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In both conditions the PHA concentration in relA/spoT mutant cells was significantly lower than in wild-form cells (p < 0.05).

Maximum cellulase production from the mutant cells was obtained within 94 h as compared to the longer incubation period (120 h) with the native strain.

Growth of wild type and mutant cells was monitored by measuring the OD600.

The phenotype displayed by mutant cells was rescued by infection with an ERRα-encoding adenovirus (AdERRα; Fig. 3C).

The specific current of menC mutant cells was only 5% (+/−2% n = 3) compared to wild type (Fig. 4).

The percentage of GFP positive mutant cells was normalized to wild type cells to obtain the relative infection efficiency.

The motility zone of the wild-type and mutant cells was measured at different times of incubation (Figure 5B).

A second phenotype observed in the mutant cells was the presence of vacuoles with an accumulation of CHMP2B mutant protein on the outer membrane, termed halos (Figure 6E).

We hypothesized that a block in gluconeogenesis in csgD mutant cells was responsible for the accumulation of TCA cycle intermediates and polyamine compounds.

To examine whether Dis3 may play a role in this pathway, centromeric silencing in dis3-54 mutant cells was first tested.

Since EGFR plays a significant role in CRC, the ability of its ligand to trigger the downstream signal in KRAS mutant cells was examined.