hRad21 overexpresses and localizes to the ALT-associated promyelocytic leukemia body in ALT cells.

Telomerase-negative immortalized cells maintain their telomeres through a telomerase-independent pathway termed alternative lengthening of telomeres (ALT). The mechanism of ALT is based on homologous recombination (HR). A hallmark of ALT cells is presence of a nuclear structure termed ALT-associated promyelocytic leukemia body (APB). Here, we demonstrated that hRAD21, an important subunit of cohesin complex, was overexpressed in ALT cells. We additionally showed that hRAD21 protein localized to APB in ALT cells. Thus, one role of hRAD21 appeared to involve telomere maintenance in ALT cells. We suggested that hRAD21 facilitated telomere HR in ALT cells by participating in APB formation.