Fig. 6
From: The FANCM-BLM-TOP3A-RMI complex suppresses alternative lengthening of telomeres (ALT)
Schematic of proposed model of FANCM-mediated ALT suppression. FANCM functions to reverse and remodel stalled replication forks that predominate in ALT telomeres. In the absence of FANCM, or through disruption of the FANCM-BTR complex, stalled forks deteriorate into double strand breaks, which provide the substrate for break-induced telomere synthesis events and the concomitant production of nascent ECTRs
