Posts Tagged 'molecular biology'



Transcriptomic analysis of the hepatopancreas response to low-pH stress in kuruma shrimp (Marsupenaeus japonicus)

Highlights

  • Low-pH stress disrupted oxidative balance in M. japonicus, suppressing SOD and CAT activities while increasing MDA levels.
  • Low-pH stress triggered 2705 DEGs in hepatopancreas linked to immunity, oxidative stress, and energy metabolism.
  • CTSDGLB1, and LGI4 are implicated in long-term immune adaptation to low pH.
  • Key pathways—lysosome, Toll-like receptor, AMPK, and PPAR signaling—were activated under low pH stress.
  • Hub genes such as NADH-GOGAT and MDHM were identified as central regulators of antioxidant defense and energy metabolism.

Abstract

Ocean acidification has emerged as a globally recognized environmental issue, posing a serious threat to marine ecosystems. To elucidate the adaptive mechanisms of Marsupenaeus japonicus under acidified conditions, both biochemical and transcriptomic analyses were performed following low-pH exposure. Biochemical assays revealed that low pH stress significantly SOD and CAT activities while markedly elevating MDA levels, indicating oxidative damage. T-AOC exhibited a transient rise followed by a sharp decline at later stages, suggesting initial activation and subsequent exhaustion of antioxidant defense. Transcriptomic profiling identified 2705 DEGs that were primarily enriched in pathways related to immune regulation, redox balance, apoptosis, and energy metabolism, including the lysosome, Toll-like receptor, and PPAR signaling pathways. Protein interaction analysis identified 9 hub genes, including NADH-GOGAT and MDHM, which may play key roles in antioxidant defense and metabolic regulation. The integration of enzyme activity and transcriptomic data indicates that acid stress initially induces oxidative imbalance, followed by compensatory activation of antioxidant and immune systems to restore cellular homeostasis. These findings provide comprehensive insights into the oxidative stress adaptation of M. japonicus and offer a genetic and physiological foundation for breeding acid-tolerant shrimp strains.

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Omics insights into ocean health: molecular adaptations and ecosystem resilience under climate stress

Despite extensive research documenting the impacts of climate change on marine ecosystems, the molecular mechanisms driving organismal and ecosystem resilience to ocean warming, acidification, and deoxygenation remain insufficiently understood. This review addresses this knowledge gap by synthesizing recent advances in omics technologies—including genomics, transcriptomics, proteomics, metabolomics, and epigenomics—that illuminate adaptive genetic, metabolic, and epigenetic processes in marine organisms. These approaches help identify climate-tolerant genetic variants, uncover metabolic pathways for stress mitigation, and reveal epigenetic modifications enabling rapid adaptation. Together, such insights are transforming biodiversity monitoring, predictive ecosystem modeling, and the evidence-based design of climate-resilient marine protected areas (MPAs) grounded in genomic and functional diversity. Studies on marine microbial communities further provide promising avenues for blue carbon ecosystem enhancement and climate mitigation. Integrating omics findings into global governance frameworks, including the United Nations Convention on the Law of the Sea (UNCLOS) and International Maritime Organization (IMO), strengthens adaptive fisheries management, spatial planning, and climate-resilient policy. Key challenges for multi-omics integration are discussed alongside innovative solutions, such as integrative analytical approaches and the adoption of standardized molecular indicators. By bridging molecular science, policy, and management, this review outlines how interdisciplinary collaboration can advance adaptive and sustainable stewardship of the ocean in an era of unprecedented environmental change.

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The negative responses and acclimation mechanisms of Neopyropia yezoensis conchocelis filaments to short- and long-term ocean acidification

Background

Ocean acidification (OA) significantly alters the carbonate chemistry of seawater, leading to a decrease of seawater pH to impact the physiological and biochemical processes of those intertidal macroalgae. Previous studies have focused on the response of macroalgae to OA at thallus stage, while the effects at filamentous stage remain insufficiently explored.

Results

This study investigated the physiological-biochemical and molecular mechanisms of the filamentous conchocelis stage (the diploid sporophyte) of Neopyropia yezoensis responding to short- (5 days) and long-term (20 days) OA (2000 ppm CO2, pH 7.53). The results showed that short-term OA rapidly inhibited the growth and photosynthesis, suppressed chlorophyll synthesis and nitrogen assimilation, and down-regulated genes associated with photosynthesis, Calvin cycle, and carbohydrate metabolism of N. yezoensis conchocelis filaments. However, N. yezoensis conchocelis filaments showed acclimation strategies under long-term OA, in terms of metabolic reorganization, prioritizing stress tolerance over growth. Further weighted gene co-expression network analysis (WGCNA) based on the metabolomic and transcriptomic results under long-term OA showed that the strategy was manifested by the accumulation of soluble sugars as osmolytes, lipid β-oxidation compensating for energy deficits, and H+ extrusion mediated via ABC transporters.

Conclusions

This study suggested time-depended responses of N. yezoensis conchocelis filaments to OA, proving the pronounced negative effects of OA on N. yezoensis conchocelis filaments, revealing N. yezoensis conchocelis filaments could acclimate to long-term OA by resource reallocation. These findings provide new insight into the survival of N. yezoensis conchocelis filaments under OA, and facilitate the development of technologies and breeding strategies for improved acidification tolerance in N. yezoensis.

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Ocean acidification enhances TiO2 nanoparticle toxicity in Oryzias melastigma: dominant role of size effects in driving bioaccumulation and hepatotoxicity

Highlights

  • OA reduces TiO₂ NPs aggregation/sedimentation, increasing NP bioaccumulation
  • NPs preferentially accumulate in liver, inducing hepatotoxicity via oxidative stress
  • Size effect outweighs biological resistance as primary NP toxicity driver under OA
  • Combined OA-NPs suppress hepatic genes, activate senescence and cell death pathways
  • First evidence quantifying hydrodynamic size dominance in OA-enhanced NP toxicity

ABSTRACT

Ocean acidification (OA) and engineered nanoparticles (NPs) pollution represent two critical global environmental challenges. Marine organisms are suffering from their combined stress. However, few studies address their combined effects, and the toxicity mechanisms of NPs under OA are largely unresolved. In this study, we investigated the responses of the marine medaka Oryzias melastigma to environmentally relevant concentration of TiO2 NPs (1.0 mg/L) under OA (pH 7.40). We found that OA alleviated the aggregation and sedimentation of NPs, and decreased the resistance ability of the marine medaka to NPs stress, leading to elevated bioaccumulation of TiO2 NPs. Notably, NPs preferentially accumulated in the liver, inducing hepatotoxicity through oxidative stress and histopathological and ultrastructural damage. Critically, an integrated biomarker approach quantified the relative contributions of size effects (58%) and biological resistance (42%) to NP toxicity under OA, demonstrating that hydrodynamic size dominates toxicity outcomes. Transcriptomic analysis further revealed suppressed hepatic gene transcription and translation, alongside activated cellular senescence and programmed cell death pathways under combined exposure. These findings provide critical insight into the combined toxicity mechanisms of NPs and OA, significantly advancing our understanding of the profound risks that NPs pose to marine ecosystems under OA conditions.

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Dulse seaweed Devaleraea mollis mitigates effects of ocean acidification on larval Pacific oysters Magallana gigas

Ocean acidification (OA), driven by upwelling and climate change, can negatively impact the ecological and economic contribution of marine calcifiers along coasts worldwide. OA interferes with calcification, particularly in early life stages, causing mortality, reduced growth, and morphological abnormalities in shellfish such as the Pacific oyster (Magallana gigas). This issue is gaining traction as climate change intensifies, placing shellfish in wild populations and farms alike at risk. Macroalgal photosynthesis by seaweed such as Pacific dulse (Devaleraea mollis) has been proposed to provide small-scale OA refuges, but few controlled experiments quantify this effect, and none have focused on larval shellfish. This study examines the potential for Pacific dulse to mitigate OA and its effects on Pacific oyster larvae. Under continuous light for 23 days, the presence of dulse resulted in a consistent increase in seawater aragonite saturation state by 0.1-0.9, and pH by 0.1-0.5 units, depending on OA condition. Newly fertilized oysters were reared for 48 hours in the absence or presence of dulse under treatments corresponding to ambient (pH 7.8, 450 μatm CO₂), future OA (pH 7.6, 800 μatm CO₂), and future OA + upwelling (pH 7.4, 1200 μatm CO₂) seawater conditions. Dulse fully mitigated OA effects on larval size that ranged from decreases of 5% to 10%. Under the future OA + upwelling treatment, dulse presence reduced the odds of underdeveloped oyster larvae at 14 hours post fertilization (hpf), and larvae with hinge abnormalities at 24 hpf, by over 50%. Dulse induced minor changes to immune response gene expression at 48 hpf. These findings highlight the benefits of seaweed when adjacent to organisms sensitive to OA. These findings will be particularly useful for shellfish farms, habitat restoration efforts, and ocean stewardship practices as a potential mitigation strategy under the changing climate.

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DNA methylation plasticity drives copepod resilience to coastal high pCO2 and cadmium pollution under multigenerational exposure

Highlights

  • Fluctuating acidification caused the most Cd multigenerational toxicity in copepods.
  • The adverse effects of acidification and Cd tended to intensify during F1-F3.
  • The copepods potentially adapted to combined exposure in F4.
  • DNA hypomethylation rendered copepods presenting the adaptive potential.

ABSTRACT

The vast majority of coastal organisms have been facing multigenerational scenarios of fluctuatingly high pCO2 and Cd pollution in their natural habitats. However, the adaptive capacity of these organisms to such combined stressors and the underlying mechanisms remain poorly understood. In this study, we conducted a multigenerational experiment (F1-F4) to investigate the adaptive responses of the marine copepod Tigriopus japonicus to combined fluctuatingly high pCO2 and Cd exposure, along with the associated mechanisms. Our findings revealed that steady high pCO2 aggravated Cd multigenerational toxicity, and it was more under fluctuating acidification. Notably, by the F4 generation, copepods potentially adapted to the combined stressors. Through transcriptomic and DNA methylation analyses of copepods from the F1 and F4 generations, we found that under combined exposure, F1 copepods likely reallocated more energy to counteract Cd toxicity; however, DNA hypermethylation inhibited Cd exclusion and detoxification/stress response pathways, ultimately compromising development and reproduction. In contrast, in the F4 generation, DNA hypomethylation enhanced processes such as cuticle repair program, compensatory mechanism (e.g., detoxification and immune response), and reproduction, consequently increasing the copepod’s fitness. These findings reveal an epigenetic basis for phenotypic acclimatization, offering marine copepods a supplementary mechanism to cope with combined stressors.

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Coupled acidification-nitrification dynamics in eutrophic estuarine waters

Highlights

  • Mid-estuary emerges as a hotspot for coupled acidification-nitrification, intensified by hydrology.
  • Nitrifier community structure adapts to acidification stress, while responds differently.
  • AOB is more sensitive to acidification in estuarine water compared to AOA.
  • Future climate change scenarios project intensified acidification and nitrification coupling in mid-estuary.

Abstract

The interplay between acidification and nitrification in estuarine systems could have profound effects on coastal biogeochemistry and ecosystem health. However, the lack of integrated field research risks oversimplifying their relationships in complex ecosystem dynamics. This study investigates the spatiotemporal covariations of acidification sensitivity and nitrification rates derived from observed inorganic carbon and nutrients data along a land-sea continuum. In the middle estuary, estuarine pH exhibited the highest sensitivity to ammonium concentration, coinciding with maximum nitrification rates. The coupling effect intensified by 40% during the transition from dry to wet hydrological conditions. Despite that microbial network complexity generally decreased with increased acidification sensitivity, ammonia-oxidizing bacterial communities are more sensitive to acidification in estuarine water compared to ammonia-oxidizing archaea. Conversely, in the lower estuary, acidification was associated with a decline in nitrification activities. Machine learning-based models suggest that climate change scenarios could exacerbate acidification and nitrification in the Pearl River Estuary, potentially amplifying their coupling effect in the middle estuary. This holistic approach not only advances our fundamental understanding of estuarine processes, also provides critical insights for policymakers and coastal managers striving to maintain the ecological integrity of these vital ecosystems in an era of rapid global change.

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The bacterial community composition of American lobster (Homarus americanus) embryos and recently hatched larvae held under different temperature and acidification conditions

Previous research investigating the microbial community of American lobster embryos has long led researchers to believe this habitat comprised only a select few bacterial taxa. However, using 16S rRNA gene sequencing, we show this community to be more diverse than previously thought. We investigated how the bacterial communities of American lobster embryos and larvae change over embryogenesis and hatching in response to two environmental variables. Ovigerous female lobsters caught from Maine and Massachusetts were held under varying temperature and pH regimes that approximated observed and predicted warming and ocean acidification conditions in the Gulf of Maine (GoM) and Southern New England (SNE). The bacterial microbiome associated with the lobster embryos was quantified from two-time points during the experiment, and larvae were collected within 12 hours of hatching. Alpha diversity increased with each life history stage, and embryo and larvae microbiomes shared little community overlap with that in the surrounding tank water. Neither environmental conditions nor lobster origin significantly altered bacterial communities, with life history stage driving alpha and beta diversity. Embryos and larvae shared three core bacterial members identified as members of the genera Rubritalea, Delftia, and Stenotrophomonas. American lobster embryos and larvae appear to have a highly selective microhabitat for bacteria that is not altered by environmental conditions. This leads us to wonder what role the microbiome may have on a developing lobster, and where the microbiome is originating if not from the surrounding seawater.

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Identification of chitinase family members in the Crassostrea gigas and the expression patterns of Cgamcase-1 under ocean acidification

Chitinase, as a crucial enzyme for the degradation of chitin, is involved in the construction of the chitin framework during the process of shell formation. In order to identify the members of the chitinase gene family in Crassostrea gigas and investigate their response to acidification, bioinformatic methods were employed to identify the chitinase family members and analyze their expression patterns. Eleven members of the chitinase family were identified from the C. gigas genome. All gene members contained the Glyco-18 domain, and some genes also contained the chitin-binding domain ChtBD2. These genes were predominantly located on chromosome 2, 5, 6, and 7. In the C. gigas, the chitinase family genes were clearly divided into two branches which were endochitinases and exochitinases. The chitinase family expressed across all developmental stages of the C. gigas larvae. With the development of larva, the expression level of five genes increased gradually. The expression levels of most chitinase family genes were higher in the mantle compared to other tissues. The acidic mammalian chitinase (Cgamcase-1) exhibited high expression level in the mantle, with the highest expression level in the outer fold (OF). The expression patterns of Cgamcase-1 in response to acidification were analyzed. After 3, 7, and 14 days of acidification stress, the mRNA expression of Cgamcase-1 in the mantle was 3.010-fold (P < 0.05), 4.557-fold (P < 0.001) and 4.129-fold (P < 0.001) of that in the control group, respectively. After 7 days of acidification stress, the mRNA expression of Cgamcase1 in OF was 3.598-fold of that in the control group (P < 0.05). In situ hybridization results revealed that the positive signals for the Cgamcase-1 probe were primarily concentrated in the epithelial cell region of the outer fold, and the intensity of the positive signals significantly increased after 7 days of acidification stress, while it significantly decreased after 14 and 28 days. The study suggested that chitinase family genes might be involved in the process of larval development and adult shell formation. Cgamcase-1 participated in chitin degradation and responding to ocean acidification. This research provided important theoretical evidence and reference for understanding the role of chitinase in the shell formation process of the C. gigas and their response mechanisms under ocean acidification.

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Molecular responses of amphipod (Parhyale darvishi), to pH stress in Persian Gulf

Climate change is driving more frequent and extreme pH fluctuations in intertidal habitats, yet the molecular mechanisms by which small crustaceans cope with acid–base stress remain poorly understood. In this study, we evaluated the transcriptional responses of the intertidal amphipod Parhyale darvishi to acute low-pH (6.0) and high-pH (9.0) challenges, simulating the extremes observed in tide pools. Following a 7-day acclimatization in aerated seawater (salinity 40–42 ppt, 24–25 °C, 12:12 h light:dark), individuals (4–7 mm length) were randomly assigned to one of three treatments: control (ambient pH 7.50–7.60), low pH (adjusted to 6.0 with 20 mL 37% HCl), or high pH (adjusted to 9.0 with 3 mL NaOH), each with two 1-L replicates containing 50 animals. After 0h, 12h and 24 h of exposure, total RNA was extracted and reverse-transcribed to cDNA. Real-time PCR assays quantified expression of five target genes: catalase (CAT), glutathione S-transferase (GST), Na⁺/K⁺-ATPase, apoptosis signal-regulating kinase 1 (ASK1), and caspase-3, with tubulin serving as the reference gene. Both pH stressors elicited significant transcriptional changes relative to controls. Under low pH, antioxidant genes CAT and GST were upregulated by approximately 2.5- and 2.1-fold, respectively, indicating activation of oxidative defense pathways. In contrast, high pH induced a more moderate antioxidant response (1.8- and 1.5-fold for CAT and GST) but triggered a pronounced apoptotic signal, with caspase-3 expression increasing nearly 3-fold. Na⁺/K⁺-ATPase transcripts rose under both treatments, reflecting osmoregulatory adjustments, while ASK1 exhibited a stronger induction in acid-stressed amphipods, suggesting stress-activated kinase signaling. These findings demonstrate that P. darvishi mounts distinct molecular responses to acid versus alkaline challenges, engaging antioxidant defenses under low pH and apoptosis-related pathways under high pH. Such differential gene expression profiles provide mechanistic insight into how intertidal amphipods cope with rapid pH swings, and underscore the utility of molecular biomarkers for assessing the resilience of coastal invertebrates under future acidification and alkalinization scenarios.

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The impact of an early exposure to 17α-ethynylestradiol on the physiology of the three-spined stickleback (Gasterosteus aculeatus) under current and future climatic scenarios

Highlights

  • RCP8.5 scenario modulated some of the long-lasting physiological responses to EE2.
  • RCP8.5-EE2 group led to sex and tissue specific responses.
  • RCP8.5-EE2 scenario resulted in lower body length at five months post-contamination.
  • RCP8.5 reduced survival rate of embryo-larval but not juvenile stages.
  • Early-life exposure to EE2 led to stickleback feminisation.
  • Early-life exposure to EE2, led to long-lasting effect on stickleback physiological responses.

Abstract

Ocean warming and acidification are climate change related drivers that impact the physiology of marine organisms and their ability to cope with future environments. Marine ecosystems are also facing pollution from an ever-growing diversity of chemical contaminants, including endocrine disruptors. A common example is the 17α-ethynylestradiol (EE2), which can affect the endocrine regulation of fish and hence potentially impact their fitness. Thus, fish have to cope to multiple climatic and chemical stresses that can interact, influencing the overall impact on fish physiology. In this study, we investigated whether the direct and carry-over effect of early exposure to EE2 (15 ng.L−1; one month during embryo-larval development) are modulated by the RCP8.5 scenario (+3°C; -0.4 pH unit). Five months post-contamination, we measured survival, growth and reproductive axis of prepubertal sticklebacks. Our findings revealed that the survival of juveniles, when exposed to EE2 during early development, is reduced under Current but not RCP8.5 scenario. Furthermore, under RCP8.5-EE2, a significantly lower body length was observed. Sex and tissue specific responses in terms of the expression profiles of genes related to development and sexual maturation was reported. Interestingly, significant interaction between RCP8.5 and EE2 was observed for the expression of ovarian aromatase (cyp19a1a), suggesting a long-lasting estrogenic effect under RCP8.5 scenario. Additionally, the skewed sex ratios and the presence of intersex individuals in both scenarios early exposed to EE2 suggested a feminization due to EE2, which could potentially disrupt sexual maturation and future reproduction. Hence, the early EE2 exposure had carry-over physiological effects on sticklebacks, and these effects can be modulated by the climate scenario. This underscores the importance of conducting long-term multi-stress studies to comprehensively understand the vulnerability on fish populations in future environments.

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Coral calcification resistance to acidification is physiologically linked with complex intracellular calcium ion dynamics between host and symbiont cells

Coral calcification is a highly complex process with numerous caveats regarding the mechanisms that dictate productivity and function. Ion homeostasis, however, is the foremost physiological process unanimously shared among Scleractinia and essential for calcification. Consequently, changes to the seawater environment may elicit adverse effects on ion homeostasis. With increasing climate shifts, the physicochemical regime of our global ocean is changing rapidly. Responses of coral calcification to physicochemical change prevail in having little uniformity on an unambiguous mechanism of resistance. Therefore, this study chose a relatively tolerant Hawaiian coral, Montipora capitata to focus efforts on understanding ion homeostasis under chemical seawater manipulation designed to limit calcification. Results indicate a physiological hormesis (two-phase adaptive response) of overall coral host gene expression that was not shared with algal symbionts and decoupled from calcification rates. The sole ion homeostatic mechanism shown was calcium ion regulation by both the host and symbiont cells. Calcium ion homeostasis was also found to be mechanistically different between winter and summer seasons. Thus, potentially indicating complex interactions between host and symbiont cells, as well as the ability for M. capitata to promote calcification under stress. Putatively synthesized here are the physiological cascades and mechanisms of resistance to environmental triggers of acidosis and seasonal change. This work provides insight into linking calcium ion homeostasis with coral resistance and aims to suggest this mechanism as biomolecular indicator used in future assessments to compare tolerance.

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Thermal and acidification gradients reveal tolerance thresholds in Pocillopora acuta recruits

Ocean warming and acidification are among the biggest threats to the persistence of coral reefs. Organismal stress tolerance thresholds are life stage specific, can vary across levels of biological organisation and also depend on natural environmental variability. Here, we exposed the early life stages of Pocillopora acuta in Kāne‘ohe Bay, Hawai‘i, USA, a common reef-building coral throughout the Pacific, to projected ocean warming and acidification scenarios. We measured ecological, physiological, biomineralisation and molecular responses across the critical transition from larvae to newly settled recruits following 6 days of exposure to diel fluctuations in temperature and pH in Control (26.8°C–27.9°C, 7.82–7.96 pHTotal), Mid (28.4°C–29.5°C, 7.65–7.79 pHTotal) and High conditions (30.2°C–31.5°C, 7.44–7.59 pHTotal). We found that P. acuta early life stages are capable of survival, settlement and calcification under all scenarios. The High conditions, however, caused a significant reduction in survival and settlement capacity, with changes in the skeletal fibre deposition patterns. Although there was limited impact on the expression of biomineralisation genes, exposure to High conditions resulted in strong transcriptomic responses including depressed metabolism, reduced ATP production and increased activity of DNA damage-repair processes, indicative of a compromised metabolic state. Collectively, our findings demonstrate that coral juveniles living in environments with large diurnal fluctuations in seawater temperature and pH, such as Kāne‘ohe Bay, can tolerate exposure to moderate projected increased temperature and reduced pH. However, under more severe environmental conditions, significant negative effects on coral cellular metabolism and overall organismal survival jeopardise species fitness and recruitment.

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Genomic analysis reveals broad adaptability of coral-killing sponge (Terpios hoshinota) under environmental stress

The coral-killing sponge, Terpios hoshinota, poses a significant ecological threat to coral reefs, exhibiting rapid expansion and competitive overgrowth. Despite its invasiveness, the genomic basis underlying its adaptability and resilience remains largely unexplored. Here, we present a high-quality genome assembly of T. hoshinota, comprising 169.4 Mb with 40,945 predicted genes. Phylogenomic analysis estimated its divergence from other demosponges during the Ordovician (~ 471 million years ago), even though its simple morphology suggests a more ancient evolutionary origin. Comparative genomic analyses revealed enrichment of genes related to substrate adhesion, innate immunity, and developmental pathways, including expansions of Wnt signaling, homeobox genes, and cell migration gene ontologies which may contribute to its aggressive growth and resilience. Transcriptomic responses under simulated climate stress conditions (heat stress at 31 °C and acidification at 700 ppm pCO₂) indicated dynamic gene regulation, with upregulation of neurotransmitter metabolism, cellular maintenance, and ion homeostasis responses. Despite these stressors, it remained stable. This suggests that T. hoshinota exhibits strong adaptability and resilience through rapid gene regulation. In conclusion, these findings provide molecular insights into T. hoshinota’s ecological success, its potential expansion under climate change, and its broader impact on coral reef ecosystems.

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A window into the effect of ocean acidification on molluscan larval shell development using a quantitative approach

Increasing atmospheric CO2 levels have led to decreased pH and calcium carbonate saturation (Ω) of seawater, a process referred to as ocean acidification. Ocean acidification is expected to reduce biomineralization by marine calcifiers, such as molluscs, and many studies have reported serious effects on molluscan shell development. However, it has not previously been possible to quantitatively compare these effects on tiny structures, such as larval shells, among and within species. We applied the measurement technique of micro-focus X-ray computed tomography (MXCT) to larval shells of the limpet Nipponacmea fuscoviridis to quantitatively trace the process of shell growth (shell thickness and shell density). Shell thickness and density significantly decreased in seawater with low Ω levels. Scanning electron microscopy (SEM) revealed that the surface structure of the shell in larvae cultured under low Ω was disturbed. Gene expression analysis showed that the development of shell-forming regions under low Ω was significantly reduced. MXCT analysis can quantify mineralization in tiny larval shells; in combination with other methods such as SEM and gene expression analysis, it can provide a novel perspective in the assessment of the impact and resilience of marine calcifiers to changes in the marine environment.

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Mapping the knowledge domain of ocean acidification impacts on marine microbial communities: visual exploration based on citespace

Ocean acidification (OA) threatens marine microbial communities that underpin global biogeochemical cycles and marine food webs, however, a systematic synthesis of research progress in this area remains limited. This study presents the first comprehensive bibliometric analysis of ocean acidification impacts on microbial ecology, analyzing 495 Web of Science publications (2005-2025) using CiteSpace to characterize the field’s evolution and identify emerging frontiers. Global collaboration spans 53 countries, led primarily by China, the United States, and Germany, with the GEOMAR Helmholtz Centre for Ocean Research prominent within institutional networks. The research focus has shifted from basic chemical parameters to complex ecosystem processes, with “responses” identified as the most active contemporary research frontier. Overall, the field has matured into a highly internationalized, interdisciplinary domain. We outline four strategic directions for future work: (1) integrating advanceds molecular technologies, including multi-omics and single-cell approaches, to resolve mechanisms; (2) expanding temporal and spatial scales through global observatory networks; (3) quantifying multiple-stressor interactions, particularly with warming and deoxygenation; and (4) connecting molecular processes to biogeochemical cycles at the ecosystem level. These findings provide a data-driven roadmap for next-generation on OA–microbe interactions, essential for predicting marine ecosystem responses to accelerating environmental change and for informing evidence-based ocean conservation policy.

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Effects of ocean acidification on intestinal homeostasis and organismal performance in a marine bivalve: from microbial shifts to physiological suppression

Highlights

  • OA stimulates the colonization of the pathogenic bacterium Mycoplasma.
  • Microbiota dysbiosis and oxidative damage trigger intestinal inflammation.
  • OA causes significant epithelial damage to the intestines of C. nobilis.
  • Physiological suppression of C. nobilis is decreased in a pH-dependent manner.

Abstract

Ocean acidification (OA) poses significant threats to marine calcifiers through multifaceted physiological disruptions. While bivalve mollusks are particularly vulnerable, the intestinal defense mechanisms against OA-induced stress remain poorly characterized. This study systematically investigated the intimate associations between the organismal physiological toxicity responses and intestinal homeostasis of Chlamys nobilis (C. nobilis) under simulated OA situations (pH 7.3–8.0) to reveal the potential physiological and biochemical damage. The results revealed that acidification stimulated pathogenic bacteria(Mycoplasma)colonization, disrupted microbiota homeostasis, and induced oxidative responses, thereby triggering intestinal inflammation and epithelial damage. Furthermore, the filtration rates and oxygen consumption rates of C. nobilis were significantly decreased in a pH-dependent manner across all the treatments, which might result from the intestinal dysfunction and the inhibition of acetylcholinesterase activities. These findings establish a link between OA-induced intestinal dysbiosis and organismal physiology, providing novel insights into the interplay between physiological performance and intestinal homeostasis under OA scenarios. The results advance our understanding of bivalve mollusk adaptation strategies and inform predictive models for its sustainability in acidifying marine ecosystems.

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Biological and genomic responses of juvenile Pacific oysters (Crassostrea gigas) to a changing ocean

Climate change, fueled by greenhouse gas emissions, is causing global atmospheric and oceanic temperatures to rise, accompanied by increased levels of carbon dioxide (CO₂) in the ocean, which has led to ocean acidification (OA). During warmer months, climate stressors (e.g. elevated temperatures), host physiology (e.g. reproductive efforts), and opportunistic pathogens like Vibrio spp. and Ostreid herpesvirus 1 (OsHV-1), coincide with each other, and exacerbate interactions into global phenomenon called oyster summer mortality syndrome, a multifactorial disease affecting oysters, particularly Crassostrea gigas (EFSA Panel on Animal Health and Welfare, 2015; Petton et al., 2015; Pernet et al., 2014). While many marine species, including bivalves (such as oysters, mussels, clams, and scallops), are adversely affected by heat and OA individually, there is relatively limited research on the combined effects of these stressors on either somatic growth or genomic responses. In this study, I investigated the individual and combined effects of temperature and pCO2 on various growth and genomic responses of juvenile Pacific oysters (Crassostrea gigas) (mean ± SD shell height: 16.6 ± 1.7 mm, wet weight: 0.47 ± 0.12 g for growth responses and shell height: 15.2 ± 1.3 mm, wet weight: 0.42 ± 0.09 g for genomic responses). Two factors (temperature and pCO2) at two levels (average summer level and IPCC-projected (RCP 8.5) future summer level) were tested in a fully-crossed experimental design, using six replicate tanks per treatment and 24 oysters per tank. Oysters were sampled at regular intervals (every 2 or 4 weeks) over 16 weeks to examine various shell biometrics (shell height, shell length, shell width, wet total weight, wet and dry shell weights, wet and dry soft-tissue weights, fan ratio, cup ratio, weight ratio) and condition index. A different subset of oysters were sampled at regular intervals (every 2 or 4 weeks) over 16 weeks for transcriptomic (RT-qPCR) analysis. Fourteen genes of interest (GOIs)—covering immunity, cellular stress, and metabolism responses—were chosen for study. The results showed that oysters were significantly impacted mostly by high temperature rather than high pCO2, both in individual and combined treatments, when analyzing both the growth and genomic results.

Growth results revealed that somatic growth, weight ratio and condition indices were negatively impacted by high temperature and minimally impacted by elevated pCO2. I found that shell growth in higher temperature conditions was growing at a faster rate than in ambient temperatures, but the amount of wet tissue in high temperature condition oysters was minimal, resulting in a higher weight ratio. Similarly, condition indices were drastically different when comparing the two temperature treatments, not pCO2. Unsupervised hierarchical clustering with principal component analysis revealed numerous clusters when comparing somatic growth, with most clusters relating to week, pCO2, and temperature. Genomic results revealed that nine of the GOIs (i.e. heat shock protein 23, heat shock protein 70, hypoxia-inducible factor 1-alpha inhibitor, V-type proton ATPase catalytic subunit A, multidrug resistance 1, toll-like receptor 7, transforming growth factor, protein kinase R, macrophage expressed protein 1) were significantly upregulated by temperature, compared to only two GOIs (metallothionein and 6-phosphofructokinase) that were significantly upregulated by pCO2. Heat shock 23 and heat shock 70 genes were deemed as being the most suitable for routine monitoring as early-warning signs of oyster summer mortality. Unsupervised hierarchal clustering with principal components analysis revealed only two major clusters when comparing genomic responses, driven primarily by temperature.

My results indicate that juvenile oysters are much more sensitive to heat exposure than high pCO2, with no additive effect of the two factors. Understanding how oyster growth and genes respond to both individual and combined climate-change stressors is crucial for improving predictions of oyster performance under future climate scenarios and for enhancing the sustainability of shellfish aquaculture systems that are increasingly affected by heatwaves and low-pH upwelling events. Ongoing research is essential to investigate oyster responses in controlled, environmentally-relevant, multi-stressor experiments, providing deeper insights into the potential impacts of concurrent climate change stressors and extremes on both natural and cultivated oyster populations.

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The effects of ocean acidification on the epiphytic bacterial community of Sargassum thunbergii via high-throughput sequencing

Marine macroalgae and their epiphytic bacteria have established a symbiotic relationship. Although the effects of ocean acidification (OA) on macroalgae have been extensively studied, its impact on these epiphytic bacteria remains unclear. This study investigated the OA-induced shifts in the epiphytic bacterial community of Sargassum thunbergii from Qingdao’s intertidal zone using 16S rDNA sequencing. The results indicated that elevated CO2 altered bacterial community structure and function, reducing diversity while maintaining dominant taxa but significantly changing their relative abundances. The abundances of Proteobacteria, Firmicutes, and Verrucomicrobiota declined, whereas Campylobacterota, Desulfobacterota, and Spirochaetota increased. The specific phyla like Cloacimonadota, Calditrichota and Entotheonellaeota also emerged. These shifts were linked to the environmental adaptability and stress resistance of epiphytic bacteria as well as the metabolic activities of the host algae, particularly in protein and fatty acid degradation.

Functional predictions revealed that OA primarily affected nitrogen and sulfur metabolism in the epiphytic bacterial community, with effects intensifying over time. Specifically, nitrogen fixation increased, while dark oxidation of sulfur compounds, dark sulfite oxidation, and dark sulfur oxidation decreased. In conclusion, ocean acidification directly induced changes in the abundance of epiphytic bacterial taxa with varying stress resistance and adaptability. Simultaneously, it promoted shifts in bacterial taxa closely associated with the host algal metabolic activities, ultimately reshaping the epiphytic bacterial community on S. thunbergii. These findings provided new insights into the macroalgae-epiphytic bacteria interactions under ocean acidification and provided important guidance for macroalgal cultivation.

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Ocean acidification disrupts the biomineralization process in the oyster Crassostrea virginica via intracellular calcium signaling dysregulation

Anthropogenically increased atmospheric carbon dioxide (pCO2) leads to ocean acidification, disrupting calcification in marine calcifiers by reducing the saturation state of calcium carbonate. Calcium is not only a crucial component in the shell and skeleton structure but also serves as an essential second messenger for regulating biomineralization across many species. Ocean acidification is well-studied as causing shell dissolution in a diversity of bivalve species by disordering calcium deposition. However, it remains unclear whether the calcium-mediated signaling pathway regulating biomineralization is also affected. This study assessed eastern oyster (Crassostrea virginica) to determine how calcium signaling responds to elevated pCO₂ and influences shell formation. Under elevated pCO2, increased intracellular calcium concentration was found in primary epithelial cell cultures from oyster mantle. Meanwhile, we observed upregulation of calmodulin, a primary sensor of intracellular calcium, while its downstream effector, calcineurin, was downregulated. In addition, four conserved shell matrix proteins (SMPs), representing shell construction conditions, were significantly upregulated in the CO2-exposed mantle cells. In vivo, larval C. virginica exhibited developmental stage-dependent alterations in calcium signaling and SMPs disarrangement stimulated by pCO2. We hypothesize that dysregulation of calcium signaling disrupts the expressions of SMPs and causes oyster shell deformation. Pharmaceutical blockage of the calcium-calmodulin binding induced abnormal expression of related genes and shell matrix changes consistent with those caused by elevated pCO2, both in vivo and in vitro. Importantly, calcineurin restored SMPs expression in CO2-treated mantle cells. These findings suggest that shell deformities under ocean acidification are related to disruption of the calcium-calmodulin signaling pathway, inhibiting calcineurin activity and affecting SMPs production.

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