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Article Addendum

Rethinking cycad metabolite research

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Pages 86-88 | Received 02 Nov 2010, Accepted 02 Nov 2010, Published online: 01 Jan 2011
 

Abstract

Cycads are among the most ancient of extant Spermatophytes, and are known for their numerous pharmacologically active compounds. One compound in particular, β-methylamino-L-alanine (BMAA), has been implicated as the cause of amyotrophic lateral sclerosis/parkinson dementia complex (ALS/PDC) on Guam. Previous studies allege that BMAA is produced exclusively by cyanobacteria, and is transferred to cycads through the symbiotic relationship between these cyanobacteria and the roots of cycads. We recently published data showing that Cycas micronesica seedlings grown without endophytic cyanobacteria do in fact increase in BMAA, invalidating the foundation of the BMAA hypothesis. We use this example to suggest that the frenzy centered on BMAA and other single putative toxins has hindered progress. The long list of cycad-specific compounds may have important roles in signaling or communication, but these possibilities have been neglected during decades of attempts to force single metabolites into a supposed anti-herbivory function. We propose that an unbiased, comprehensive approach may be a more appropriate means of proceeding with cycad biochemistry research.

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Figures and Tables

Figure 1 A representative chromatographic separation of a Cycas micronesica leaf sample displaying a large number of peaks. Each of these peaks corresponds to a compound which illustrates the chemical complexity of the cycad metabolome.

Figure 1 A representative chromatographic separation of a Cycas micronesica leaf sample displaying a large number of peaks. Each of these peaks corresponds to a compound which illustrates the chemical complexity of the cycad metabolome.

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