Detecting the Influence of Cell Cycle Regulatory Proteins on Human Telomeres

Maintenance of genome stability depends on an appropriate response to deoxyribonucleic acid (DNA) damage. This response is based on a complex network of signaling pathways that activate numerous processes and ultimately lead to damage repair and cellular survival or cell death. Thus, a relationship between telomeres and DNA-damage checkpoints seems inevitable. This is based on the fact that a gene responsible for ataxia telangiectasia (A-T), a master controller of cellular pathways and networks orchestrating the responses to DNA damage, influences telomere metabolism as well as the function of cell cycle regulatory proteins. In mitotic cells, ataxia telangiectasia mutant (ATM) is required for a DNA damage-dependent signal-transduction cascade that activates multiple cell cycle checkpoints. Interestingly, ATM and telomeres influence several common functions. When ATM is missing, several cellular processes are affected, and this results in a variety of disease phenotypes. Some of the common metabolic abnormalities, such as poor growth, have been linked to lack of ATM as well as loss of telomeres.