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Recently, Zhang et al. presented that stationary phase atg mutant cells shows higher spontaneous petite frequencies up to 6% than about 3% in WT cells [16].
The CP12 protein which was also found to be differentially expressed in wild type and mutant cells shows a redox-dependent binding to Calvin cycle enzymes in cyanobacteria as well as in chloroplasts [16].
Comparing wild-type cells with mutant cells shows that loss of CHD4 does not dramatically change the transcriptional landscape of early embryonic cells, as cells generally cluster by stage of embryo rather than by genotype.
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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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