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The effect of exogenous β-N-methylamino-l-alanine (BMAA) on the diatoms Phaeodactylum tricornutum and Thalassiosira weissflogii

Journal article
Authors Sandra Lage
Linnea Ström
Anna Godhe
Sara Rydberg
Published in Harmful Algae
Volume 58
Pages 85-92
ISSN 1568-9883
Publication year 2016
Published at Department of marine sciences
Linnaeus Centre for Marine Evolutionary Biology (CEMEB)
Pages 85-92
Language en
Links dx.doi.org/10.1016/j.hal.2016.08.00...
Keywords β-N-methylamino-l-alanine, Phaeodactylum tricornutum, Thalassiosira weissflogii, Ammonia, Physiological role
Subject categories Marine ecology


β-N-methylamino-l-alanine (BMAA), a non-protein amino acid with neurodegenerative features, is known to be produced by cyanobacteria, diatoms and a dinoflagellate. BMAA research has intensified over the last decade, and knowledge has been gained about its bioaccumulation in aquatic and terrestrial ecosystems, toxic effects in model organisms and neurotoxicity in vivo and in vitro. Nevertheless, knowledge of the actual physiological role of BMAA in the producing species or of the ecological factors that regulate BMAA production is still lacking. A few studies propose that BMAA functions to signal nitrogen depletion in cyanobacteria. To investigate whether BMAA might have a similar role in diatoms, two diatom species – Phaeodactylum tricornutum and Thalassiosira weissflogii – were exposed to exogenous BMAA at environmental relevant concentrations, i.e. 0.005, 0.05 and 0.5 μM. BMAA was taken up in a concentration dependent manner in both species in the BMAA free fraction and in the protein fraction of T. weissflogii. As a result of the treatments, the diatom cells at some of the time points and at some of the BMAA concentrations exhibited lower concentrations of chlorophyll a and protein, in comparison to controls. At the highest (0.5 μM) concentration of BMAA, extracellular ammonia was found in the media of both species at all time points. These results suggest that BMAA interferes with nitrogen metabolism in diatoms, possibly by inhibiting ammonium assimilation via the GS/GOGAT pathway.

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