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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.