Table 1.

Interactions at the NPC and functional consequences.

Lesion type	NPC component associated with lesion	Cell cycle phase of association	Mediators (NPC interaction dependent on)	Function of relocalization	Reference
Persistent DSB (HO	Nup84 (ChIP)	G1/S/G2	Slx5/8	Increase survival	Nagai et al. (2008);
break, no donor for	Nup133 (ChIP)		Mec1/Tel1	Promote gene conversion	Kalocsay, Hiller and
repair)	Nic96 (ChIP)		Swr1	Promote ectopic BIR	Jentsch (2009); Oza
	Nup49 (Imaginga, b)		Mms21	Promote MMEJ	et al. (2009); Horigome
			Siz2	Suppress GCRs	et al. (2014, 2016)
			Smc5/6e
Subtelomeric DSB	Nup84 (ChIP)	N/D	Kinesin14 (Cik1, Kar3)	Increase survival	Therizols et al. (2006);
			Cohibin (Lrs4, Csm1)	Promote end joiningf	Chung et al. (2015)
			Swr1e	Promote Rad52-dependent BIR
Eroded telomere	Nup49 (ChIP,	Senescing	Slx5/8	Relocalize to pores from NE	Khadaroo et al. (2009);
	(Imaginga)	cells	Siz1/Siz2	Promote Rad52-dependent	Churikov et al. (2016)
			Rad9/Rad24e	type II recombination
Collapsed fork	Nup49 (Imaginga, b)	S	-	Increase survival	Nagai et al. (2008)
by HU + MMSc				Promote fork restart
Collapsed fork at	Nup49 (Imagingb)	S	Nup84	Reduce repeat breakage and	Su et al. (2015)
CAG repeatsd	Nup84 (ChIP)		Slx5/8	instability
				Suppress Rad52-dependent HR

^aColocalization of fluorescently tagged pore protein with the lesion in either wild-type or nup133ΔN mutant cells (which clusters NPCs to one side of the nucleus; Doye, Wepf and Hurt 1994).

^bPreferential localization of the lesion at the periphery of the nucleus (zone 1) by zoning analysis.

^cInduced collapsed fork by treatment with 0.2 M HU and 0.03% MMS.

^d(CAG)₇₀ or (CAG)₁₃₀ repeat tracts.

^eMutant causes partial delocalization.

^fConcluded to be NHEJ in Therizols et al. (2006), but a significant fraction (at least 40%) had what is now accepted as a MMEJ signature.