Figure 7: Kinesin-14 promotes DSB mobility.
From: Perinuclear tethers license telomeric DSBs for a broad kinesin- and NPC-dependent DNA repair process
(a–c) Mobility of Rad52–YFP foci calculated by mean square displacement (MSD) analysis. Percentage of cells with diffusion coefficient D>10−3 μm2 s−1 is included in parentheses. (a,b) Mobility of non-telomeric BIR-repaired DSBs is shown (N=49). (c) Mobility of subtelomeric (SubTEL) DSBs is shown (N=84). (d) Model depicting BIR-dependent repair processes at subtelomeric and internal DSBs tested. Swr1-dependent Htz1 incorporation allows kinesin-14 to target BIR-repairable DSBs to the nuclear pore subcomplex Nup84 for repair. Cohibin-dependent perinuclear telomere tethering licenses subtelomeric DSBs for this repair process by promoting kinesin-14 recruitment to damaged DNA. DSBs may increase their association with the inner nuclear membrane protein Mps3 along the nuclear envelope before being ultimately targeted to Nup84. DSB targeting to and release from Nup84 via kinesin-14 is performed via non-catalytic and catalytic functions of the complex, respectively. Kinesin-14 performs its role in part via cooperation with microtubules. Dashed arrows symbolize events that promote DSB targeting to the NPC. Green kinesin-14 and arrows highlight DSB targeting to Nup84. Red kinesin-14 and arrows highlight DSB release from Nup84.
