Cool temperature acclimation in toxigenic Microcystis aeruginosa PCC 7806 and its non-toxigenic mutant.

Cool temperature acclimation in toxigenic Microcystis aeruginosa PCC 7806 and its non-toxigenic mutant.
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产毒铜绿微囊藻 PCC 7806 及其非产毒突变体的低温驯化。

DOI:
10.1101/2023.08.28.555099
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发表时间:
2023
期刊:
bioRxiv : the preprint server for biology
影响因子:
--
通讯作者:
Wilhelm,StevenW
Wilhelm,StevenW
中科院分区:
--
文献类型:
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作者:
Stark,GwendolynF;Martin,RobbieM;Smith,LauraE;Wei,Bofan;Hellweger,FerdiL;Bullerjahn,GeorgeS;McKay,RMichaelL;Boyer,GregoryL;Wilhelm,StevenW

文献摘要

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对于铜绿微囊藻PCC 7806,温度从26° C降低到19° C,在连续培养的生长期间,每个细胞的微囊藻毒素配额加倍。在这里,我们测试了微囊藻毒素的增加是否提供了M。通过比较细胞浓度、细胞生理学和转录组学推断的代谢,铜绿假单胞菌PCC 7806在低温生长期间具有适合性优势。铜绿假单胞菌PCC 7806 ΔmcyB.光生理数据结合转录组学数据揭示了突变株在19° C下生长期间的代谢变化,其中包括增加的电子汇和非光化学淬灭。增加基因表达的谷胱甘肽依赖性peroxiredoxin在冷处理过程中观察到,这表明补偿机制,以抵御活性氧在突变体中的微囊藻毒素的情况下。我们的观察结果强调了长期防御策略在氧化应激管理中的潜在选择性优势(即,制造微囊藻毒素)与产生细胞成分以主动消散或降解氧化应激剂的短期主动策略相比。
For Microcystis aeruginosa PCC 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 provided M. aeruginosa PCC 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 strain M. aeruginosa PCC 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) vs the shorter-term proactive strategy of producing cellular components to actively dissipate or degrade oxidative stress agents.