Light and the transcriptional response of the microcystin biosynthesis gene cluster

Citation
M. Kaebernick et al., Light and the transcriptional response of the microcystin biosynthesis gene cluster, APPL ENVIR, 66(8), 2000, pp. 3387-3392
Citations number
45
Categorie Soggetti
Biology,Microbiology
Journal title
APPLIED AND ENVIRONMENTAL MICROBIOLOGY
ISSN journal
00992240 → ACNP
Volume
66
Issue
8
Year of publication
2000
Pages
3387 - 3392
Database
ISI
SICI code
0099-2240(200008)66:8<3387:LATTRO>2.0.ZU;2-E
Abstract
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 mu ltifunctional enzyme complex, consisting of both peptide synthetase and pol yketide synthase modules coded for by the mcy gene cluster. The recent iden tification of the mcy genes in the production of microcystin synthetase for the first time provides an avenue to study the regulation of microcystin p roduction at a genetic level. In this study, nl. aeruginosa PCC7806 was gro wn either under continuous light of various intensities or under low light with subsequent short-term exposure to different light intensities and qual ities 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 intensitie s and red light. Blue light and certain artificial stress factors (methylvi ologen and NaCl) led to reduced transcript amounts. There appeared to be tw o light thresholds, between dark and low light (16 mu mol of photons m(-2) s(-1)), and medium (31 mu mol of photons m(-2) s(-1)) and high light (68 mu mol of photons m(-2) s(-1)), at which a significant increase in transcript ion occurred. Our findings show that the effect of light on microcystin syn thetase production is due to light quality and is initiated lit certain thr eshold intensities, which are not necessarily reflected by observed intrace llular toxin bioactivity.