FIG 6.

Model for the regulation of DmdB activity in Ruegeria pomeroyi DSS-3. During carbon and energy limitation, DmdB1 overcomes DMSP inhibition as ADP concentrations increase as a result of decreasing cellular energy charge. The resulting stimulation of the demethylation pathway increases the energy charge and lowers ADP concentrations until DMSP inhibition is restored. A different chain of events may explain the role of DmdB2. The levels of DmdA activity and MMPA are likely set by the availability of free THF. During rapid growth, methyl-THF is oxidized, yielding high intracellular levels of free THF and MMPA. The increased levels of MMPA reverse the DMSP inhibition of DmdB2 and lead to rapid production of acetaldehyde and MeSH. These additional energy sources spare the pools of methyl-THF, leading to a depletion of free THF and a decline in MMPA production. In addition, the oxidation of MeSH leads to H₂O₂ production, resulting in oxidative stress and slowing DMSP-dependent growth. The slowdown in growth reduces the demand for methyl-THF, causing a depletion of free THF. Alternatively, both enzymes may be active during growth on methionine when MMPA is produced in the absence of DMSP.