented spots that can develop into skin cancer. XERODERMA PIGMENTOSUM
Cockayne syndrome ( CS ), also called Neill- Dingwall syndrome , is a rare and fatal autosomal recessive neurodegenerative disorder. In contrast to cells with normal repair capability, CSA and CSB deficient cells are unable to preferentially repair UV-induced cyclobutane pyrimidine dimers in the template strand of actively transcribed genes. It is named after English physician Edward Alfred Cockayne who first described it in 1936. COCKAYNE SYNDROME
RECENT RESEARCH
Dynamic maps of UV damage formation and repair for the human genome Jinchuan Hu , Ogun Adebali, Sheera Adar, and Aziz Sancar