Allison Smith

I study the mechanisms underlying species distributions. In particular, I take into account adaptations of animals and bacteria that allow them to survive and reproduce in complex and often hostile physical and chemical environments. It is the beginning of the big data era, and I leverage as many data, software, and code resources as possible to address research questions over large spatial and long temporal scales. I work on a variety of projects which are described in the following sections.

Hypoxic zones are expanding and temperatures are increasing in the global open ocean. I determine the effects of these environmental changes on marine ecosystems by understanding how animals respond to hypoxia simultaneously with temperature. Different species have different hypoxia tolerances. One of the primary mechanisms underlying hypoxia tolerance is blood-oxygen binding, which is sensitive to temperature. Blood-oxygen binding is measured as the oxygen pressure in the blood at which whole blood is 50% oxygenated, called P₅₀. A low P₅₀ means that respiratory pigments in the blood of an organism equilibrate to 100% oxygenation at lower oxygen pressures, and the organism is more hypoxia tolerant.

Temperature alters hypoxia tolerance by shifting the P₅₀ of organisms. The effect of temperature is measured as the heat of oxygenation (ΔH) which is the amount of heat energy released (negative ΔH) or absorbed (positive ΔH) when oxygen binds to respiratory pigments. If ΔH is negative, then colder temperatures decrease P₅₀, which increases hypoxia tolerance. If ΔH is positive, then colder temperatures increase P₅₀, which decreases hypoxia tolerance. Marine orgnanisms swim between warmer, well-oxygenated waters near the surface of the ocean and colder, less-oxygenated waters in the deeper ocean. The shift in P₅₀ increases the hypoxia tolerance of species with a negative ΔH and decreases the hypoxia tolerance of species with a positive ΔH. To explore these traits in the global pelagic ocean, I developed a metric called the P₅₀ depth to map the fundamental niche of blood-oxygen binding thresholds. The P₅₀ depth, defined as the shallowest depth in the ocean where pO₂ = P₅₀, represents a key physiological transition point between dexoxygenated and oxygenated blood in the ocean water column. This metric can be used to link blood-oxygen binding to the environment over large spatial scales, providing a mechanistic perspective on habitat suitability and zonation in hypoxic regions.

Ocean hypoxia is related to the activity of heterotrophic bacteria on detrital particles sinking from the surface ocean. Parameterizations for particles in ocean models are largely based on an empirical curve fit to sediment trap data and do not include critical biological processes that may be altered by climate change. I created the microbial remineralization model to link bacterial activity to decomposition and remineralization of particles in the water column. The microbial remineralization model explicitly describes the interactions between sinking particles and heterotrophic bacteria using 9 state variables - particulate organic carbon (POM) as well as bacteria (PB and DB), active exoenzyme (EP, ED), inactive exoenzyme (XP, XD), and hydrolysate (HP, HD) associated with two physical environments, dissolved and particulate. The first application of the model has been to determine the role of bacterial group behavior in particle remineralization. Major findings were: diffusion and advection caused rapid loss of hydrolysate and exoenzymes from particles; exoenzyme production based on bacterial abundance consistent with quorum sensing behavior emerged as a property of the model; and bacterial uptake and retention of hydrolysate altered bacterial production and remineralization depths.

Thermal physiology of intertidal mussels

The intertidal habitat is a model ecosystem for studying the effects of climate change on species biogeographic ranges because many intertidal species are living near their physiological limits along the steep environmental gradients between marine and terrestrial environments. A major result of my research has been to determine that there is regional variability in lethal temperatures at mussel bed upper zonation limits. Temperature has long been hypothesized to be a main factor determining upper shore limits everywhere so this finding contrasts with the prevailing paradigm for rocky intertidal ecosystems. I then used a biophysical model to determine that variability in % contact between mussels and underlying substrates may be the mechanism leading to observations of patchy mortality in mussel beds after heat waves at all shore levels.