<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Banerjee, Swarnendu</style></author><author><style face="normal" font="default" size="100%">Subramanian, Abhishek</style></author><author><style face="normal" font="default" size="100%">Chattopadhyay, Joydev</style></author><author><style face="normal" font="default" size="100%">Sarkar, Ram Rup</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Exploring the role of GS-GOGAT cycle in microcystin synthesis and regulation - a model based analysis</style></title><secondary-title><style face="normal" font="default" size="100%">Molecular Biosystems</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">DEC</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">13</style></volume><pages><style face="normal" font="default" size="100%">2603-2614</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">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.</style></abstract><issue><style face="normal" font="default" size="100%">12</style></issue><work-type><style face="normal" font="default" size="100%">Article</style></work-type><custom3><style face="normal" font="default" size="100%">Foreign</style></custom3><custom4><style face="normal" font="default" size="100%">2.781</style></custom4></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Banerjee, Swarnendu</style></author><author><style face="normal" font="default" size="100%">Sarkar, Ram Rup</style></author><author><style face="normal" font="default" size="100%">Chattopadhyay, Joydev</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Effect of copper contamination on zooplankton epidemics</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of Theoretical Biology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Bistability</style></keyword><keyword><style  face="normal" font="default" size="100%">Chemical contamination</style></keyword><keyword><style  face="normal" font="default" size="100%">Daphnia-parasite</style></keyword><keyword><style  face="normal" font="default" size="100%">Hormesis</style></keyword><keyword><style  face="normal" font="default" size="100%">Host-resource</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2019</style></year><pub-dates><date><style  face="normal" font="default" size="100%">MAY</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">469</style></volume><pages><style face="normal" font="default" size="100%">61-74</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Infectious disease and chemical contamination are increasingly becoming vital issues in many ecosystems. However, studies integrating the two are surprisingly rare. Contamination not only affects the inherent host-resource interaction which influences the epidemic process but may also directly affect epidemiological traits via changes in host's behaviour. The fact that heavy metal such as copper is also an essential trace element for organisms, further increase complexity which make predicting the resultant effect of contamination and disease spread difficult. Motivated by this, we model the effect of copper enrichment on a phytoplankton-zooplankton-fungus system. We show that extremely deficient or toxic copper may have a destabilizing effect on the underlying host-resource dynamics due to increased relative energy fluxes as a result of low host mortality due to fish predation. Further, on incorporating disease into the system, we find that the system can become disease-free for an intermediate range of copper concentration whereas it may persist for very less copper enrichment. Also, we predict that there may exist vulnerable regions of copper concentration near the toxic and deficient levels, where the parasite can invade the system for a comparatively lower spore yield. Overall, our results demonstrate that, the effect of contamination may be fundamental to understanding disease progression in community ecology. (C) 2019 Elsevier Ltd. All rights reserved.&lt;/p&gt;</style></abstract><work-type><style face="normal" font="default" size="100%">Article</style></work-type><custom3><style face="normal" font="default" size="100%">Foreign</style></custom3><custom4><style face="normal" font="default" size="100%">1.833</style></custom4></record></records></xml>