Figure 3.

Telomere nondisjunction mechanically disturbs spindle elongation and leads to the formation of anaphase chromatin bridges. (A) Single cell analysis of spindle elongation during mitotic progression in the absence (gray lines, n = 22) or in the presence of 10 µm Napp1 (red, n = 13, and green, n = 4 lines). In the presence of 10 µm Napp1, cells displaying telomere segregation defects and merotelic attachments are shown in red, whereas cells with telomere nondisjunction defects are shown in green. (B) Mean rate of spindle elongation for the different phenotypes shown in A. (C) Example of a fine chromatin bridge seen after Aurora inhibition with correctly segregated kinetochores. (D) Percentage of anaphase chromatin bridges, merotely, and aneuploidy phenotypes in control (n = 206), after Aurora inhibition (n = 293), or in cells deleted for the monopolin subunit Pcs1 (n = 221). Light gray, anaphase bridges; dark gray, merotely; white, aneuploidy. Error bars indicate SD obtained from three independent experiments.

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