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Biology subjects

Garcia, F. C.

Publications and source records attributed to Garcia, F. C..

11 recordsLinked to original sources

Self-generated oxygen limitation drives coral outcomes during marine heatwaves

Marine heatwaves cause massive, but often patchy coral bleaching. Why neighboring colonies often respond differently remains unresolved. Here, we show that interactions between metabolic demand and flow-mediated resupply generate heterogeneous oxygen microenvironments inside branching corals under heat stress. During the 2023 and 2024 Red Sea heatwaves, high-frequency in situ measurements revealed hypoxic to near-anoxic interbranch conditions despite well-oxygenated surrounding seawater. In 2023, neighboring colonies developed divergent oxygen regimes preceding paling and bleaching; in 2024, stronger and earlier thermal stress was associated with recurrent nighttime near-anoxia before tissue disintegration and mortality. A physics-based three-dimensional fluid-metabolism model reproduced these patterns. Oxygen depletion and coral impacts emerged when metabolic oxygen demand exceeded flow-mediated resupply. Organism-scale variability in oxygen regimes may explain divergent coral fate under shared heatwave exposure.

ecology↗

Warming exacerbates fungal pathogenicity to drive physiological collapse and microbiome reorganization in octocorals

Corals are increasingly threatened by climate change, yet the interplay between ocean warming and fungal infection remains experimentally underexplored. Here, we demonstrate that thermal stress exacerbates the pathogenicity of the fungus Aspergillus sydowii, driving physiological collapse and functional reorganization in the octocoral Sclerophytum sp. We deployed a 34-day mesocosm heat-stress experiment and quantified performance, mortality, and taxonomic and functional microbiome shifts. Combined heat and fungal exposure proved highly lethal, causing 45% mortality compared to 7% under heat exposure alone. Re-isolation from diseased nubbins implicates A. sydowii as the causal agent. Metagenomic profiling indicated that physiological collapse was underpinned by a functional transition from mutualism to antagonism in the microbiome. Specifically, combined heat and fungal stress triggered a depletion of ankyrin- and WD40-repeat proteins - hallmarks of symbiotic stability - concurrent with a surge in genes involved in fungal cell wall degradation and secondary metabolite biosynthesis. While surviving holobionts recovered full photosynthetic efficiency after combined stress, their microbiomes did not revert to baseline. Instead, they assembled into a taxonomically distinct configuration characterized by enrichments of sulfate-reducers (Thermodesulfobacteriota) and thermotolerant phototrophs (Thermosynechococcales). This suggests that despite the rapid photosystem recovery, the holobiont retained a complex legacy of thermal and biotic stress across both its internal chemical microenvironment and its microbiome. These findings highlight the decoupled recovery processes of different holobiont components, demonstrating that even though some corals may survive severe climate-driven disease, they emerge as ecologically reorganized entities.

ecology↗

Pathogen priming reveals host immune training and microbiome conditioning in corals

UNSTRUCTURED ABSTRACTIn several species, vaccine-like approaches, where hosts are primed through controlled pathogen exposure, have proven effective in enhancing responses to subsequent infections. This principle remains unexplored in corals. Here, we demonstrate that chronic exposure to non-lethal concentrations of live or inactivated Vibrio coralliilyticus primes the coral holobiont to counter subsequent infections under heat stress. Non-primed corals experienced greater heat stress pathogen-driven bleaching and a significant decline in their photosynthetic efficiency compared to primed samples. These results were linked to microbiome conditioning and host gene expression modulation, including a layered, fine-tuned immune and cellular response to microbial invasion. This proof-of-concept challenges strictly innate immune responses in corals and positions immune priming and microbiome conditioning as integrated mechanisms of coral holobiont resilience. Together, these findings can contribute to redefine coral immunity concepts and lay the groundwork for developing new microbiome-based strategies to enhance coral health for reef conservation under climate change. LAY SUMMARYCoral reefs are increasingly threatened by rising seawater temperatures and disease. Unlike vertebrates, corals do not possess a classical adaptive immune system, so they have been thought to rely only on innate defenses. However, our study shows that corals may be more capable than previously believed. We demonstrate that exposing corals to non-lethal doses of a widespread bacterial pathogen can train them to better withstand subsequent infections under heat stress. Corals that were not pre-exposed suffered more pathogen caused bleaching and showed a stronger decline in physiological performance, while those that were primed were more resilient. This improved resistance appears to come from two coordinated processes. First, the corals associated bacterial community shifted in a way that seems to help protect the host. Second, the coral itself adjusted its gene expression, mounting a more effective and controlled response to infection. These findings suggest that corals may be able to remember past exposures and respond more effectively to future infections, even without a traditional adaptive immune system, providing a foundation for developing new strategies to support coral resilience.

microbiology↗

Coral Probiotics Buffer Adjacent Ecosystem-Level Responses to Extreme Marine Heatwave

Probiotics can enhance coral thermal tolerance, yet their ecosystem-level effects remain unknown. Here, we present the first long-term in-situ test of whether coral-targeted probiotics influence adjacent cryptobenthic reef communities during a record marine heatwave. Probiotics were applied to Pocillopora favosa and Acropora spp. coral colonies for 18 months, spanning the fourth global bleaching event. Cryptobenthic communities were assessed using biomimetic monitoring structures integrating biodiversity surveys, molecular profiling, microbial network analyses, and metabolic assays. Before the heatwave, probiotic and control patches were comparable across structural, microbial, and functional metrics. Following thermal stress, control patches exhibited pronounced losses of cryptobenthic invertebrate abundance and taxonomic breadth, microbial network fragmentation, and net carbonate dissolution. In contrast, probiotic-treated patches retained higher biodiversity, cohesive microbial interaction architectures, and positive calcification. These findings demonstrate that coral-targeted probiotics can scale from host-level intervention to buffer adjacent ecosystem-level responses to extreme marine heatwaves under accelerating climate change. TeaserA coral-targeted probiotic strategy enhances multi-trophic resilience under heat stress.

microbiology↗

Probiotic and postbiotic treatment in situ during a marine heat wave improves coral health and promotes specific metabolic and microbiome changes

Microbial therapies are emerging as promising tools for coral protection against heat stress, yet such application was not tested in situ. We tested two coral-derived probiotic consortia and their heat-killed counterparts (postbiotics) on bleaching Acropora cf. valida in the Red Sea during a marine heatwave. Over 15 days, both live and one of the heat-killed treatments maintained photosynthetic efficiency (Fv/Fm), whereas placebo-treated corals exhibited significant thermal stress-induced decline. 16S rRNA gene sequencing profiling showed enrichment of putatively beneficial genera (e.g., Terasakiispira spp., Pseudoalteromonas spp.), and untargeted metabolomics resolved treatment-specific metabolic signatures that differed among consortia and between live and inactivated formulations. These molecular fingerprints illuminate specific underlying protective mechanisms and host-microbiome interactions under heat stress. Together, our results position microbial therapies (probiotics and specific postbiotics) as field-validated, mechanism-informed interventions capable of minimizing impacts on corals during real-world thermal extremes and provide design cues for scalable deployment.

microbiology↗

Proteome-based investigation of O-GlcNAcylation in a C. elegans model of Ageing and Alzheimer's disease: Functional Support for Earlier Hypothesis-Generating Findings

The monosaccharide N-acetyl-glucosamine (GlcNAc), which dynamically modifies serine and threonine residues of nuclear and cytoplasmic proteins, is a key regulator of numerous biological processes. Investigating O-GlcNAc modification in vivo and in vitro remains challenging, making animal models essential for gaining powerful insights into this post-translational modification. In this study, we conducted a proteomic analysis for identifying O-GlcNAc-modified proteins in both early and adult larval stages of N2 wild-type Caenorhabditis elegans and in aex-3p::tau(V337M), a nematode model of ageing and Alzheimers disease using a high-resolution nano-LC-ESI mass spectrometry approach. We found that O-GlcNAcylation in C. elegans is developmentally regulated and is disrupted in a tauopathy model. Wild-type worms transition from RNA processing in larvae to broader regulation of RNA metabolism and protein stability, whereas tau-expressing worms display stress- and signalling-related features. O-GlcNAcylated PDI-2 emerges as a candidate regulator of protein quality control and decrease of O-GlcNAc levels suggests competition with hyperphosphorylated tau. These findings position O-GlcNAcylation as a context-dependent modulator of proteostasis with therapeutic relevance for tauopathy.

biochemistry↗

Tracking of in vivo O-GlcNAcylation in an Alzheimer's Disease and Aging C. elegans Model

We investigated O-linked {beta}-N-acetylglucosamine (O-GlcNAc), a post-translational modification, in an in vivo Caenorhabditis elegans model of Alzheimers Disease and aging. Employing a chemoenzymatic labeling strategy combined with an automated image processing approach, we analyzed both post-hatching and adult stages of wild-type N2 and transgenic strain expressing human tau V337M under the aex-3 promoter (aex-3p::tau(V337M)). Labeled O-GlcNAc proteins were visualized using fluorescence microscopy and quantified using a region-of-interest-based image analysis pipeline. Morphometric characterization revealed an age-dependent increase in O-GlcNAcylation in wild-type worms, while the AD model showed a progressive decline. In middle-aged transgenic nematodes, O-GlcNAc-labeled regions of interest shifted from anterograde to predominantly retrograde movement, suggesting that aging and neurodegeneration alter O-GlcNAc trafficking dynamics, potentially reflecting impaired synaptic support or enhanced clearance in C. elegans. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=133 SRC="FIGDIR/small/659071v2_ufig1.gif" ALT="Figure 1"> View larger version (26K): org.highwire.dtl.DTLVardef@10d6816org.highwire.dtl.DTLVardef@12ca2d8org.highwire.dtl.DTLVardef@17742b2org.highwire.dtl.DTLVardef@bbc33b_HPS_FORMAT_FIGEXP M_FIG C_FIG

systems biology↗

Bacterial inoculation manipulates the coral epigenome

Environmental shifts can cause epigenetic modifications in corals, which are associated with changes in gene expression and physiology, though it remains unclear if associated bacteria can also induce such changes. Here, we inoculated nubbins of the coral Pocillopora verrucosa with an opportunistic pathogen, Vibrio coralliilyticus, and/or a coral probiotic, Cobetia sp., and subjected the nubbins to heat stress. We show that pathogen exposure led to distinct DNA methylation changes compared to the control, probiotic, and co-inoculation groups. We also demonstrate that DNA methylation correlates with coral gene expression and highlight genes altered by pathogen inoculation that showed similar responses in their expression and methylation. Notably, the coral probiotic was able to mitigate specific epigenetic changes, which correlated with increased stress resilience and higher coral survival rates. Thus, bacterial-induced changes to the coral epigenome may instigate long-term changes in host resilience.

molecular biology↗

Species interactions amplify the temperature dependence of microbial community respiration

The respiratory release of CO2 by microbes is a dominant component of the global carbon cycle. However, large uncertainties exist about the effects of climatic warming on the respiration of microbial communities due to lack of mechanistic, empirically-tested theory that accounts for dynamic species interactions. We developed a general mathematical model which predicts that thermal sensitivity of microbial community respiration increases as species interactions become more positive, i.e., change from competition to facilitation. This is because facilitation disproportionately increases positive feedbacks between the thermal sensitivities of species-level metabolic and biomass accumulation rates at warmer temperatures. We experimentally validated this prediction in bacterial communities of 8 taxa, finding that a shift from competition to facilitation after a month of co-adaptation caused a 60% increase in the thermal sensitivity of their respiration relative to de novo communities that had not co-adapted. Thus, rapid changes in species interactions can profoundly change the temperature-dependence of microbial community respiration and should be considered in climate change models.

ecology↗

Dissolved organic matter and heterotrophic prokaryotes diel patterns reveal enhanced growth at the mesopelagic fish layer during daytime

Contrary to epipelagic waters, where biogeochemical processes closely follow the light and dark periods, little is known about diel cycles in the oceans mesopelagic realm. Here, we monitored the dynamics of dissolved organic matter (DOM) and planktonic heterotrophic prokaryotes every 2 h for one day at 0 and 550 m (a depth occupied by vertically migrating fish during light hours) in oligotrophic waters of the central Red Sea. We additionally performed predator-free seawater incubations of samples collected from the same site both at midnight and at noon. Comparable in situ variability in microbial biomass and dissolved organic carbon concentration suggests a diel supply of fresh DOM in both layers. The presence of fish in the mesopelagic zone during daytime promoted a sustained, longer growth of larger prokaryotic cells. The specific growth rates were consistently higher in the noon experiments from both depths (surface: 0.34 vs. 0.18 d-1, mesopelagic: 0.16 vs. 0.09 d-1). Heterotrophic bacteria and archaea in the mesopelagic fish layer were also more efficient at converting DOM into new biomass. These results suggest that the oceans twilight zone receives a consistent diurnal supply of labile DOM from diel vertical migrating fishes, enabling an unexpectedly active community of heterotrophic prokaryotes.

ecology↗

Red blood cell-derived extracellular vesicles mediate intercellular communication in ischemic heart failure

Extracellular vesicles (EV) mediate intercellular signaling by transferring their cargo to recipient cells. Red blood cell (RBC)-derived EVs constitute a significant proportion of circulating EVs and have been implicated in regulating immune responses. Here, we describe a transgenic mouse model for fluorescent-based mapping of RBC-EV target cells based on the functional transfer of EV-contained Cre-recombinase to target cells. In a murine model of ischemic heart failure, we detect an increase in RBC-EV-targeted cardiomyocytes in the hearts and microglial cells in the brains. Cells targeted by RBC-EVs present an enrichment of genes implicated in cell proliferation and metabolism pathways compared to non-recombined (non-targeted) cells. Cardiomyocytes targeted by RBC-EVs are more likely to demonstrate cellular markers of DNA synthesis and proliferation, suggesting functional significance of EV-mediated signaling. In conclusion, we leverage our mouse model for mapping of RBC-EV targets in murine ischemic heart failure to demonstrate quantitative and qualitative changes in RBC-EV recipients.

cell biology↗