March 17, 1998
The problem for phytoplankton in a continually mixed hydrodynamic regime is that they are subjected to a wide range of light and potentially a wide range of nutrient availabilty. Optimization to one condition does not necessarily maximize growth or insure their survival.
My assumption is that survival is more important than optimization (this will be discussed elsewhere), and that for a species to survive in a fluctuating envirornment it needs to maintain a level of intraspecific variability. This variablility could be at the genetic level, the gene expression/metabolism level, or at the physiological history level. I will discuss these three below.
Although we general consider algae to be clones and that clones have nearly identical genetic makeup, there are several mechanisms that lead to intraspecific genetic variability. The most obvious mechanism is sexual reproduction. Many algae have cell cycles and sexual reproduction events. This should be examined more in terms of cell-to-cell diversity of response. Another mechanism that could be operating in the cyanobacteria would be transposons. These have been shown to be highly active in the archaebacteria such that in a one-liter culture of *** started from a single cell, only 30?? something percent of the cells are genetically identical. This genetic variablity would have to make a difference in expression patterns of key genes for environmental response inorder for this mechanism to be directly valuable to the species.
Individual cell history has been used to explain differential responses of individuals to environmental conditions. For examples, cells that were recently mixed to the surface from deep water would expect to have different response than individual cells that had just been at saturating light intensities. Models that address this have been based on a Lagrangian ??? that divides the water column into packets that mix around.
Individual cell physiologies can also be effected by cell size, stage in the cell division cycle, and storage of either nutrient or photosynthate. Most laboratory experiments would attempt to minimize these inter-individual differences through some type of controlled pre-conditioning of the culture. Although this is desireable for studying a response to a particular factor, it doesn't give us a workable idea of how much variation there will be between individuals in a population under natural conditions. A good example of this would be the physiological variation caused by cell cycle differences that were explored by Chisholm and Vaulot? with consideration for Gq.
An interesting case in this would be to study the physiological diversity in populations that have long periods of stable conditions. Do they converge toward the predicted optimum condition (as assumed in the optimization models) or do they maintain a higher level of physiological diversity.
Regulation by the two-component system (gene and enzyme levels) creates a complex system of feedback, feedforward and other interactions. These systems are usually considered to be deterministic in the Monod model of regulation, i.e. if there is a new substrate or absence of a substrate that a particular genetic expression response will happen.
I would like to compare the deterministic view of the two component model (such as the STELLA models that I use in class) with a complex view of the same system. I have set up simple NK models of a pathway to show how this works. The interactions between the nodes leads to a complex system that has basins. With a simple three step pathway there are several ways to set up the model and each has different consequences for regulation. These simple examples illustrate the importance of the concepts of basins, periodic attractors and also lead to questions about how simple changes in the regulation scheme could shift basins.
I need to expand this to look at a more detailed model of light and nutrient use as a complex system. The first steps will be to try to understand what the meaning of having a system that is in a periodic basin. A cell that is cycling through the states in a periodic attractor might respond differently than a cell, in the same basin, but at another state in the same basin. This would lead to metabolic variablility that is not based on cell histroy as described above. One example of this is the oscillations in glucose metabolism (text book).
The next project will be to demonstrate (dream up) a plausible metabolic mechanism that could lead to shifting from one basin to another. If there are four or five enzyme clusters, each with their own genes and enzyme regulation systems, are their some links that could be changed at a semi-permanent level (i.e. not in the DNA code or protein sequence). I will look at protein modification such as phosphorylation/dephos or adenylation (seen in N metabolism and N2 fixation paper by Ohki) as potential changes, and then explore how such a small change will lead to a shift in basin - meaning a complete shift in metabolic patterns. If I can argue that shift-up shift-down could be such a change in basins, I think people will understand the utility of the complex network approach.
The current paradigm for competitive exclusion is that under a set of conditions the species that can use the resourses more efficiently would exclude the other species. This is a very special case for speciation, especially it seems in the aquatic environment. Even so, much of our work is based or benchmarked agains optimal physiological solutions to environmental conditions.
What we are trying to examine is what factors allow species to survive, how important are these factors, and given their importance how far from "optimal" will the real community production be. Terrestrial plant physiologists/ecologists are wrestling with this problem in the context of climate change (see Bazzaz 1996). In a way, the difference between "optimal" biochemical and biophysical estimates for productivity and our measurements of community primary productivity is actually a measure of the importance of survival through pre-investment in adaptability. If we can sort out how much is due to predator deterance and avoidance, hydrodynamic loss, and pre-investment then we will have a much better idea of the strategies for survival.
are there developmental patterns in unicellular algae not undergoing sexual division stages (see Goodwin 1994)
hormone communication (cAMP in the OK lake)
complex system with herbivores and nutrient availablilty
what is ruderal