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Sodium channel mutation leading to saxitoxin resistance in clams increases risk of PSP

Alternative titleSodium channel mutation responsible for saxitoxin resistance in clams increases risk of PSP
DOIResolve DOI: https://doi.org/10.1038/nature03415
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Affiliation
  1. National Research Council Canada. NRC Institute for Marine Biosciences
FormatText, Article
Subjectbivalves; PSP; toxins; public health
Abstract
Bivalve molluscs, the primary vectors of paralytic shellfish poisoning (PSP) in humans, show marked inter-species variation in their capacity to accumulate PSP toxins (PSTs)1 which has a neural basis2, 3. PSTs cause human fatalities by blocking sodium conductance in nerve fibres4, 5. Here we identify a molecular basis for inter-population variation in PSP resistance within a species, consistent with genetic adaptation to PSTs. Softshell clams (Mya arenaria) from areas exposed to 'red tides' are more resistant to PSTs, as demonstrated by whole-nerve assays, and accumulate toxins at greater rates than sensitive clams from unexposed areas. PSTs lead to selective mortality of sensitive clams. Resistance is caused by natural mutation of a single amino acid residue, which causes a 1,000-fold decrease in affinity at the saxitoxin-binding site in the sodium channel pore of resistant, but not sensitive, clams. Thus PSTs might act as potent natural selection agents, leading to greater toxin resistance in clam populations and increased risk of PSP in humans. Furthermore, global expansion of PSP to previously unaffected coastal areas6 might result in long-term changes to communities and ecosystems.
Publication date
Terms of use
  • 2005 Nature Publishing Group
In
  • Nature 434, no. 7034 (7 April 2005): 763–767.
LanguageEnglish
Peer reviewedYes
NRC numberNRCC 55500
1383
NPARC number3538490
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Record identifier854ab3a5-9f89-4556-b2f0-fc1e349c20a7
Record created2009-03-01
Record modified2020-04-07

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