|
In constructing a house, builders need to make sure its framework is solid before they can continue to build the rest of the house following the framework. Likewise, DNA building uses mechanisms for identifying and repairing damaged DNA to make sure that certain processes in the cell cycle is finished before further construction can begin.
The accurate transmission of genetic information from one cell to its daughter cells is essential to the survival of all organisms. Within a faithful transmission, there is a constant need for cells to repair DNA damage caused by internal and external environmental sources (ie. UV/gamma radiation, oxygen biproducts and other chemicals). One mechanism that cells uses to repair their DNA damage is to give themselves a chance to repair, meaning halting their cycle engines in order to accurately repair any damages before continuing replication. Such a mechanism is termed checkpoint arrest. We know very little about the molecular analysis of feedback controls and how a cell senses damage and arrests its cycle. At present, we are still learning about the signals generated by monitoring mechanisms and how these signals arrest the cell cycle engine. For the last decade, researchers have been studying the mechanics of cell cycle regulation and checkpoint control due to its connection to the characteristics of cancer cells.
Cancer cells do not use checkpoint repair mechanisms to correct their DNA damages, thus they grow without restraint. One of the ways researchers are studying cell cycle checkpoints in relation to cancer is in studying the human genetic disorder ataxia-telangiectasia (A-T), characterized by an early death, sensitivity to radiation and a predisposition to cancer. The interest in A-T is due to the discovery of a human homologue of a yeast gene responsible for checkpoint arrest. Working with yeast as a model, researchers have inducible cancer cells with mutations that have broken checkpoint repair mechanisms. In studying these mutants and their defective checkpoints, we will be able to understand more clearly the molecular origins of cancer and in the future, develop a cure.
|
