Common fragile sites are locations on chromosomes that commonly exhibit gaps and breaks and are seen to occur in cells that have been cultured under conditions that partially inhibit DNA replication — such as folate deficiency. These sites are deleted and rearranged in many tumors but are controlled by mechanisms that have remained unclear. In the December 13
Casper et al. used three different techniques to inactivate or disable ATR expression in human cell cultures with deficient ATM from patients with ataxia-telangiectasia. They observed that the replication checkpoint kinase ATR, but not ATM, is critical for maintenance of fragile site stability. ATR deficiency resulted in fragile...