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. Author manuscript; available in PMC: 2017 Jul 1.
Published in final edited form as: Nat Genet. 2017 May 29;49(7):1148–1151. doi: 10.1038/ng.3883

Figure 3. SAC deficiency and CIN caused by TRIP13 loss-of-function is rescued with wild type but not mutant TRIP13.

Figure 3

(a) Quantification of chromosome segregation errors of TRIP13-mutated patient lymphoblasts expressing H2B-mNeon or co-expressing GFP-TRIP13 wt. Each bar depicts the mean of 3-4 experiments ±SEM, >85 cells in total. P-values ≤ 0.05 from an unpaired Student’s t-test are shown. Addition of GFP-TRIP13 wt to patient 1 cells reduced the rate of chromosome missegregation.

(b) Analysis of mitotic delay as in (Fig 1d) of nocodazole-treated patient lymphoblasts expressing H2B-mNeon or co-expressing GFP-TRIP13 wt. Mean of three experiments ±SEM, >35 cells in total. Patient 1 cells expressing GFP-TRIP13 now maintain mitotic arrest.

(c) Analysis of mitotic delay as in (Fig 1d) and (b) of nocodazole-treated HCT116 wt or HCT116 TRIP13 KO cells expressing H2B-mNeon, co-expressing GFP-TRIP13 wt, or co-expressing TRIP13 p.Arg354X. Mean of three experiments ± SEM, >45 cells in total. HCT116 wt and TRIP13 KO + TRIP13 wt cells both maintain mitotic arrest unlike TRIP13 KO and TRIP13 KO + TRIP13 p.Arg354X cells.

Key: patient 1, ID_0644; wt, wild-type; KO, knockout; CIN, chromosomal instability; SAC, spindle assembly checkpoint; SEM, standard error of the mean