Genotype and host microbiome alter competitive interactions between Microcystis aeruginosa and Chlorella sorokiniana
Genotype and host microbiome alter competitive interactions between Microcystis aeruginosa and Chlorella sorokiniana
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DOI：
10.1016/j.hal.2020.101939
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发表时间：
2020-11-01
期刊：
影响因子：
6.6
通讯作者：
Denef, Vincent J.
中科院分区：
文献类型：
--
作者：
Schmidt, Kathryn C.;Jackrel, Sara L.;Denef, Vincent J.
蓝藻有害藻华（cyanoHAB）的频率和规模持续增加，威胁着全球淡水生态系统和服务。在北温带湖泊中，蓝藻在初夏出现，继绿藻之后成为主要的浮游植物群，这种模式被认为是由温度和生物可利用营养物质的变化介导的。为了了解这种演替模式的其他驱动因素，我们的研究使用相互入侵实验来检查铜绿微囊藻（cyanoHAB 的主要贡献者）和绿藻 Chlorella sorokiniana 之间的竞争相互作用。我们考虑了可能影响这些相互作用的两个因素：（1）菌株变异，特别强调肝毒素微囊藻毒素基因的存在或缺失，以及（2）宿主相关细菌。我们使用了有毒的铜绿微囊藻 PCC 7806（产生微囊藻毒素的菌株）、PCC 7806 的无毒突变体、无毒的铜绿假单胞菌 PCC 9701（不产生微囊藻毒素的菌株）和 C. sorokiniana。每种生物体都不含所有细菌（即无菌的），并重新引入定义的细菌群落以产生其异种的对应物。通过 C. sorokiniana 的配对异种和配对无菌种群与两种微囊藻菌株之一之间的相互入侵实验来评估竞争性相互作用，每个菌株分别进行评估。使用流式细胞术和随机森林模型快速区分和量化浮游植物种群密度，准确度达 99%。我们发现，M. aeruginosa PCC 7806（而非菌株 PCC 9701）可以从 C. sorokiniana 稳态种群的低丰度中增殖。此外，细菌的存在使得绿脓杆菌 PCC 7806 能够以比无菌生长时更高的种群密度生长成已建立的 C. sorokiniana 种群。相反，当铜绿分枝杆菌占优势时，C. sorokiniana 只能从低密度增殖到 PCC 9701 菌株中，而且只有在无菌条件下。缺乏产生微囊藻毒素能力的 PCC 7806 突变体的行为与有毒的野生型相似，这意味着微囊藻毒素并不是造成两种野生型菌株之间观察到的竞争能力差异的原因。当 PCC 7806 M. aeruginosa 被引入 C. sorokiniana 培养物时，微囊藻毒素 (MC) 的定量显示，当宿主相关细菌不存在时，每个细胞的 MC 数量是两种物种培养物中存在的两倍。我们的结果表明，铜绿微囊藻与 C. sorokiniana 竞争的能力是由参与微囊藻毒素产生的基因之外的基因组差异决定的，并表明宿主相关细菌在介导浮游植物种间相互作用中的重要作用。这些结果扩大了我们对浮游植物演替的关键驱动因素以及淡水有害蓝藻水华的建立和持久性的理解。
Cyanobacterial harmful algal blooms (cyanoHABs) continue to increase in frequency and magnitude, threatening global freshwater ecosystems and services. In north-temperate lakes cyanobacteria appear in early summer, succeeding green algae as the dominant phytoplankton group, a pattern thought to be mediated by changes in temperature and bioavailable nutrients. To understand additional drivers of this successional pattern our study used reciprocal invasion experiments to examine the competitive interaction between Microcystis aeruginosa, a dominant contributor to cyanoHABs, and the green alga Chlorella sorokiniana. We considered two factors that may impact these interactions: (1) strain variation, with a specific emphasis on the presence or absence of the gene for the hepatotoxin microcystin, and (2) host-associated bacteria. We used toxic M. aeruginosa PCC 7806 (microcystin producing strain), a non-toxic mutant of PCC 7806, non-toxic M. aeruginosa PCC 9701 (non-microcystin producing strain), and C. sorokiniana. Each organism was available free of all bacteria (i.e., axenic) and with a re-introduced defined bacterial community to generate their xenic counterparts. Competitive interactions were assessed with reciprocal invasion experiments between paired xenic and paired axenic populations of C. sorokiniana and one of the two Microcystis strains, each assessed separately. Flow cytometry and random forest models were used to rapidly discriminate and quantify phytoplankton population densities with 99% accuracy. We found that M. aeruginosa PCC 7806, but not strain PCC 9701, could proliferate from low abundance in a steady-state population of C. sorokiniana. Further, the presence of bacteria allowed M. aeruginosa PCC 7806 to grow to a higher population density into an established C. sorokiniana population than when grown axenic. Conversely, when M. aeruginosa was dominant, C. sorokiniana was only able to proliferate from low density into the PCC 9701 strain, and only when axenic. The mutant of PCC 7806 lacking the ability to produce microcystin behaved similarly to the toxic wild-type, implying microcystin is not responsible for the difference in competitive abilities observed between the two wild-type strains. Quantification of microcystins (MCs) when PCC 7806 M. aeruginosa was introduced into the C. sorokiniana culture showed two-fold more MCs per cell when host associated bacteria were absent compared to present in both species cultures. Our results show that the ability of M. aeruginosa to compete with C. sorokiniana is determined by genomic differences beyond genes involved in microcystin toxin generation and indicate an important role of host-associated bacteria in mediating phytoplankton interspecies interactions. These results expand our understanding of the key drivers of phytoplankton succession and the establishment and persistence of freshwater harmful cyanobacterial blooms.