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Biology subjects

Lamarre, S. G.

Publications and source records attributed to Lamarre, S. G..

3 recordsLinked to original sources

Social experience influences thermal sensitivity: lessons from an amphibious mangrove fish

Understanding factors affecting ectothermic fishes capacity to cope with warming temperature is critical given predicted climate change scenarios. We know that a fishs social environment introduces plasticity in how it responds to high temperature. However, the magnitude of this plasticity and the mechanisms underlying socially-modulated thermal responses are unknown. Using the amphibious, selfing hermaphroditic mangrove rivulus fish (Kryptolebias marmoratus) as a model, we tested three hypotheses: 1) social stimulation affects physiological and behavioural thermal responses of isogenic lineages of fish, 2) social experience and acute social stimulation result in distinct physiological and behavioural responses, and 3) a desensitization of thermal receptors is responsible for socially modulated thermal responses. To test the first two hypotheses, we measured the temperature at which fish emerged (i.e., pejus temperature) with acute warming with socially naive, isolated fish and socially experienced fish. Our results did not support our first hypothesis as fish socially-stimulated by mirrors during warming (i.e., acute social stimulation) emerged at similar temperatures as isolated fish. However, in support of our second hypothesis, prior social experience resulted in fish emerging at a higher temperature than socially naive fish suggesting an increase in pejus temperature with social experience. We measured whole-body cortisol concentrations of socially naive and socially experienced fish and determined that socially experienced fish had significantly higher cortisol concentrations than socially naive fish. To test our third hypothesis, we exposed socially experienced and naive fish to capsaicin, an agonist of TRPV1 thermal receptors. Socially experienced fish emerged at significantly higher capsaicin concentrations than socially naive fish suggesting a desensitization of their TRPV1 thermal receptors. Collectively, our data indicate that past and present social experiences impact the behavioural response of fish to high temperature. We also provide novel data suggesting that social experience affects the capacity of fish to perceive warm temperature.

physiology↗

Phenotypic plasticity during diel cycling hypoxia in Arctic char (Salvelinus alpinus)

Oxygen concentration naturally fluctuates in aquatic environments. Due to increased eutrophication caused by anthropic activities, this phenomenon could be amplified and result in a daily cycle of alternating normoxic and hypoxic conditions. At the metabolic level, lack of oxygen and reoxygenation can both have serious repercussions on fish due to fluctuations in ATP supply and demand and an elevated risk of oxidative burst. Thus, fish must adjust their phenotype to survive and equilibrate their energetic budget. However, their energy allocation strategy could imply a reduction in growth which could be deleterious for their fitness. Although the impact of cyclic hypoxia is a major issue for ecosystems and fisheries worldwide, our knowledge remains however limited. Our objective was to characterise the effects of cyclic hypoxia on growth and metabolism in fish. We monitored growth parameters (specific growth rate, condition factor), hepatosomatic and visceral indexes, relative heart mass and hematocrit of Arctic char (Salvelinus alpinus) exposed to thirty days of cyclic hypoxia. We also measured the hepatic protein synthesis rate, hepatic triglycerides as well as muscle glucose, glycogen and lactate, and quantified hepatic metabolites during this treatment. Arctic char appeared to acclimate well to oxygen fluctuations. The first days of cyclic hypoxia induced a profound metabolome reorganisation in the liver. However, fish rebalanced their metabolic activities and successfully maintained their growth and energetic reserves after one month of cyclic hypoxia. These results demonstrate the impressive ability of fish to cope with their changing environment. Summary statementThis study characterizes the metabolic adjustments performed by Arctic char when coping with one month of cyclic hypoxia. Fish reached a new phenotype by defending their growth and energy stores.

physiology↗

Reduced Shmt2 expression impairs mitochondrial folate accumulation and respiration, and leads to uracil accumulation in mouse mitochondrial DNA

BackgroundAdequate cellular thymidylate (dTMP) pools are essential for preservation of nuclear and mitochondrial genome stability. Previous studies have indicated that disruption in dTMP synthesis in the nucleus leads to increased uracil misincorporation into DNA affecting genome stability. To date, the effects of impaired mitochondrial dTMP synthesis in non- transformed tissues have been understudied. ObjectiveThis study aimed to determine the effects of decreased serine hydroxymethyltransferase 2 (Shmt2) expression and dietary folate deficiency on mitochondrial DNA integrity and mitochondrial function in mouse tissues. MethodsLiver mitochondrial DNA (mtDNA) content, and uracil content in liver mtDNA was measured in Shmt2+/- and Shmt2+/+ mice weaned onto either a folate-sufficient control diet (2 mg/kg folic acid, C) or a modified diet lacking folic acid (0 mg/kg folic acid, FD) for 7 wks. Shmt2+/- and Shmt2+/+ mouse embryonic fibroblasts (MEF cells) were cultured in defined culture medium containing either 0 or 25 nM folate to assess proliferative capacity and mitochondrial function. ResultsShmt2+/- mice exhibited 48-67% reduction in SHMT2 protein levels in tissues. Interestingly, Shmt2+/- mice consuming the folate-sufficient C diet exhibited a 25% reduction in total folate in liver mitochondria. There was also a >20-fold increase in uracil in liver mtDNA in Shmt2+/- mice consuming the C diet, and dietary folate deficiency also increased uracil content in mouse liver mtDNA from both Shmt2+/+ and Shmt2+/- mice. Furthermore, decreased Shmt2 expression in MEF cells reduced cell proliferation, mitochondrial membrane potential, and oxygen consumption rate. ConclusionsThis study demonstrates that Shmt2 heterozygosity and dietary folate deficiency impair mitochondrial dTMP synthesis, as evidenced by the increased uracil in mtDNA. In addition, Shmt2 heterozygosity impairs mitochondrial function in MEF cells. These findings suggest that elevated uracil in mtDNA may impair mitochondrial function.

biochemistry↗