PSP toxin release from the cyanobacterium <i>Raphidiopsis brookii</i> D9 (Nostocales) can be induced by sodium and potassium ions

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dc.contributor.authorSoto-Liebe, Katia
dc.contributor.authorMendez, Marco A.
dc.contributor.authorFuenzalida, Loreto
dc.contributor.authorKrock, Bernd
dc.contributor.authorCembella, Allan
dc.contributor.authorVasquez, Monica
dc.date.accessioned2025-01-24T00:06:55Z
dc.date.available2025-01-24T00:06:55Z
dc.date.issued2012
dc.description.abstractParalytic shellfish poisoning (PSP)toxins are a group of naturally occurring neurotoxic alkaloids produced among several genera of primarily freshwater cyanobacteria and marine dinoflagellates. Although saxitoxin (STX) and analogs are all potent Na+ channel blockers in vertebrate cells, the functional role of these compounds for the toxigenic microorganisms is unknown. Based upon the known importance of monovalent cations (such as sodium) in the maintenance of cellular homeostasis and ion channel function, we examined the effect of high extracellular concentrations of these ions on growth, cellular integrity, toxin production and release to the external medium in the filamentous fresh-water cyanobacterium, Raphidiopsis brookii D9; a gonyautoxins (GTX2/3) and SIX producing toxigenic strain. We observed a toxin export in response to high (17 mM) NaCl and KCl concentrations in the growth medium that was not primarily related to osmotic stress effects, compared to the osmolyte mannitol. Addition of exogenous PSP toxins with the same compositional profile as the one produced by R. brookii D9 was able to partially mitigate this effect of high Na+ (17 mM). The PSP toxin biosynthetic gene cluster (sxt) in D9 has two genes (sxtF and sxtM) that encode for a MATE (multidrug and toxic compound extrusion) transporter. This protein family, represented by NorM in the bacterium Vibrio parahaemolyticus, confers resistance to multiple cationic toxic agents through Na+/drug antiporters. Conserved domains for Na+ and drug recognition have been described in NorM. For the D9 sxt cluster, the Na+ recognition domain is conserved in both SxtF and SxtM, but the drug recognition domain differs between them. These results suggest that PSP toxins are exported directly in response to the presence of monovalent cations (Na+, K+) at least at elevated concentrations. Thus, the presence of both genes in the sxt cluster from strain D9 can be explained as a selective recognition mechanism by the SxtF/M transporters for GTX2/3 and SIX. We propose that these toxins in cyanobacteria could act extracellularly as a protective mechanism to ensure homeostasis against extreme salt variation in the environment. (C) 2012 Elsevier Ltd. All rights reserved.
dc.fuente.origenWOS
dc.identifier.doi10.1016/j.toxicon.2012.09.001
dc.identifier.eissn1879-3150
dc.identifier.issn0041-0101
dc.identifier.urihttps://doi.org/10.1016/j.toxicon.2012.09.001
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/101880
dc.identifier.wosidWOS:000311177500014
dc.issue.numero7
dc.language.isoen
dc.pagina.final1334
dc.pagina.inicio1324
dc.revistaToxicon
dc.rightsacceso restringido
dc.subjectCyanobacteria
dc.subjectRaphidiopsis brookii
dc.subjectPSP toxins
dc.subjectIonic effect
dc.subjectCyanotoxin export
dc.subjectMATE proteins
dc.subject.ods13 Climate Action
dc.subject.ods15 Life on Land
dc.subject.ods06 Clean Water and Sanitation
dc.subject.ods14 Life Below Water
dc.subject.odspa13 Acción por el clima
dc.subject.odspa15 Vida de ecosistemas terrestres
dc.subject.odspa06 Agua limpia y saneamiento
dc.subject.odspa14 Vida submarina
dc.titlePSP toxin release from the cyanobacterium <i>Raphidiopsis brookii</i> D9 (Nostocales) can be induced by sodium and potassium ions
dc.typeartículo
dc.volumen60
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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