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. Author manuscript; available in PMC: 2020 Mar 15.
Published in final edited form as: Methods. 2018 Aug 24;157:56–65. doi: 10.1016/j.ymeth.2018.08.009

Figure 4: SMT of Halo-lamin A mutants.

Figure 4:

(A) Disease relevant mutations in lamin A were introduced and imaged by SMT as in Figure 1. Molecules within the nucleus, both at the periphery and in the nucleoplasm, were analyzed. Stacked bar graphs represent the ratio of diffuse (grey), fast bound (orange), and slow bound molecules (blue). Mutations are organized by respective disease outcome. Exposure time 30 ms; acquisition time 200 ms; 900 images per cell. CM, cardiomyopathy defect; EDMD, Emery-Dreifuss muscular dystrophy; FPLD, Dunnigan-type familial partial lipodystrophy; MAD, Mandibuloacral dysplasia; WRN, Werner syndrome. Values represent means and 95% confidence intervals of at least 10 cells and 2 experiments.

(B) Fast bound (orange; left y-axis) and slow bound dwell times (blue; right y-axis) from molecules in (A).