The transcription factor and tumour suppressor P53 is known to interact with NER-associated regulatory proteins and thus is important in the NER response. modifications is important in determining its fate. Failure of these DNA damage response steps can lead to cellular proliferation and DL-Methionine oncogenic development, causing skin cancer, hence these chromatin changes are critical for a proper response to UV-induced injury. Keywords:chromatin, UV, apoptosis, repair, histone, SWI/SNF == 1. Chromatin == Eukaryotic cells compact their DNA into repeating arrays of nucleosomes comprised of 146 bp of DNA wrapped around an octamer of histone proteinsa tetramer of H3 and H4 flanked by two H2A and H2B dimers [1], otherwise known as chromatin. A fifth histone protein, H1, promotes chromatin DL-Methionine structure of DL-Methionine a higher order by facilitating the compaction of nearby nucleosomes at the entry and exit points. Linker DNA connects these core proteins, which is typically 3050 bp in length [2]. Chromatin has been subdivided into two functionally distinct classes. Firstly, euchromatin which is decondensed in the interphase of the cell cycle and contains most of the actively transcribed genes, and secondly heterochromatin which remains condensed throughout the whole cell cycle and contains mostly inactive genes [3,4]. Each core histone contains a globular domain and anN-terminal tail protruding from the nucleosome. The nucleosome is in a constant dynamic equilibrium between a fully wrapped state and a collection of partially unwrapped states. This unwrapping transiently exposes buried DNA sites for access. However the conversion between these states is dynamic and rapid. Any process that requires access to DNA must therefore overcome this chromatin structural barrier [5]. This nucleosomal structure is the platform for which many variations, modifications and binding of proteins all impact DNA and cell functions. A number of chromatin remodelling complexes use adenosine 5-triphosphate (ATP) to alter chromatin structure, making the DNA accessible to the proteins which bind chromatin and regulate cellular processes. This can influence the epigenetic modifications of various histones, as well as the alteration of theN-terminal tail of chromatin by histone chaperones, in turn influencing the dynamic state of chromatin [6]. These chromatin-remodelling factors are important in the link between chromatin structure and cellular processes such as transcription, replication, recombination, aging, repair, cell cycle control, death signalling and responses to external stimuli such as ultraviolet (UV) radiation. == 2. UV Damage and the Cellular Response == Chromatin is under constant threat from both endogenous and exogenous sources. Among these sources, UV radiation is one of the most EP prevalent inducers of DNA damage in our environment. The photolesions induced by UV inhibit the replication of DNA, as well as transcription thus causing genomic instability [7]. If they are not repaired prior to cell division, these photolesions can result in an incorrect nucleotide, or mutation, being incorporated into newly synthesised DNA. When UV reaches the skin, a major part of it is reflected, while the rest is absorbed. UVB DL-Methionine radiation (290320 nm) is absorbed mostly by the upper epidermal layers, while UVA (320400 nm) DL-Methionine penetrates deeper into the skin, reaching the basal layer of the epidermis [8]. UVB radiation has been shown to cause different types of DNA damage, including the formation of dimeric photoproducts between adjacent pyrimidine dimers on each strand. There are two major types of these lesions induced by UV irradiation: cyclobutane pyrimidine dimers (CPDs) and Pyrimidine (64) Pyrimidone photoproducts (6-4PPs). Although UVA has also been shown to result in the formation of pyrimidine dimers [9,10], it requires.