Fig 6. A model to describe the known Rad52-mediated mechanisms that function at telomeres during replicative senescence.

Replication forks traveling through subtelomeric and telomeric sequences frequently encounter impediments to their progression. A fork collapse would leave a truncated telomere, which can be elongated by telomerase (far left). In the absence of telomerase (gray box), the truncated telomere can be repaired by BIR. Fork impediments can be dealt with via error-free PRR. Blocks of lagging and leading strand synthesis can be repaired via Rad5-independent and Rad5-dependent error-free PRR, respectively.