Abstract
Produced by cyanobacteria and some plants, BMAA is considered as an important environmental factor in the occurrence of some neurodegenerative diseases. Neither the underlying mechanism of its toxicity, nor its biosynthetic or metabolic pathway in cyanobacteria is understood. Interestingly, BMAA is found to be toxic to some cyanobacteria, making it possible to dissect the mechanism of BMAA metabolism by genetic approaches using these organisms. In this study, we used the cyanobacterium Anabaena PCC 7120 to isolate BMAA-resistant mutants. Following genomic sequencing, several mutations were mapped to two genes involved in amino acids transport, suggesting that BMAA was taken up through amino acid transporters. This conclusion was supported by the protective effect of several amino acids against BMAA toxicity. Furthermore, targeted inactivation of genes encoding different amino acid transport pathways conferred various levels of resistance to BMAA. One mutant inactivating all three major amino acid transport systems could no longer take up BMAA and gained full resistance to BMAA toxicity. Therefore, BMAA is a substrate of amino acid transporters, and cyanobacteria are interesting models for genetic analysis of BMAA transport and metabolism.
Highlights
The neurotoxin β-N-methylamino-l-alanine (BMAA) is a non-protein amino acid, first identified from Cycas in 1967 [1]
In order to select the most suitable report for further genetic characterization, we compared the growth of these two strains in the presence of different concentrations of BMAA in the growth medium
We provided evidence that BMAA enters the cells through the proteaginous amino acid transport systems in the cyanobacterium Anabaena
Summary
The neurotoxin β-N-methylamino-l-alanine (BMAA) is a non-protein amino acid, first identified from Cycas in 1967 [1]. The underlying mechanism is not understood, the accumulation of BMAA in brain tissues is found to be associated with neurodegenerative diseases such as amyotrophic lateral sclerosis, Parkinson’s disease, and Alzheimer’s disease [2,3,4,5]. It is postulated as one of the environmental factors that contribute to the relatively high rate of dementia in Finland [6]. The production of BMAA by cyanobacteria is considered as an important environmental factor affecting human health [17]. Despite the extensive studies, the biosynthesis and metabolic pathways of BMAA remain largely unknown, and the hypothetical pathways recently proposed still lack experimental support [18,19]
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