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. Author manuscript; available in PMC: 2021 Jun 1.
Published in final edited form as: Curr Opin Cell Biol. 2020 Feb 24;64:25–33. doi: 10.1016/j.ceb.2020.01.011

Figure 1. Surveillance and repair of nuclear pores and small nuclear envelope ruptures.

Figure 1.

A: The surveillance system is poised as Chm7 and Heh1 are segregated on either side of the nuclear envelope by NTRs and NPCs. Cartoon models of Chm7 (orange) and Heh1 (green) depicting predicted winged helix (WH) domains and a microtubule interacting and transport (MIT) domain interacting motif (MIM) alongside established LAP2-Emerin-MAN1 (LEM) and nuclear export sequences (NES). B: Disruption of the nuclear envelope caused by defective nuclear pore biogenesis or nuclear envelope rupture results in the local meeting Chm7 and Heh1. Binding of Heh1 to Chm7 leads to its activation, which likely triggers polymer formation (depicted by an opening of the Chm7 structure). C: A co-polymer of Chm7 and Heh1 (orange/green) helps to seal the membrane likely with help from other ESCRT proteins including Vps4 (not shown, see Table 1). D: The nuclear envelope is repaired, and nuclear-cytoplasmic compartmentalization is reestablished. E: Unregulated surveillance leads to a hyper-activation of Chm7/CHMP7, which drives aberrant membrane expansion at micronuclei and at the INM and might directly cause DNA damage. In all panels: nuclear pore complex, blue; outer and inner nuclear membranes, brown; cytoplasm, yellow; nucleoplasm, purple.