bioRxiv Science⌕ Search

bioRxiv · 10.1101/2025.04.22.650023

Plasticity and genetics shape thermal tolerance in non-native populations of the European green crab (Carcinus maenas)

Abstract

Temperature is a major driver of individual performance in ectotherms, with this impact depending on stressor intensity and duration. Differences in individual response across temperature, time, and populations are shaped by the interplay between evolutionary adaptation and phenotypic plasticity. Some populations are able to thrive in novel and changing environments despite limited genetic diversity, raising the question of how plasticity and adaptation interact after significant genetic diversity loss. The European green crab (Carcinus maenas) is a textbook example of this phenomenon: invasive populations boast a broad thermal tolerance and exceptional thermal flexibility even after repeated genetic bottlenecks. Despite this loss of diversity overall, prior work has found a strong population-level association between variation at a specific extended genomic region (supergene), cold tolerance, and sea surface temperature. We conducted a series of three experiments using righting response to characterize sublethal thermal tolerance and plasticity in introduced green crab populations, then determined if these factors were associated with supergene genotype for individual adult crabs. Crabs showed signs of stress after exposure to a 30{degrees}C heat shock in one experiment. Interestingly, a second experiment exposing C. maenas to repeated 24-hour heat shocks showed that prior heat shock conferred beneficial plasticity during a subsequent event. The third experiment examined cold acclimation over multiple timepoints up to 94 hours. At 5{degrees}C, certain crabs exhibited an acclimatory response where righting slowed dramatically at first, and then gradually sped up after a longer period of cold exposure. Several crabs failed to right at 1.5{degrees}C, which could be indicative of dormancy employed to reduce energy consumption in colder conditions. There were no significant relationships between individual plasticity and supergene genotype in any experiment. Linking population-level genetic associations with individual-level physiology is complex, and reflects the impact of environmental conditions such as temperature throughout life history in shaping adult phenotype. Our results highlight the robust thermal tolerance and plasticity that adult green crabs maintain despite a substantial reduction in genetic diversity, and underscore the importance of probing population-level genotype-phenotype associations at the individual level.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Venkataraman, Y. R., Kelso, J. C., Payne, C., Freitas, H. L., Kohler, J., Tepolt, C. K.. 2025-04-26. Plasticity and genetics shape thermal tolerance in non-native populations of the European green crab (Carcinus maenas). https://doi.org/10.1101/2025.04.22.650023

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Rad and Phospholamban are Key Drivers of the Ventricular Adrenergic Response and Stress-Induced Arrhythmia

The adrenergic response is a fundamental mechanism that regulates heart rate (chronotropy), cardiac contractility (inotropy) and relaxation (lusitropy). Adrenergic stress is also a recognized trigger of arrhythmia in disease. Yet, our understanding of the underlying molecular basis remains incomplete. Protein kinase A (PKA) and the calcium/calmodulin-dependent kinase II (CaMKII) phosphorylate multiple targets proposed to participate in the adrenergic response, including the GTP-binding protein Rad, phospholamban (PLB) and ryanodine receptor 2 (RyR2). Here we demonstrate that phosphorylation of both Rad and PLB is necessary for inotropy and lusitropy. We show that changes in cardiac contractility and relaxation are primarily dependent on intracellular calcium handling. Finally, we report that Rad and PLB control stress-induced arrhythmogenesis, despite the phosphorylation of other pro-arrhythmic targets. We have identified the essential molecular components of the adrenergic response, resolving a long-standing debate in cardiac excitation-contraction coupling and refining current models of sympathetic regulation in health and disease.

physiology↗

MCT6 is an intestinal Lac-Phe exporter required for metformin-associated weight loss

Metabolites are increasingly recognized as circulating molecules that regulate physiology, yet the mechanisms that couple intracellular production to organism-wide action remain poorly defined. Using the anorexigenic metabolite Lac-Phe as a tractable system, we identify the orphan transporter MCT6 (SLC16A5) as a physiologic intestinal Lac-Phe exporter. This mechanism controls the extent to which intracellularly synthesized Lac-Phe acquires systemic activity. MCT6 transports Lac-Phe, mediates its cellular efflux, and is required for maintaining its blood levels in mice following strong glycolytic stimuli. Both global and intestinal epithelial-specific deletion of MCT6 confers resistance to metformin-associated weight loss on a high-fat diet. Bypassing the transport defect with exogenous Lac-Phe normalizes the body weight phenotype of MCT6-KO mice. Together, these data connect MCT6 to metformin pharmacology and intestinal lactate metabolism, and more generally underscore the importance of transporter-mediated release in the conversion of an intracellular metabolic state into a circulating metabolite effector.

physiology↗

DEPP1 connects nutrient and oxygen availability to maintenance of muscle mass

Nutrients and oxygen are sensed within the muscle to control growth and disruption of either signal is sufficient to lead to muscle atrophy. While nutrient limitation is sensed via a conserved transcriptional atrophy program (commonly referred to as atrogenes) dictated via the Forkhead box O (FoxO) transcription factors, how low oxygen promotes muscle loss remains unknown. Accordingly, the downstream mechanisms that initiate muscle loss when oxygen and nutrients are limiting are only partly understood. Here, we find Hypoxia Inducible Factor (HIF), the master regulator of our adaptation to low oxygen, is necessary and sufficient to mediate muscle loss under hypoxia in mice. RNA sequencing in skeletal muscle isolated from starved or hypoxic mice identifies Decidual Protein Induced by Progesterone 1 (Depp1), which is induced in skeletal muscle when nutrients or oxygen is limiting via FoxO1 and HIF activation, respectively. Whole body Depp1 loss in mice reduces muscle loss under fasting and hypoxia and skeletal muscle Depp1 overexpression is sufficient to mediate muscle atrophy. Mechanistically, Depp1 localizes to the mitochondria and is necessary to control autophagy activation and mitochondrial degradation in skeletal muscle. Taken together, our studies nominate Depp1 as a new atrogene necessary for muscle loss under multiple atrophy scenarios involving FoxO and HIF.

physiology↗