Transcriptomic signatures across a critical sedimentation threshold in a major reef-building coral.

Sedimentation is a major cause of global near-shore coral reef decline. Although the negative impacts of sedimentation on coral reef community composition have been well-documented, the effects of sedimentation on coral metabolism in situ have received comparatively little attention. Using transcriptomics, we identified gene expression patterns changing across a previously defined sedimentation threshold that was deemed critical due to changes in coral cover and community composition. We identified genes, pathways, and molecular processes associated with this transition that may allow corals, such as Porites lobata, to tolerate chronic, severe sedimentation and persist in turbid environments. Alternative energy generation pathways may help P. lobata maintain a persistent stress response to survive when the availability of light and oxygen is diminished. We found evidence for the expression of genes linked to increased environmental sensing and cellular communication that likely allow P. lobata to efficiently respond to sedimentation stress and associated pathogen challenges. Cell damage increases under stress; consequently, we found apoptosis pathways over-represented under severe sedimentation, a likely consequence of damaged cell removal to maintain colony integrity. The results presented here provide a framework for the response of P. lobata to sedimentation stress under field conditions. Testing this framework and its related hypotheses using multi-omics approaches can deepen our understanding of the metabolic plasticity and acclimation potential of corals to sedimentation and their resilience in turbid reef systems.

Rapid, high-throughput phenotypic profiling of endosymbiotic dinoflagellates (Symbiodiniaceae) using benchtop flow cytometry.

Endosymbiotic dinoflagellates (Family Symbiodiniaceae) are the primary producer of energy for many cnidarians, including corals. The intricate coral-dinoflagellate symbiotic relationship is becoming increasingly important under climate change, as its breakdown leads to mass coral bleaching and often mortality. Despite methodological progress, assessing the phenotypic traits of Symbiodiniaceae in-hospite remains a complex task. Bio-optics, biochemistry, or "-omics" techniques are expensive, often inaccessible to investigators, or lack the resolution required to understand single-cell phenotypic states within endosymbiotic dinoflagellate assemblages. To help address this issue, we developed a protocol that collects information on cell autofluorescence, shape, and size to simultaneously generate phenotypic profiles for thousands of Symbiodiniaceae cells, thus revealing phenotypic variance of the Symbiodiniaceae assemblage to the resolution of single cells. As flow cytometry is adopted as a robust and efficient method for cell counting, integration of our protocol into existing workflows allows researchers to acquire a new level of resolution for studies examining the acclimation and adaptation strategies of Symbiodiniaceae assemblages.

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

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.