Ontology highlight
ABSTRACT:
PROVIDER: PRJNA383026 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5452095.fastq.gz | Fastqsanger.gz | |||
| SRR5452096.fastq.gz | Fastqsanger.gz |
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Project description:Abstract Ocean warming elevates metabolic rates in marine ectotherms but often constrains energetic resources, causing an imbalance between supply and demand. Transient hypoxia is near-ubiquitous across the world’s coral reefs and may exacerbate this imbalance, yet its effects on the energetics of reef fishes remain poorly understood. In this study, we assess the metabolic costs incurred by a cryptobenthic reef fish exposed to oxygen fluxes measured on the world’s hottest coral reefs in the Arabian/Persian Gulf. Hypoxia-exposure induced an 8.67% increase in aerobic metabolic rate over the six hours following reoxygenation, and resulted in an estimated 2.87% increase in total daily metabolic rate (mg O2 kg -1 day-1). This energetic cost did not coincide with detectable changes in anaerobic metabolism but was accompanied by increased activity during reoxygenation and a strong, acute transcriptomic response in genes related to oxygen-sensing. Oxygen availability on the reefs declined below the threshold for inducing such energetic costs on over half (56.04%) of the days throughout the summer, potentially leading to substantial cumulative costs. Such energetic costs represent an additional and previously under-appreciated consequence of hypoxia in coral reef environments that may exacerbate the temperature-induced mismatches between energy supply and demand, a key balance affecting growth and fitness.
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Project description:Persian Arabian Gulf Coral Symbiodiniaceae Targeted loci environmental
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Project description:Mesophotic coral reefs have been proposed as refugia for corals, providing shelter and larval propagules for shallow-water reefs that are disproportionately challenged by global climate change and local anthropogenic stressors. Yet, knowledge of the capacity of coral larvae to adjust to different depth environments is still limited. In this study, planulae of the reef-building coral Stylophora pistillata from 5-8 and 40-44 m depth in the Gulf of Aqaba were tested in a long-term in situ translocation experiment for their ability to settle and acclimate to reciprocal depth conditions. We assessed survival rates, photochemical, physiological and morphological characteristics, as well as gene expression variations in juveniles grown at different depths, comparing them to non-translocated adults, juveniles and planulae. We found high mortality rates among mesophotic-origin planulae, irrespective of translocation depth. Gene expression patterns suggested that deep planulae lacked settlement competency and experienced increased developmental stress upon release. Symbiont photochemical acclimation to depth occurred rapidly within 8 days, with symbiont populations showing changes in photochemical traits but no symbiont species shuffling between deep and shallow juveniles. In contrast, coral host physiological and morphological acclimation were less evident. We observed minimal overlap in gene expression patterns between different life stages and depths, indicating that gene expression significantly depends on life stage. The study also identified a set of DEGs associated with initial stress responses following translocation, lingering stress response, and environmental effects of depth. In conclusion, though our data reveal rapid symbiont acclimation, host acclimation to match deep coral phenotypes was incomplete within 60 days for planulae translocated to different depths. These results have implications for understanding the ecological significance of mesophotic reefs as potential larval sources in the face of environmental stressors.
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Project description:Ulcerative colitis is a chronic inflammatory disorder for which a definitive cure is still missing. This is characterized by an overwhelming inflammatory milieu in the colonic tract where a composite set of immune and non-immune cells orchestrate its pathogenesis. Over the last years, a growing body of evidence has been pinpointing gut virome dysbiosis as underlying its progression. Nonetheless, its role during the early phases of chronic inflammation is far from being fully defined. Here we show the gut virome-associated Hepatitis B virus protein X, most likely acquired after an event of zoonotic spillover, to be associated with the early stages of ulcerative colitis and to induce colonic inflammation in mice. It acts as a transcriptional regulator in epithelial cells, provoking barrier leakage and altering mucosal immunity at the level of both innate and adaptive immunity. This study paves the way to the comprehension of the aetiopathogenesis of intestinal inflammation and encourages further investigations of the virome as a trigger also in other scenarios. Moreover, it provides a brand-new standpoint that looks at the virome as a target for tailored treatments, blocking the early phases of chronic inflammation and possibly leading to better disease management.
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