Essay --

INTRODUCTIONDouble stranded breaks (DSB) occur frequently in eukaryotic cells. It can 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. and so it is very important to repair it before the cell undergoes further division. Two mechanisms of repair system can occur in the cell homologous recombination (HR) and non homologous DNA end 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 remodelers are essential to open the DNA. One way of DNA being packaged is to wrap around a 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 homologous repair. Experiments were conducted to determine whether nucleolin,a protein with chaperone activity, works as a chromatin remodeler and promotes dissociation of histones from nucleosome in areas of double stranded break. In addition to this, further investigation was done to determine its role in recruitment of repair factors. During transcription, 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 test whether nucleolin has FACT-like histone chaperone activity out-of-pocket 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 component for recruiting repair factors like XRCC4, RPA 32 et cetera. absence of nucleolin not only affects nucleosome disassembly but decreases 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 recruitment of resultant repair factors. It not only expanded my fellowship of protein (nucleolin) structure and function, but also enhanced my ability to analyze the role the various 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. Understanding such mechanisms is useful to advance further in the field of medicine to hold diseases caused by mutation.