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Applied and Environmental Microbiology, August 2000, p. 3387-3392, Vol. 66, No. 8
0099-2240/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Light and the Transcriptional Response of the Microcystin Biosynthesis Gene Cluster

Melanie Kaebernick,1,2 Brett A. Neilan,1,* Thomas Börner,2 and Elke Dittmann2

School of Microbiology and Immunology, University of New South Wales, Sydney 2052, Australia,1 and Institute for Biology (Genetics), Humboldt University, Berlin, Germany2

Received 16 March 2000/Accepted 5 May 2000

Microcystin, a hepatotoxin known to be the cause of animal and human deaths, is produced by the bloom-forming cyanobacterium Microcystis aeruginosa in freshwater bodies worldwide. The toxin is produced nonribosomally via a multifunctional enzyme complex, consisting of both peptide synthetase and polyketide synthase modules coded for by the mcy gene cluster. The recent identification of the mcy genes in the production of microcystin synthetase for the first time provides an avenue to study the regulation of microcystin production at a genetic level. In this study, M. aeruginosa PCC7806 was grown either under continuous light of various intensities or under low light with subsequent short-term exposure to different light intensities and qualities and various stress factors. RNase protection assays were employed to observe the level of mcyB and mcyD transcription under each condition. Both mcyB and mcyD transcript levels were increased under high light intensities and red light. Blue light and certain artificial stress factors (methylviologen and NaCl) led to reduced transcript amounts. There appeared to be two light thresholds, between dark and low light (16 µmol of photons m-2 s-1), and medium (31 µmol of photons m-2 s-1) and high light (68 µmol of photons m-2 s-1), at which a significant increase in transcription occurred. Our findings show that the effect of light on microcystin synthetase production is due to light quality and is initiated at certain threshold intensities, which are not necessarily reflected by observed intracellular toxin bioactivity.

* Corresponding author. Mailing address: School of Microbiology and Immunology, University of New South Wales, Sydney 2052, Australia. Phone: 61-2-93853235. Fax: 61-2-93851591. E-mail: b.neilan{at}unsw.edu.au.

Applied and Environmental Microbiology, August 2000, p. 3387-3392, Vol. 66, No. 8
0099-2240/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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