APLF (C2orf13) Is a Novel Component of Poly(ADP-Ribose) Signaling in Mammalian Cells

Abstract

The Acknowledgment section was inadvertently omitted and should appear as shown below. ACKNOWLEDGMENTS F.C.-L. is a recipient of an EMBO long-term fellowship (ALTF956-2006). K.W.C. is funded by the MRC (G0400959 and G0600776), BBSRC (BB/C516595/1), and the European Community (integrated project DNA Repair LSHG-CT-2005-512113).

The DNA Damage Response: Making It Safe to Play with Knives

“…XRCC1 and LIG3 are recruited to SSBs in a PARP1-dependent manner and promote SSB repair following DNA end processing by XRCC1 interacting proteins, such as DNA polymerase β, PNK and the nucleases APE1, APTX and APLF (Caldecott, 2008). APLF is dependent on the PBZ motif for its recruitment to DNA damage sites (Bekker-Jensen et al, 2007; Kanno et al, 2007; Rulten et al, 2008). …”

The PARP Side of the Nucleus: Molecular Actions, Physiological Outcomes, and Clinical Targets

“…7B) (Ahel et al, 2008; Eustermann et al, 2010; Isogai et al, 2010; Rulten et al, 2008). It was originally identified in CHFR (checkpoint protein with FHA and RING domains), APLF (aprataxin PNK-like factor), and other proteins involved in DNA repair and checkpoint control proteins (Ahel et al, 2008; Rulten et al, 2008). Functional analyses have demonstrated that the actions of CHFR in the antephase checkpoint are blocked by mutations in the PBZ motif or by inhibition of poly(ADP-ribose) synthesis (Ahel et al, 2008).…”

“…Functional analyses have demonstrated that the actions of CHFR in the antephase checkpoint are blocked by mutations in the PBZ motif or by inhibition of poly(ADP-ribose) synthesis (Ahel et al, 2008). PAR binding by the PBZ in APLF is required for targeting the protein to DNA strand breaks and may also serve to suppress further PAR synthesis (Rulten et al, 2008). These results provided the first evidence of functional consequences for PAR binding through a specific motif.…”

Nonhomologous end joining: A good solution for bad ends

“…However, APLF also promotes assembly of higher order NHEJ complexes indirectly, through its ability to bind to Poly (ADP ribose) chains (PAR) [67]. PAR is added to chromatin and repair factors near the site of strand breaks by Poly (ADP ribose) polymerases (PARPs) (reviewed in [68]), and this promotes recruitment of APLF through a pair of tandemly repeated PAR binding zinc finger (PBZ) motifs in its C-terminus [69]. Finally, APLF has a C-terminal nucleosome assembly protein-1 (NAP1)-like motif that is sufficient for partial nucleosome assembly and disassembly in vitro [70].…”

“…APLF is one such factor and, as noted above, has been shown to stabilize the assembly of NHEJ core factors at breaks directly through multiple protein-protein interactions [14]. However, APLF could also promote dynamic changes in the stability and composition of complexes present at strand breaks; its PBZ domains can interact with uncharacterized factors already present at the strand break after they are modified by PAR [67, 69]. APLF may also interact simultaneously with XRCC1 or XRCC4 [41, 42], Ku, [14, 66] and PAR [69], thus acting as a physical and inducible link between multiple strand break repair pathways (e.g.…”