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Topic

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

Department of Biology

Date & location

• Monday, July 28, 2025
• 10:00 A.M.
• Virtual Defence

Examining Committee

Supervisory Committee

• Dr. Amanda Bates, Department of Biology, ßÉßɱ¬ÁÏ (Co-Supervisor)
• Dr. Chris Pearce, Department of Biology, UVic (Co-Supervisor)
• Dr. Helen Gurney-Smith, Department of Biology, UVic (Member)

External Examiner

• Dr. Timothy Green, Centre for Shellfish Research, Vancouver Island University

Chair of Oral Examination

• Dr. Annalee Lepp, Department of Gender Studies, UVic

Abstract

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.