4.5 Article

Calcium homeostasis disruption initiates rapid growth after micro-fragmentation in the scleractinian coral Porites lobata

Journal

ECOLOGY AND EVOLUTION
Volume 12, Issue 9, Pages -

Publisher

WILEY
DOI: 10.1002/ece3.9345

Keywords

calcium homeostasis; coral; gene expression; stress response; transcriptome

Funding

  1. University of Guam Sea Grant Master's Thesis Research Supplemental Grants
  2. National Science Foundation's Established Program [OIA-1457769, OIA-1946352]

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This study utilized RNA-seq technology to investigate the physiological responses of Porites lobata colonies to physical fragmentation and outplanting. The results demonstrate significant impacts of fragmentation and outplanting on energy production, calcium homeostasis, antioxidant expression, and protein turnover in the coral host. These findings shed light on the physiological mechanisms that enable rapid wound healing and stabilization in response to physical injury in corals.
Coral reefs are ecosystems under increasing threat from global climate change. Coral restoration is a tool for preserving the biological and ecological function of coral reefs by mitigating coral loss and maintaining the structural integrity and complexity of reefs. To generate the necessary stock for coral restoration, larger coral colonies are usually fragmented to generate smaller specimens for outplanting, taking advantage of the high regenerative ability of corals. In this study, we utilized RNA-seq technology to understand the physiological responses of Porites lobata colonies to physical fragmentation and outplanting, which have thus far not been characterized. Our results demonstrate that P. lobata fragments undergoing physical injury recover through two distinct phases: rapid wound regeneration of the cut margins, followed by a slower growth phase that cements the colony to the substrate. Our study found rapid physiological responses to acute physical injury and outplanting in the coral host that involved significantly increased energy production, calcium homeostasis disruption, and endoplasmic reticulum (ER) stress leading to increased antioxidant expression and rates of protein turnover. Our results suggest that phosphoinositide-mediated acute calcium homeostasis disruption stimulates wound recovery processes in response to physical injury. Symbiont gene expression revealed extremely low gene differences in response to fragmentation, growth, and outplanting. These results provide insight into the physiological mechanisms that allow for rapid wound healing and stabilization in response to physical injury in corals.

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