Exploring the role of GS–GOGAT cycle in microcystin synthesis and regulation – a model based analysis. Issue 12 (16th October 2017)

• Record Type: Journal Article
• Authors: Banerjee, Swarnendu; Subramanian, Abhishek; Chattopadhyay, Joydev; Sarkar, Ram Rup
• Is Part Of: Molecular bioSystems. Volume 13:Issue 12(2017)
• Page Start: 2603
• Page End: 2614
• Publication Date: 2017-10-16
• Subjects: Molecular biology -- Periodicals; Biochemistry -- Periodicals; 571.7405
• DOI: 10.1039/c7mb00342k
• Languages: English
• ISSNs: 1742-206X

Abstract

Abstract : First kinetic model of microcystin regulation that explains the biochemical and gene regulatory events linking environmental nitrogen change with microcystin. Abstract : Toxic cyanobacteria blooms populate water bodies by consuming external nutrients and releasing cyanotoxins that are detrimental for other aquatic species, producing a significant impact on the plankton ecosystem and food web. To exercise population-level control of toxin production, understanding the biochemical mechanisms that explain cyanotoxin regulation within a bacterial cell is of utmost importance. In this study, we explore the mechanistic events to investigate the dependence of toxin microcystin on external nitrogen, a known regulator of the toxin, and for the first time, propose a kinetic model that analyzes the intracellular conditions required to ensure nitrogen dependence on microcystin. We hypothesize that the GS–GOGAT cycle is manipulated by variable influx of different intracellular metabolites that can either disturb or promote the balance between the enzyme microcystin synthetase and substrate glutamate to produce variable microcystin levels. As opposed to the popular notion that nitrogen starvation increases microcystin synthesis, our analyses suggest that under certain intracellular metabolite regimes, this relationship can either be completely lost or reversed. External nitrogen can only complement the conditions fixed by intracellular glutamate, glutamine and 2-oxoglutarate. This mechanistic understanding can provide an experimentally testable hypothesis for exploring the less-known biology of microcystin synthesis and designing specific interventions.