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BAK基因敲低可延缓造礁珊瑚的白化过程,并减轻其氧化性DNA损伤。

BAK knockdown delays bleaching and alleviates oxidative DNA damage in a reef-building coral.

作者信息

Majerová Eva, Steinle Camryn, Drury Crawford

机构信息

Hawai'i Institute of Marine Biology, University of Hawai'i at Mānoa, Kāne'ohe, HI, USA.

出版信息

Commun Biol. 2025 Aug 13;8(1):1216. doi: 10.1038/s42003-025-08671-y.

DOI:10.1038/s42003-025-08671-y
PMID:40804160
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12350770/
Abstract

As climate change threatens marine ecosystems, efforts to restore coral reefs using resilient corals are increasing. This conservation approach remains limited by our understanding of cellular mechanisms of resilience and trade-offs. Here, we demonstrate that downregulation of pa-BAK stabilizes the coral-algal endosymbiosis and slows bleaching during acute heat stress in Pocillopora acuta through coordinated expression of gene clusters. The improvement in thermal tolerance was closely related to the downregulation efficiency in individual corals. Oxidative DNA damage, a hallmark of thermal stress response, was prevented in corals with stabilized symbiosis, likely through a decrease in mitochondrial ROS release. We hypothesize that this manipulation causes a cascading molecular response, which may impact other traits such as oxidative mitochondrial damage, proving detrimental over the longer term. Developing our understanding of heat-stress defense mechanisms that promote stability in the coral-algal symbiosis is fundamental for effective modern coral reef restoration practices based on improving ecosystem resilience.

摘要

随着气候变化对海洋生态系统构成威胁,利用具有恢复力的珊瑚来恢复珊瑚礁的努力日益增加。这种保护方法仍然受到我们对恢复力细胞机制和权衡理解的限制。在此,我们证明,通过基因簇的协调表达,下调pa-BAK可稳定珊瑚-藻类内共生关系,并减缓尖锐鹿角珊瑚在急性热应激期间的白化现象。耐热性的提高与单个珊瑚中的下调效率密切相关。氧化DNA损伤是热应激反应的一个标志,在共生关系稳定的珊瑚中可预防,可能是通过线粒体ROS释放的减少。我们推测,这种操作会引发级联分子反应,这可能会影响其他特征,如线粒体氧化损伤,从长远来看可能是有害的。深入了解促进珊瑚-藻类共生关系稳定性的热应激防御机制,对于基于提高生态系统恢复力的有效现代珊瑚礁恢复实践至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79ce/12350770/465a19ae704a/42003_2025_8671_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79ce/12350770/055ee3f98a2a/42003_2025_8671_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79ce/12350770/0e1cde94f37a/42003_2025_8671_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79ce/12350770/d18fe4948113/42003_2025_8671_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79ce/12350770/465a19ae704a/42003_2025_8671_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79ce/12350770/055ee3f98a2a/42003_2025_8671_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79ce/12350770/0e1cde94f37a/42003_2025_8671_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79ce/12350770/d18fe4948113/42003_2025_8671_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79ce/12350770/465a19ae704a/42003_2025_8671_Fig4_HTML.jpg

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Comparative physiology reveals heat stress disrupts acid-base homeostasis independent of symbiotic state in the model cnidarian Exaiptasia diaphana.
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