Table 1. Interaction matrix of the gene regulatory network for the glycolytic mode.
PfkA | FbaA | GapA | Pgk | Eno | PykF | Cya | Crp | Fis | GyrAB | GyrI | TopA | RpoS | RssB | stable RNAs | FruR | |
pfkA | 0 | − | − | − | − | − | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | − |
fbaA | 0 | −(−/+) | −(−/+) | −(−/+) | −(−/+) | − | + | + | 0 | 0 | 0 | 0 | 0 | 0 | 0 | − |
gapA | 0 | −(−/+) | −(−/+) | −(−/+) | −(−/+) | − | + | + | 0 | 0 | 0 | 0 | 0 | 0 | 0 | − |
pgk | 0 | −(−/+) | −(−/+) | −(−/+) | −(−/+) | − | + | + | 0 | 0 | 0 | 0 | 0 | 0 | 0 | − |
eno | 0 | − | − | − | − | − | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | − |
pykF | 0 | − | − | − | − | − | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | − |
cya | 0 | 0 (−) | 0 (−) | 0 (−) | 0 (−) | + | − | − | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 |
crp | 0 | 0 (+) | 0 (+) | 0 (+) | 0 (+) | − | + | + | − | 0 | 0 | 0 | 0 | 0 | 0 | 0 |
fis | 0 | 0 | 0 | 0 | 0 | 0 | − | − | − | + | − | − | 0 | 0 | 0 | 0 |
gyrAB | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | − | − | + | + | 0 | 0 | 0 | 0 |
gyrI | 0 | 0 | 0 | 0 | 0 | 0 | + | + | 0 | 0 | 0 | 0 | + | 0 | 0 | 0 |
topA | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | + | + | − | − | + | 0 | 0 | 0 |
rpoS | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | − | 0 | 0 |
rssB | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | + | 0 | 0 | 0 |
rrn | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | + | 0 | 0 | 0 | 0 | 0 | 0 | 0 |
fruR | 0 | − | − | − | − | − | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | − |
The matrix describes the effect of regulators (column) on genes (rows). Plus signs stand for activation of a gene by a regulator, and minus signs for inhibition. In determining the signs, we excluded the direct effect of a slow variable on itself when the latter is due to non-specific protein degradation through decay and growth dilution [18]. Signs in brackets correspond to interactions whose signs are different in the case of allosteric regulation (that is, they are changed when using model instead of model ). The double sign for the effect of enzymes FbaA, GapA and Pgk on genes fbaA, gapA and pgk describes the combined control of free FruR and CrpcAMP in the presence of allosteric regulation. In particular, the regulation exerted by free FruR leads to an inhibition, whereas a positive regulation arises from allosteric effects via CrpcAMP.