Abstract
The phytotoxin, syringomycin, produced by Pseudomonas syringae pv. syringae caused the cellular efflux of K + in cell suspensions of Rhodotorula pilimanae and Saccharomyces cerevisiae. K + levels in the suspension media increased 3–10-fold within 2 min after adding syringomycin (1.5 μg/ml). As shown previously, syringomycin also stimulated the uptake of tetraphenylphosphonium (TPP) ions 10-fold. Although valinomycin (10 μM) and nigericin (10 μM) inhibited and N,N′-dicyclohexylcarbodiimide (DCCD) (50 μg/ml) stimulated TPP uptake, these ienophores had no effect on K + efflux. However, carbonylcyanide m-chlorophenylhydrazone (CCCP) induced K + efflux and inhibited TPP uptake. We conclude that syringomycin causes K + efflux and that this effect is independent of the toxin's action on the DCCD-sensitive H +-ATPase. Also syringomycin is not acting as a K + ionophore such as valinomycin or nigericin, nor does its action resemble that of the protonophore CCCP.
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