In July 2016, East Bank of Flower Garden Banks (FGB) National Marine Sanctuary experienced a localized mortality event (LME) of multiple invertebrate species that ultimately led to reductions in coral cover. Abiotic data taken directly after the event suggested that acute deoxygenation contributed to the mortality. Despite the large impact of this event on the coral community, there was no direct evidence that this LME was driven by acute deoxygenation, and thus we explored whether gene expression responses of corals to the LME would indicate what abiotic factors may have contributed to the LME. Gene expression of affected and unaffected corals sampled during the mortality event revealed evidence of the physiological consequences of the LME on coral hosts and their algal symbionts from two congeneric species (Orbicella franksi and Orbicella faveolata). Affected colonies of both species differentially regulated genes involved in mitochondrial regulation and oxidative stress. To further test the hypothesis that deoxygenation led to the LME, we measured coral host and algal symbiont gene expression in response to ex situ experimental deoxygenation (control = 6.9 ± 0.08 mg L−1, anoxic = 0.083 ± 0.017 mg L−1) in healthy O. faveolata colonies from the FGB. However, this deoxygenation experiment revealed divergent gene expression patterns compared to the corals sampled during the LME and was more similar to a generalized coral environmental stress response. It is therefore likely that while the LME was connected to low oxygen, it was a series of interconnected stressors that elicited the unique gene expression responses observed here. These in situ and ex situ data highlight how field responses to stressors are unique from those in controlled laboratory conditions, and that the complexities of deoxygenation events in the field likely arise from interactions between multiple environmental factors simultaneously.

中文翻译：

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珊瑚分子对局部死亡事件和异位脱氧反应的交叉点

2016 年 7 月，花园岸 (FGB) 国家海洋保护区东岸经历了多种无脊椎动物物种的局部死亡事件 (LME)，最终导致珊瑚覆盖面积减少。事件发生后立即采集的非生物数据表明，急性脱氧导致了死亡。尽管这一事件对珊瑚群落产生了巨大影响，但没有直接证据表明这次 LME 是由急性脱氧驱动的，因此我们探讨了珊瑚对 LME 的基因表达反应是否表明哪些非生物因素可能导致了 LME 。在死亡事件期间采样的受影响和未受影响的珊瑚的基因表达揭示了 LME 对来自两个同类物种的珊瑚宿主及其藻类共生体的生理影响的证据。法兰氏圆球菌和蜂窝轮虫）。两个物种受影响的菌落对涉及线粒体调节和氧化应激的基因进行了差异性调节。为了进一步检验脱氧导致 LME 的假设，我们测量了珊瑚宿主和藻类共生体基因表达对异位实验脱氧的反应（对照 = 6.9 ± 0.08 mg·L−1, 缺氧 = 0.083 ± 0.017 mg·L−1）在健康的情况下福维奥拉塔FGB 的殖民地。然而，这种脱氧实验揭示了与 LME 期间采样的珊瑚相比不同的基因表达模式，并且更类似于广义的珊瑚环境应激反应。因此，虽然 LME 与低氧有关，但一系列相互关联的应激源很可能引发了此处观察到的独特基因表达反应。这些原位和非原位数据强调了现场对应激源的反应与受控实验室条件下的反应有何不同，并且现场脱氧事件的复杂性可能是由多个环境因素同时相互作用引起的。