Bacterial Quorum-Sensing Signal Arrests Phytoplankton Cell Division and Impacts Virus-Induced Mortality.
Bacterial Quorum-Sensing Signal Arrests Phytoplankton Cell Division and Impacts Virus-Induced Mortality.
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DOI：
10.1128/msphere.00009-21
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发表时间：
2021-05-12
期刊：
影响因子：
4.8
通讯作者：
Whalen KE
中科院分区：
文献类型：
--
作者：
Pollara SB;Becker JW;Nunn BL;Boiteau R;Repeta D;Mudge MC;Downing G;Chase D;Harvey EL;Whalen KE
细菌和浮游植物在海洋中形成密切的联系，这是由化学化合物的交换驱动的。细菌信号2-庚基-4-喹诺酮（HHQ）减缓浮游植物的生长;然而，负责的机制仍然未知。浮游植物和异养细菌之间的相互作用通过控制初级生产、构建海洋食物网、介导碳输出和影响全球气候，从根本上塑造了海洋生态系统。分泌的化合物促进了植物毒素-细菌的相互作用;然而，将这些化学信号、它们的作用机制以及它们所产生的生态后果联系起来仍然是一个根本性的挑战。细菌群体感应信号2-庚基-4-喹诺酮（HHQ）诱导立即，但可逆的，细胞停滞（无细胞分裂或死亡）在球石藻Emiliania huxleyi;然而，负责的机制仍然未知。使用转录组学和蛋白质组学的方法结合诊断生化和荧光细胞为基础的测定，我们表明，HHQ暴露导致浮游植物的S期停滞与DNA损伤的积累和缺乏修复一致，尽管诱导的DNA损伤反应（DDR）。虽然这种影响是可逆的，HHQ暴露的浮游植物也受到保护，从病毒死亡率，归因于一个新的作用，群体感应信号在调节多营养相互作用。此外，我们的数据表明，在现场测量HHQ与增强微型和纳米浮游生物生物量的领域相吻合。我们的研究结果表明，细菌通信信号作为新兴的参与者，可能是帮助构建整个海洋复杂微生物群落的因素之一。细菌和浮游植物在海洋中形成密切的联系，这是由化学化合物的交换驱动的。细菌信号2-庚基-4-喹诺酮（HHQ）减缓浮游植物的生长;然而，负责的机制仍然未知。在这里，我们表明，HHQ暴露导致浮游植物DNA损伤的积累，并阻止其修复。虽然这种影响是可逆的，但HHQ暴露的浮游植物也减轻了病毒死亡率，提高了这种复杂相互作用的生态后果。进一步的结果表明，HHQ可能靶向参与核苷酸生物合成和DNA修复的浮游植物蛋白，这两者都是病毒成功的关键目标。我们的研究结果支持微生物线索作为海洋生态系统中的新兴参与者，为细菌通信信号如何介导种间和界间行为提供了一个新的机制框架。
Bacteria and phytoplankton form close associations in the ocean that are driven by the exchange of chemical compounds. The bacterial signal 2-heptyl-4-quinolone (HHQ) slows phytoplankton growth; however, the mechanism responsible remains unknown. Interactions between phytoplankton and heterotrophic bacteria fundamentally shape marine ecosystems by controlling primary production, structuring marine food webs, mediating carbon export, and influencing global climate. Phytoplankton-bacterium interactions are facilitated by secreted compounds; however, linking these chemical signals, their mechanisms of action, and their resultant ecological consequences remains a fundamental challenge. The bacterial quorum-sensing signal 2-heptyl-4-quinolone (HHQ) induces immediate, yet reversible, cellular stasis (no cell division or mortality) in the coccolithophore Emiliania huxleyi; however, the mechanism responsible remains unknown. Using transcriptomic and proteomic approaches in combination with diagnostic biochemical and fluorescent cell-based assays, we show that HHQ exposure leads to prolonged S-phase arrest in phytoplankton coincident with the accumulation of DNA damage and a lack of repair despite the induction of the DNA damage response (DDR). While this effect is reversible, HHQ-exposed phytoplankton were also protected from viral mortality, ascribing a new role of quorum-sensing signals in regulating multitrophic interactions. Furthermore, our data demonstrate that in situ measurements of HHQ coincide with areas of enhanced micro- and nanoplankton biomass. Our results suggest bacterial communication signals as emerging players that may be one of the contributing factors that help structure complex microbial communities throughout the ocean. IMPORTANCE Bacteria and phytoplankton form close associations in the ocean that are driven by the exchange of chemical compounds. The bacterial signal 2-heptyl-4-quinolone (HHQ) slows phytoplankton growth; however, the mechanism responsible remains unknown. Here, we show that HHQ exposure leads to the accumulation of DNA damage in phytoplankton and prevents its repair. While this effect is reversible, HHQ-exposed phytoplankton are also relieved of viral mortality, elevating the ecological consequences of this complex interaction. Further results indicate that HHQ may target phytoplankton proteins involved in nucleotide biosynthesis and DNA repair, both of which are crucial targets for viral success. Our results support microbial cues as emerging players in marine ecosystems, providing a new mechanistic framework for how bacterial communication signals mediate interspecies and interkingdom behaviors.