Cool temperature acclimation in toxigenicMicrocystis aeruginosaPCC 7806 and its non-toxigenic mutant

Author:

Stark Gwendolyn F.,Martin Robbie M.,Smith Laura E.,Wei Bofan,Hellweger Ferdi L.,Bullerjahn George S.ORCID,McKay R. Michael L.ORCID,Boyer Gregory L.,Wilhelm Steven W.ORCID

Abstract

AbstractForMicrocystis aeruginosaPCC 7806, temperature decreases from 26° C to 19° C double the microcystin quota per cell during growth in continuous culture. Here we tested whether this increase in microcystin providedM. aeruginosaPCC 7806 with a fitness advantage during colder-temperature growth by comparing cell concentration, cellular physiology, and the transcriptomics-inferred metabolism to a non-toxigenic mutant strainM. aeruginosaPCC 7806 ΔmcyB. Photo-physiological data combined with transcriptomic data revealed metabolic changes in the mutant strain during growth at 19° C, which included increased electron sinks and non-photochemical quenching. Increased gene expression was observed for a glutathione-dependent peroxiredoxin during cold treatment, suggesting compensatory mechanisms to defend against reactive oxygen species are employed in the absence of microcystin in the mutant. Our observations highlight the potential selective advantages of a longer-term defensive strategy in management of oxidative stress (i.e.,making microcystin)vsthe shorter-term proactive strategy of producing cellular components to actively dissipate or degrade oxidative stress agents.ImportanceThrough comparisons of a microcystin-producing wildtype strainM. aeruginosaPCC 7806 and a non microcystin-producing mutant,M. aeruginosaPCC 7806ΔmcyB, our observations highlight defensive (microcystin production)vsactive (production of degradation enzymes and increased electron sinks) strategies for dealing with cold-temperature induced oxidative stress as well as associated physiological changes. This work increases our understanding of microcystin’s intracellular function, and the role it may play in bloom ecology. In combination with other studies, this work begins to experimentally establish a mechanistic foundation to better understand cold-to-warm seasonal transitions from toxigenic to non-toxigenic strains frequently observedin situ.

Publisher

Cold Spring Harbor Laboratory

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