notes/mechanistic_models.htm
There are three fundamentally different underlying model for phytoplankton physiology:
| short description | example | |
| optimization | optimization of cellular composition and efficiency leading to maximum growth rate or least loss | Shuter 1979 |
| survival | ensuring survival through rough times by using storage or other non-optimal, high cost strategies | Parnas and Cohen 1976 |
| Multiple Annoyance Hypothesis |
multiple low levels of toxic side products limit the growth through interference with metabolism |
These models represent very different approaches to understanding how phytoplankton cell structure is linked to the processes of regulation and growth in algae. These are not "meta-models" in the sense of Burmaster (****). Each model requires its own set of parameters and experimental approaches. This short paper intends to ellucidate the differences between these three approaches and explore the potential for bringing these together.
Optimization
measuring processes and components such as carbon fixation and chlorophyll or photosynthetic units
addresses molecular efficiency of each component (mol C fixed per mol C per time)
allocation of components within the cell that leads to maximum growth rate under those conditions
classical example is the sun shade adaptation
models based on minimum cost or maximum production in a competitive environment
Survival
diversity within species, phenotypic plasticity under different conditions
example diatom size differences between generations
differences in gene structure
good models from vascular plant literature
individual based models such as Rueter -
based on genetic algorithm
MAH
low levels of toxins or supra-optimal conditions
examples from trace metals
Zinc squeeze from Sunda
measure side products at very low levels
balance of secondary metabolism
There is a list of phenomena that cant be adequately explained by any of the three models. These phenomenon are usually explained by invoking larger context; Godel's theorem. When the larger context is invoked however, the argument becomes more circular. Maybe these models could be used together to explain the response without invoking the larger context.
Oscillation
why would metabolism oscillate
how can the over-capacity be explained in the context of optimal models
examples - the metabolic flux models for enzymes - see Bi335 website
Crashes
peroxidation cascade (Sakamoto et al ---)
imbalanced metabolism
Viruses
lower growth rate allows higher density
John Rueter
February 19, 2001