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(G ) Average MT disassembly rates from time-lapse imaging of wild type (black), wild type expressing cin4 -Q73L for 90 min, and constitutive cin4 -Q73L mutant cells (shown in pink).
(F ) Durations of pause events from time-lapse imaging of wild type (black), wild type expressing cin4 -Q73L for 90 min, and constitutive cin4 -Q73L mutant cells (shown in pink).
(H ) Average length of astral MTs (aMT) per yeast cell measured, for wild type (black), wild type expressing cin4 -Q73L for 90 min, and constitutive cin4 -Q73L mutant cells (shown in pink).
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Finally, ~16% of mutant cells showed division defects (Figs 2b and S2d,e).
NF1 mutant cells show activation of RAS/MAPK signaling, so a counter-screen in RAS mutant carcinoma cells was performed to exclude common RAS-pathway driven genes.
In addition, analysis of DNA plasmids recovered from Ku86 mutant cells showed an increased use of microhomologies at the nonhomologous end joining junctions, and displayed a significantly higher frequency of DNA insertions compared to control cells.
Indeed, delg mutant cells showed an identical COX activity compared to control (Fig. 5B).
In contrast, delg null mutant cells showed a strong decrease in staining.
In addition, Δctf4 and Δelg1 mutant cells show partially overlapping phenotypes.
As seen in Fig. 2D, delg mutant cells showed a strong reduction in NAO.
In contrast, the elongated and deformed ssn8 mutant cells showed uneven cellular organization.
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