Friday, March 15, 2019
INTRODUCTIONDouble stranded breaks (DSB) occur frequently in eukaryotic cells. It finish be caused by many factors such as ultra violet radiation, reactive oxygen species, ionizing radiation et cetera (Lieber,2010). DNA damage leads to rapid growth of tumor leading to cancer. Hence it is very important to unsex it before the cell undergoes supercharge division. Two mechanisms of repair system can occur in the cell homological recombination (HR) and non homologous DNA residue joining (NHEJ). These repair systems along with their mechanism and the repair factors associated with it has been analyzed in this paper. In order for repair factors to access the DNA that are packaged, chromatin granule remodelers are essential to open the DNA. One way of DNA macrocosm packaged is to wrap around a social structure known as nucleosome. Thus, the authors have focused on the disscociation of nucleosome and the role of chromatin remodeler during the process of nonhomologous and homologo us repair. Experiments were conducted to determine whether nucleolin,a protein with chaperone activity, works as a chromatin remodeler and promotes disassociation of histones from nucleosome in areas of forficate stranded break. In addition to this, further probe was done to determine its role in enlisting of repair factors. During placement, chromatin remodelers such as switch/sucrose nonfermentable (SWI/SNF) and facilitates chromatin transportation (FACT) eliminates H2A/H2B dimer allowing transcription factor to interact with DNA (Belotserkovskaya,2003). Experiments involving knockdown of FACT subunit was conducted to prove whether nucleolin has FACT-like histone chaperone activity due to its role in H2A/H2B dimer removal in areas of double strand breaks. If the results of knoc... ... MRN complex. In addition to this, nucleolin is a vital persona for recruiting repair factors like XRCC4, RPA 32 et cetera. Absence of nucleolin not only affects nucleosome dismantling but decr eases the efficiency of double stranded break repair. Hence, this paper allowed further analysis of the different repair systems that occur in DNA double stranded break site at different cell cycles and the enlisting of resultant repair factors. It not only expanded my knowledge of protein (nucleolin) structure and function, but also enhanced my ability to analyze the role the discordant components that are involved in repair system. Further analysis of recruitment of Asf1 and factors that affect the rate of nucleolin function can be performed in future. mind such mechanisms is useful to advance further in the field of medication to prevent diseases caused by mutation.