Fig. 7: Structural modeling of Drosophila SSE and human ESPL1 in complex with Lamin C/Lamin A EXXR motif.
From: An evolutionarily conserved role for separase in the regulation of nuclear lamins
A Predicted structures of the catalytic domains of Drosophila SSE (blue, residues 1–634) and human ESPL1(green, residues 1709–2120), shown in top and side views. The putative substrate-binding cleft is indicated (black ovals). Right panels depict close-up views of the electrostatic surface potential at the substrate-binding site, with the Lamin C/Lamin A EXXR motif in stick representation. B Model of Separase function in lamin regulation. In normal cells (left panel) Separase (red ovals), in addition to binding chromatin (not shown for clarity) localizes at the nuclear rim, where it interacts with A-type (green filaments) and B-type lamins (purple filaments). Upon Separase loss (right panel), B-type lamins are reduced, A-type lamins accumulate in the cytoplasm, forming aggregates (green rectangles), and nuclear membrane integrity is compromised, leading to invaginations and disrupted chromatin-membrane interactions.
