Table 2.
Gene | glc | gl | succ | ac | Reference |
---|---|---|---|---|---|
aceA | +/+ | +/+ | −/− | (58) | |
aceB | −/− | (58) | |||
aceEF* | −/+ | (60) | |||
ackA | +/+ | (61) | |||
acn | −/− | −/− | (58) | ||
acs | +/+ | (61) | |||
cyd | +/+ | (62) | |||
cyo | +/+ | (62) | |||
eno† | −/+ | −/+ | −/− | −/− | (30) |
fba∥ | −/+ | (30) | |||
fbp | +/+ | −/− | −/− | −/− | (30) |
frd | +/+ | +/+ | +/+ | (60) | |
gap | −/− | −/− | −/− | −/− | (30) |
glk | +/+ | (30) | |||
gltA | −/− | −/− | (58) | ||
gnd | +/+ | (30) | |||
idh | −/− | −/− | (58) | ||
mdh†† | +/+ | +/+ | +/+ | (63) | |
ndh | +/+ | +/+ | (59) | ||
nuo | +/+ | +/+ | (59) | ||
pfk† | −/+ | (30) | |||
pgi‡ | +/+ | +/− | +/− | (30) | |
pgk | −/− | −/− | −/− | −/− | (30) |
pgl | +/+ | (30) | |||
pntAB | +/+ | +/+ | +/+ | (29) | |
ppc§ | ±/+ | −/+ | +/+ | (63, 64) | |
pta | +/+ | (61) | |||
pts | +/+ | (30) | |||
pyk | +/+ | (30) | |||
rpi | −/− | −/− | −/− | −/− | (30) |
sdhABCD | +/+ | −/− | −/− | (58) | |
sucAB | +/+ | −/+ | −/+ | (60) | |
tktAB | −/− | (30) | |||
tpi** | −/+ | −/− | −/− | −/− | (30) |
unc | +/+ | ±/+ | −/− | (66–68) | |
zwf | +/+ | +/+ | +/+ | (30) |
Results are scored as + or − meaning growth or no growth determined from in vivo/in silico data. The ± indicates that suppressor mutations have been observed that allow the mutant strain to grow. In 68 of 79 cases the in silico behavior is the same as the experimentally observed behavior. glc, glucose; ac, acetate; gl, glycerol; succ, succinate.
The in vivo aceAE strain is able to grow under anaerobic growth conditions by using the pyruvate formate lyase.
† The in silico pfk strain is able to grow by increasing the PPP flux ≈ 5× and using the pps gene product to overcome PEP deficiency.
‡ The in silico pgi strain is unable to grow with glycerol or succinate as the carbon source because it is unable to synthesize glycogen and one carbohydrate component in the lipopolysaccharide. These are likely nonessential components of the biomass.
§ The grow on glycerol and glucose is possible through the utilization of the glyoxylate bypass. Constitutive mutations in the glyoxylate bypass can suppress the ppc phenotype.
¶ The in silico eno strain is able to grow by the synthesis and degradation of serine.
∥ There is evidence that fba has an inhibitory effect on stable RNA synthesis (65). Such an inhibition cannot be predicted by FBA.
The inability of tpi mutants to grow on glucose may be related to the accumulation of dihydroxyacetone phosphate, which leads to the formation of the bactericidal compound methylglyoxal (30).
†† Very slow growth on glycerol and succinate.