In E. coli, the ptsG gene encoding the glucose-specific transporter
(enzyme EIIBC) of the phosphotransferase system is known
to play a central role in CCR and the inducer exclusion mechanism
(Gosset, 2005). In order to relieve CCR and to utilize glucose and
xylose simultaneously, the chromosomal ptsG gene was disrupted
in the JHS01169 strain, resulting in the construction of the
JHS01300 strain losing the glpK, yqhD and ptsG genes. To investigate
the effect of the ptsG deletion, JHS01169/pCPaGG and
JHS01300/pCPaGG were cultivated in R/5 medium with 5 g/L glucose
and 3 g/L xylose (Fig. 2A and B). While JHS01300/pCPaGG consumed
2.1 g/L of xylose (70% of initial xylose concentration),
JHS01169/pCPaGG utilized only 0.6 g/L of xylose in 15 h. The final
cell mass (3.8 g/L) and glycerol concentration (3.5 g/L) of
JHS01300/pCPaGG were 15% and 46% higher than those of
JHS01169/pCPaGG, respectively (Table 3). Especially, deletion of
ptsG considerably increased the xylose consumption rate of
JHS01300/pCPaGG by a 3.5-fold, relative to that of JHS01169/
pCPaGG. Deletion of ptsG certainly increased xylose consumption
and glycerol production by the relief of CCR, and reduced glucose
consumption rate, of which phenomena were coincided with the
previous report (Hernandez-Montalvo et al., 2001). Meanwhile,
30% of xylose initially added still remained when glucose was
depleted at 15 h (Fig. 2B), indicating that modulation of CCR was
not enough for the recombinant E. coli strain to utilize glucose
and xylose in the same consumption rate. Thus, an additional strategy
for more efficient utilization of xylose during glucose consumption
should be devised.