BMAA Inhibits Nitrogen Fixation in the Cyanobacterium Nostoc sp. PCC 7120

Lotta Berntzon,Ulla Rasmussen,Johan Eriksson,Birgitta Bergman,Sven Erasmie,Narin Celepli

doi:10.3390/md11083091

Abstract

Cyanobacteria produce a range of secondary metabolites, one being the neurotoxic non-protein amino acid β-N-methylamino-L-alanine (BMAA), proposed to be a causative agent of human neurodegeneration. As for most cyanotoxins, the function of BMAA in cyanobacteria is unknown. Here, we examined the effects of BMAA on the physiology of the filamentous nitrogen-fixing cyanobacterium Nostoc sp. PCC 7120. Our data show that exogenously applied BMAA rapidly inhibits nitrogenase activity (acetylene reduction assay), even at micromolar concentrations, and that the inhibition was considerably more severe than that induced by combined nitrogen sources and most other amino acids. BMAA also caused growth arrest and massive cellular glycogen accumulation, as observed by electron microscopy. With nitrogen fixation being a process highly sensitive to oxygen species we propose that the BMAA effects found here may be related to the production of reactive oxygen species, as reported for other organisms.

Highlights

Cyanobacteria produce a vast range of secondary metabolites, and yet the functions of these compounds remain largely unknown
PCC 7120, hereafter Nostoc 7120) selected as the test organism was previously reported to produce being the neurotoxic non-protein amino acid β-N-methylamino-L-alanine (BMAA) [5], which was verified for our strain using LC-MS/MS
Since BMAA may be an environmental factor triggering human neurodegeneration, it is of great importance to elucidate the role of BMAA in this human-related context, and to better comprehend the nature and significance of BMAA in cyanobacteria

Summary

Introduction

Cyanobacteria produce a vast range of secondary metabolites, and yet the functions of these compounds remain largely unknown. Toxin-producing cyanobacteria are globally widespread in both aquatic and terrestrial environments, the biosynthesis of the cyanotoxins is restricted to a limited number of genera within the cyanobacterial phylum. Some of the best-known examples of toxins produced by cyanobacteria are microcystins (Microcystis spp. and Anabaena spp.), nodularin (Nodularia spumigena), and anatoxin-a (Anabaena flos-aquae and Phormidium spp.) [1,2]. As toxin-producing cyanobacteria often form massive surface accumulations, known as blooms, in aquatic environments, including touristic and recreational coastal areas, the production of toxins is considered a nuisance and a potential health issue. Genome sequencing of toxic bloom-forming cyanobacteria has revealed an array of biosynthetic gene clusters involved in toxin production and has facilitated a deeper understanding of the role and regulation of such bioactive compounds [3,4]

Results

Discussion

Conclusion