Essay --

INTRODUCTION echo cosmic stringed corners (DSB) occur frequently in eukaryotic cellular phones. It can be caused by many factors such as ultra violet radiation, thermolabile oxygen species, ionizing radiation et cetera (Lieber,2010). DNA damage leads to rapid growth of tumour leading to cancer. Hence it is very important to restore it before the cell undergoes further division. Two mechanisms of haunt 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 take for repair factors to access the DNA that are packaged, chromatin remodelers are crucial to open the DNA. One way of DNA being packaged is to confine around a structure known as nucleosome. Thus, the authors have centre on the disscociation of nucleosome and the role of chromatin remodeler during the process of nonhomologous and homologous repa ir. Experiments were conducted to determine whether nucleolin,a protein with chaperone bodily function, works as a chromatin remodeler and promotes dissociation of histones from nucleosome in areas of divalent 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 act with DNA (Belotserkovskaya,2003). Experiments involving knockdown of FACT subunit was conducted to test whether nucleolin has FACT-the likes of 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 component for recruiting repair factors like XRCC4, RPA 32 et cetera. Absence of nucleolin not only affects nucleosome disasse mbly but decreases the cogency of double stranded break repair. Hence, this paper allowed further analysis of the dispa arrange 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 knowledge of protein (nucleolin) structure and function, but excessively enhanced my ability to analyze the role the various components that are complicated 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 multipurpose to advance further in the field of medicine to prevent diseases caused by mutation.