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. 2017 Nov 10;28(1):69–89. doi: 10.1038/cr.2017.139

Figure 5.

Figure 5

Filia-Floped interact with Blm and promote its recruitment to replication forks. (A) Physical association of Filia, Floped, Blm and Trim25 in ESCs with or without HU treatment. (B) Blm and Trim25 localized at replication forks in ESCs under the normal (upper panel) and HU treatment (lower panel) conditions. (C) Blm knockdown impaired stalled fork restart in ESCs after HU treatment. (D) Blm regulated stalled fork restart in a protein dosage-dependent manner. (E) Depletion of Filia (Filia-KO) or Floped (Floped-KO) from ESCs decreased the recruitment of Blm and Trim25 to replication forks, double depletion (Double KO) resulted in a more severe phenotype. (F) FiliaS151A was as defective as Filia-Floped double deficiency in recruiting Trim25 and Blm to replication forks, whereas FiliaS151D functioned as effectively as WT Filia. (G) Ectopic expression of WT Filia and/or Floped in NIH3T3 cells stimulated the recruitment of Trim25 and Blm to replication forks. However, expression of FiliaS151A had no effect. (H) Ectopic expression of FiliaS151A in NIH3T3 cells impaired Blm recruitment induced by Floped. Data are represented as mean ± SEM. **P < 0.01, ***P < 0.001.