RESEARCH INTERESTS

My research focuses on how links between energy metabolism and oxidative stress influence animal life-history strategies and trade-offs involved with growth rate and senescence. I am also interested in the effects of environmental change on animal physiology, and the costs and limitations of mitochondrial plasticity, and their relationships to ecology. I aim to incorporate multidisciplinary knowledge, including chemistry, bioenergetics, animal physiology and ecology, eventually to describe the proximate and ultimate causes of the persistent variability in the animal performance such as metabolic rate, growth rate, feeding capacities, within a population and species. Most of my current work focuses on fishes, but I have several ongoing and previous researches on birds, mammals and amphibian.


CURRENT RESEARCH PROJECTS

fish in individual tankI am currently working on a broad project looking at the variability of metabolic traits at different scales, from the sub-cellular mechanisms to the population consequences, using fish as study species. The project is run by Neil Metcalfe and funded by an ERC advanced grant. The project also involves Sonya Auer, Eugenia Martin and Graeme Anderson. The project aims to incorporate multidisciplinary knowledge, including chemistry, bioenergetics, animal physiology and ecology. My current main research themes are listed below.

The role of mitochondrial efficiency in whole-animal performance

Links between energy metabolism and animal performance have been demonstrated in a number of contexts. Interestingly, however, most of this work has been performed using oxygen consumption as an estimate of ATP production, while in reality mitochondria vary in the amount of ATP generated per molecule of oxygen consumed (P/O ratio). Focusing on liver and skeletal muscle mitochondria, this project investigates the role that the P/O ratio play in shaping the growth rate of an organism, and how environmental factors such as temperature and food availability may affect this relationship. This project is being conducted in collaboration with Christos Chinopoulos (Semmelweis University, Hungary) and Colin Selman (University of Glasgow, UK).

Salin, K., Villasevil, E., Auer, S., Anderson, G., Selman, C., Metcalfe, N., and Chinopoulos, C. (2016) Simultaneous measurement of mitochondrial respiration and ATP production in tissue homogenates and calculation of effective P/O ratios. Physiological Reports, 4(20), e13007. (doi:10.14814/phy2.13007PDF
Salin, K., Auer, S. K., Rudolf, A. M., Anderson, G. J., Selman, C., and Metcalfe, N. B.(2016) Variation in metabolic rate among individuals is related to tissue-specific differences in mitochondrial leak respiration.Physiological and Biochemical Zoology, 89(6), pp. 511-523. (doi:10.1086/688769PDF

The role of oxidative stress in animal life-history trade-offs

Understanding the role of reactive oxygen species (ROS) in influencing life-history trade-offs is of growing interest in ecology, due to their effect in generating oxidative stress and in turn the senescence of the organism. However, there have been virtually no measurements of ROS in an ecological context due to the complexity and specialized nature of the available methods. This project aims to improve our understanding of oxidative balance by measurement of in vivo ROS levels using a probe, MitoB, targeting the mitochondria in living animals.

The development of this cutting-edge method is based on a cross-disciplinary collaboration with a chemist – Richard Hartley  and a specialist in mass-spectrometry – Bill Mullen. Using this new technique, we have shown that in fact the relationship between the rate of oxygen consumption and the rate of production of ROS is in the opposite direction to that usually assumed. I am currently developing the method in the red blood cells of birds to allow longitudinal study of oxidative stress, in collaboration with Pat Monaghan and Antoine Stier.

Salin, K., Auer, S. K., Villasevil, E. M., Anderson, G. J., Cairns, A. G., Mullen, W., Hartley, R. C., and Metcalfe, N. B.(2017) Using the MitoB method to assess levels of reactive oxygen species in ecological studies of oxidative stress. Scientific Reports, 7, 41228. (doi: 10.1038/srep41228PDF
Salin, K., Auer, S. k., Rudolf, A. M., Anderson, G. J., Cairns, A. G., Mullen, W., Hartley, R. C., Selman, C., and Metcalfe, N. B.(2015) Individuals with higher metabolic rates have lower levels of reactive oxygen species in vivo. Biology Letters, 11(9), 20150538. (doi:10.1098/rsbl.2015.0538PDF

Links among oxygen consumption, ATP production and ROS generation

Unravelling the association between oxygen consumption and ATP production and ROS generation in living organisms is crucial to our understanding of the effects of energy metabolism on cellular oxidative stress and senescence. Indeed, the mechanistic dependence of the production of ATP and ROS on oxygen consumption has often led to the assumption that higher rates of oxygen consumption will result in greater ATP and ROS generation. However, the relationship between the rate of oxygen consumption, ATP production and ROS generation is not straightforward. My work and others have shown that the relationship can be in many different directions, depending on the context. The effect of this relationship on individual fitness is expected to be context dependent as high P/O ratio may allow individuals to maximise growth efficiency by reducing oxygen and food requirements, but is likely to generate a cost in term of oxidative stress.

The next step of this project is to determine the links among oxygen consumption, ATP production and ROS generation in individual animals by combining technological breakthroughs to carry out high-resolution respirometry, ATP assay, and in vivo ROS levels (as explained above).

Salin, K., Auer, S. K., Rey, B., Selman, C., and Metcalfe, N. B.(2015) Variation in the link between oxygen consumption and ATP production, and its relevance for animal performance. Proceedings of the Royal Society of London Series B: Biological Sciences, 282(1812), 20151028. (doi:10.1098/rspb.2015.1028PDF

Determination of mitochondrial adaptations to environmental stressors

The influence of mitochondrial bioenergetics extends into all of biology since the mitochondria supply the energy that fuels organismal functions. However, the perceived status of mitochondria has recently increased even further with research showing that mitochondria are part of interactive networks connecting changes in oxygen concentration, pH and temperature with cell signalling, energy (ATP) supply and oxidative stress. Mitochondrial plasticity can buffer detrimental effects of global change up to a certain threshold. Specifically, in order to better predict the evolutionary potential and persistence of populations under climate change, this project examines how oxidative stress and other variables related to mitochondrial energy efficiency affect the ability of animals to respond to an environmental stressor.

I am currently conducting a study to test whether animals that have higher mitochondrial coupling efficiency have a higher efficiency of protein growth, as a consequence of a greater capacity for investment in somatic growth under limited food access, in collaboration with Ian McCarthy (University of Bangor) and Simon Lamarre (University of Moncton).

Salin, K., Auer, S. K., Anderson, G. J., Selman, C., and Metcalfe, N. B.(2016) Inadequate food intake at high temperatures is related to depressed mitochondrial respiratory capacity. Journal of Experimental Biology, 219(9), pp. 1356-1362. (doi:10.1242/jeb.133025PDF

PREVIOUS RESEARCH PROJECTS

Postdoctoral project:

The evolutionary consequences of physiological adaptation in striped mice coping with dry events.
This project was funded by a grant from the National Research Foundation of South Africa to establish a phSalinK-STRIPED MOUSE PROJECTysiological profile of animals that cope and fail to cope with an extreme dry season. The environment experienced by the South African striped mouse is characterized by a dry season during the summer (from December to April), which reduces plant growth and subsequently food availability. Most of the mice die during this period (only 1 to 20% survive). Two theories, the allostasis and reactive scope models, could explain whether individual animals succeed or fail in coping with this event. These two models have been compared using field data collection collected from wild mice. From August 2012 to May 2013, I collected data in the field at the Geogap nature reserve in order to quantify the physiological status of the mice before, during and after the dry season. The physiological variables that were recorded included their basal metabolic rate, their energy reserves (glucose, ketone bodies and blood uric acid), glucocorticoid levels, leukocyte profile and levels of oxidative stress.

PhD project:

The relationship between mitochondrial efficiency, oxidative balance and growth in amphibians.
During my PhD I studied the physiological mechanisms underlying life-history traits in amphibians. The aim was to highlight relationships between life-history trajectory and energy metabolism (including its oxidative cost). I mainly focused on the growth rates of amphibians. As well as investigating mitochondrial functioning and the link between ATP production and ROS generation as a bioenergetic constraint, I also considered the “cascade” of functional steps in resource metabolism from the ingestion of food to the supply of ATP, and assessed oxidative balance parameters through integrative measurements. Across the successive elements in the energy processing chain, the degree of mitochondrial coupling appeared as a keystone determining the energy allocation to traits such as growth. Moreover, the results suggested that the oxidative constraint should first be estimated at the level of pro-oxidant generation, but also that the resources allocated to anti-oxidant defences must be integrated to have a reliable overview of the oxidative cost underlying the senescence process. Overall, my results led to the suggestion that mitochondrial efficiency is a fundamental mechanism of life-history interactions, leading to applications in multiple disciplines since mitochondrial performance is subject to hormonal changes, genetic variability, food composition and availability, environmental temperature, etc. and can affect different levels of biological organization.

Roussel, D., Salin, K., Dumet, A., Romestaing, C., Rey, B., and Voituron, Y. (2015) Oxidative phosphorylation efficiency, proton conductance and reactive oxygen species production of liver mitochondria correlates with body mass in frogs. Journal of Experimental Biology, 218(20), pp. 3222-3228. (doi:10.1242/jeb.126086PDF
Salin, K., Roussel, D., Rey, B., and Voituron, Y. (2012) David and Goliath: a mitochondrial coupling problem? Journal of Experimental Zoology Part A: Ecological Genetics and Physiology, 317(5), pp. 283-293. (doi:10.1002/jez.1722PDF
Salin, K., Luquet, E., Rey, B., Roussel, D., and Voituron, Y. (2012) Alteration of mitochondrial efficiency affects oxidative balance, development and growth in frog (Rana temporaria) tadpoles. Journal of Experimental Biology, 215(5), pp. 863-869. (doi:10.1242/jeb.062745PDF

Masters projects:

I conducted two studies as part of my Masters degree: the first looked at the alteration of mitochondrial coupling in liver and muscle during shivering and non-shivering thermogenesis in ducklings exposed to cold; the other one investigated the physiological adaptations displayed by a subterranean fish during a starvation event.

Salin, K., Voituron, Y., Mourin, J., and Hervant, F. (2010) Cave colonization without fasting capacities: an example with the fish Astyanax fasciatus mexicanusComparative Biochemistry and Physiology. Part A: Molecular and Integrative Physiology, 156(4), pp. 451-457. (doi:10.1016/j.cbpa.2010.03.030PDF
Salin, K., Teulier, L., Rey, B., Rouanet, J.-L., Voituron, Y., Duchamp, C., and Roussel, D. (2010) Tissue variation of mitochondrial oxidative phosphorylation efficiency in cold-acclimated ducklings. Acta Biochimica Polonica, 57(4), pp. 409-412. (PMID: 21125027PDF
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