In a recent development, researchers have discovered mutation in genes responsible for cell division disrupts the replication process of the genomes and promotes cancer. The research suggests accumulation of mutations in human genes promotes tumor formation along with developing resistance to treatments. Biologists at the University of Geneva reveal that precocious entry of human genome in replication phase leading to molecular collisions on the DNA thereby induces new mutations.
Cell division into two daughter cells must replicate the entire genome and transcribe partly to synthesize new proteins. Cell division is notably controlled by specific genes, which includes proton-oncogenes Myc and Cyclin E. The overexpression of these genes or mutation into oncogenes, for instance due to exposure of cells to a carcinogen, leads to reckless cell growth that promotes tumor formation. Researchers are vying to understand the reason behind accumulation of mutation in cells with activated oncogenes.
Mutation of Genes for Cell Division Disrupts Replication Process
The replication of the entire DNA, which nears to 6.4 billion pairs of nucleotides in only few hours, involves the cell to organize preparation of the process at large number of sites on each chromosome simultaneously. Termed replication origins, the position and spacing of these locations need to be controlled in a way so that replication occurs smoothly and efficiently.
Researchers at University of Geneva have developed a method to detect the origin of replication on all chromosomes. This involves separating and sequencing the newly made DNA from cells that have very recently entered replication phase, so as to map sites on the genome where replication has kicked off. The method particularly developed for human cells provides high degree of sensitivity and resolution.