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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, Δctf4 and Δelg1 mutant cells show partially overlapping phenotypes.

Indeed, mutant cells show growth and sporulation defects at high temperature and under optimal culture conditions.

During imaginal disc growth, Slbp mutant cells show defects in S phase and proliferate more slowly than control cells.

Repair of these DSBs likely occurs in a process involving Ku and Ligase IV, since mutant cells show an extreme sensitivity to etoposide [36], [37], [38].

Such null mutant cells show even higher levels of chromosome damage than patient cells [8], [17] reflecting rescue by the hypomorphic p70-nibrin protein present in patient cells.

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.

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.