Maintaining normal telomere length and integrity is critical for correct cell function and to avoid senescence-like growth arrest. In an Advanced Online Publication in
Garcia-Cao et al. studied telomeres in mouse embryonic fibroblast (MEF) cells generated from mice lacking combinations of Rb proteins (Rb1, Rbl1 and Rbl2). Double and triple knockout cells had significantly elongated telomeres compared with controls. Most of the telomeres in these cells were elongated by the sixth passage in culture. These telomeres appear to be functional and there was no significant increase in end-to-end chromosomal fusions. The long-telomere phenotype was not associated with changes in telomerase activity.
The authors propose that inactivation of Rb function by viral oncoproteins may be a mechanism to induce telomere lengthening and sustain tumor cell growth.