Abstract
In the presence of excess sulfate, cysteine synthesis in pumpkin leaves is not limited by sulfate reduction but by the availability of O-acetylserine. Feeding of O-acetylserine or its metabolic precursors S-acetyl-CoA and CoA to leaf discs enhanced the incorporation of [35S]sulfate into reduced S compounds, mainly into cysteine, at the cost of lowered H2S emission; the uptake and reduction of sulfate is not affected by these treatments. .beta.-Fluoropyruvate, an inhibitor of the generation of S-acetyl-coenzyme A via pyruvate dehydrogenase, stimulated H2S emission in response to sulfate. This stimulation is overcompensated by addition of O-acetylserine, S-acetyl-CoA or CoA. Apparently in the presence of high amounts of sulfate, excess S is reduced and emitted as H2S into the atmosphere. The H2S emitted seems to be produced by the liberation from a precursor of cysteine rather than by cysteine desulfhydration.