Table 2.
Interactions at the NE and functional consequences.
| Lesion type | NE component associated with lesion | Cell cycle phase of association | Mediators (NE interaction dependent on) | Function of tethering | Reference |
|---|---|---|---|---|---|
| Persistent DSB (HO break, no donor for repair) | Mps3 (ChIP, Imaginga) Heh2 (ChIP) | S/G2 | Rad51, Rad52, Rad9/Rad24, H2A.Zc, Swr1, INO80 (Arp8) SMC5/6 (Nse5), Mms21, Rtt107 | Delays HR repair Repress uSCR Repress HR with an ectopic donor Promote GCRs in NP mutants Recruit telomerase | Kalocsay, Hiller and Jentsch (2009); Oza et al. (2009); Horigome et al. (2014, 2016) |
| Cdc13 | |||||
| Slowly repaired DSB (30 kb resection required for SSA) | Mps3 (ChIP) | N/D | N/D | Unclear (repair is dependent on Rad52, partially on Nup84) | Oza et al. (2009); Chung et al. (2015) |
| Repairable DSB (HO break, ectopic donor on different chromosome) | Mps3 (ChIPb, Imaginga) | N/D | N/D | Suppress HR with an ectopic donor | Oza et al. (2009); Horigome et al. (2014) |
a
Preferential localization of the lesion at the periphery of the nucleus (zone 1) is lost in the mps3ΔN mutant.
b
Repairable DSBs do not show a zone 1 increase by imaging or bind to Mps3 by ChIP (Nagai et al.2008; Oza et al.2009).
c
H2A.Z is encoded by the HTZ1 gene; NE interaction is also lost in htz1-K126R, K133R non-sumoylatable mutants (Kalocsay, Hiller and Jentsch 2009) or the htz1ΔM6 mutant that doesn't bind SWR-C, but retains its Mps3 inner nuclear membrane localization function (Gardner et al.2011; Horigome et al.2014).