Figure 2.

Putative mechanisms of resection regulation by Fun30 and Rad9 (adapted from Bantele, 2018). As Rad9 is a chromatin-binding protein without apparent catalytic activity, at least two mechanisms of resection inhibition can be envisioned (upper part). First, Rad9 could directly block or slow down the progression of nucleases either by inhibiting the nucleases (A) or by stabilizing chromatin in a configuration that is non-permissive to resection (B) for example by inhibiting Fun30, if the latter was required to help overcome resection-inhibition by nucleosomes. Fun30 could also promote resection by several different mechanisms (lower part). As a nucleosome remodeler, Fun30 could either act through chromatin (C), or by removing Rad9 from chromatin (D). The action through chromatin could involve its putative remodeling activities and potentially H2A/H2B dimer exchange, which might affect γH2A and H2A.Z dynamics or repositioning of nucleosomes by nucleosome sliding (C, right side).