## 2 Results
\begin{table}
\begin{tabular}{c c c c} \hline \hline
**Strain:** & **LJ110** & **GL3** & **GL4** \\ \hline \hline \multirow{2}{*}{\
\begin{tabular}{c} MM-agar \\ + (\(\mu\)/v) \\ \end{tabular} } & \multirow{2}{*}{
\begin{tabular}{c} No C-source \\ \end{tabular} } & \multirow{2}{*}{-} & \multirow{2}{*}{-} \\ \cline{2-2} \cline{4-4}  & & & \\ \cline{2-2} \cline{4-4}  & D-Glucose & Normal (1) & - & Small (2) \\ \cline{2-2} \cline{4-4}  & Glycerol & Normal (1) & \multicolumn{1}{c}{Small (1)} \\ \cline{2-2} \cline{4-4}  & Lactate (pH 7.0) & Small (1) & Small (1) & Small (1) \\ \cline{2-2} \cline{4-4}
0.5\% C-source & Mannitol & Normal (1) & - & - \\ \cline{2-2} \cline{4-4}  & Succinate (pH 7.0) & Small (1) & Small (1) & Small (1) \\ \cline{2-2} \cline{4-4}  & Sorbitol & Normal (1) & - & Small (2) * \\ \cline{2-2} \cline{4-4}  & D-Xylose & Small (1) & - & Small (2) \\ \cline{2-2} \cline{4-4}  & Maltose & Normal (1) & - & - \\ \cline{2-2} \cline{4-4}  & D-Galactose & Small (1) & - & - \\ \cline{2-2} \cline{4-4}  & Gluconate (pH 7.0) & Normal (1) & Small (2) & Small (1) \\ \cline{2-2} \cline{4-4}  & L-Arabinose & Normal (1) & Small (2) & Small (2) \\ \cline{2-2} \cline{4-4}  & Lactose & Normal (1) & - & - ** \\ \hline \hline \end{tabular}
\end{table} 
Table 2: Growth phenotypes of wild type LJ110 and mutant strains GL3 and GL4 on agar plates. LB-agar; minimal medium (MM)-agar [50] with 0.5% C-source (\(w\)/\(v\)). normal = single colonies with a diameter of \(\geq\)1 mm; small = colonies with a diameter \(\leq\)1 mm; in grey = barely visible; = no growth; * = occurrence of papillae after several days of incubation. ** Lactose-minus due to gene insertion (1) colonies evaluated after 1 day of incubation at 37 \({}^{\circ}\)C; (2) colonies evaluated after 2 days of incubation at 37 \({}^{\circ}\)C. Average of at least three independent biological replicates. For details see Section 4. We hypothesized that--by prolonged incubation on MM agar plates with glucose as sole carbon source--mutant colonies of GL3 might appear due to activation of the inherent chromosomal genes _fsaA_ and/or _fsaB_ genes which could suppress the glucose-negative phenotype. However, even after a prolonged incubation of 3 weeks, no such suppressor mutants appeared. Growth on glucose, however,  
Figure 2: Growth behavior of wt LJ110 (**a**) and triple mutant strain, GL3 (**b**) on glucose or fructose as carbon sources. Shake flask growth on MM with fructose and 100 \(\upmu\)M IPTG (\(\bullet\)) or on MM with glucose and 100 \(\upmu\)M IPTG (\(\square\)). At 37 \({}^{\circ}\)C, 200 rpm. Average values of two biological replicates are presented. Both strains were inoculated from MM fructose overnight cultures. Note that the time axis is different in the two graphs. For details see Section 4.  
could be restored in strain GL3 when it was transformed with a plasmid carrying wild type _pfkA_ gene (pJNTN-m-L-_pfkA_; Table 3) (data not shown). We take this as evidence that the growth deficiency of strain GL3 mainly lies in its inability to degrade F6P or glucose 6-phosphate (G6P) by the EMP route (due to blockage of both PFKs) or by the hexose monophosphate (HMP) route (lack of glucose 6-phosphate dehydrogenase).