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.
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.
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