Allison Smith

computational marine biology

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RESEARCH

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.

Blood-oxygen binding in the pelagic ocean:

negative ΔH

positive ΔH

O2

O2

O2

O2

H

H

H

H

Temp (°C)

Temp (°C)

+

+

+

+

+

+

4O2

4H+

heat

4H+

4O2

+

+

heat

0

15

30

0

15

30

H

H

O2

O2

O2

O2

H

H

0

100

200

400

T

T

50

600

P50

P50

P50

P50

800

more

hypoxia

tolerant

less

hypoxia

tolerant

0

0

1

2

3

4

0

1

2

3

4

1000

pO2 (kPa)

pO2 (kPa)

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.

Bacterial remineralization of sinking particles

Bacterial Activity on

Particles (POM)

Microbial Remineralization

Model

Particle Flux Attenuation

in the Ocean

Mass Transfer

POM (mg m-2 d-1)

0

Mortality

ED

XP

Decay

POM

XD

1000

EP

Decay

Action

HP

Uptake

HD

2000

DOCs

PB

Bacteria (B)

Uptake

Mortality

Growth

Growth

Exoenzyme (E,X)

3000

DB

Hydrolysate (H)

Sinking

Transfer Direction

4000

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

Upper limit of a mussel bed
Mytilus californianus 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.