Organism Size and Environmental Variation

Much of what follows addresses how size differences affect environmental relationships (extending comments in Chap. 4), but it is worthwhile to start with some commonalities. Monod has famously said (personal communication reported by Koch 1976, p. 47) that “what is true of E. coli is also true of the elephant, only more so” by which he probably meant that they had many biochemical reactions in common (this likely was from Monod’s closing conference synopsis at Cold Spring Harbor, see Monod and Jacob [1961]). Koch, however, continues in his own words (p. 47) about their ecological parallels...There never was a single E. coli, nor a single elephant, on which Darwins law has not operated separately, and equally; it has done so on them and on all their ancestors. The law of survival of the fittest has been obeyed, and the little E. coli has survived” Both organisms have passed the screen of natural selection within the context of what is possible for each of them. For the elephant, coping has involved../“many more cells, much more DNA, more neurons, and the ability to walk and do other things that E. coli cannot do.” For the bacterium, it has involved extensive phenotypic plasticity and extreme genotypic versatility.

It should be added that what the elephant does as a genetic individual comprising one huge mass of coordinated, differentiated cells, the E. coli genetic individual does as a diffuse, essentially undifferentiated clone. Most of the elephant’s cells, being internal, are buffered from exterior fluctuations, but they do have to contend with such things as pathogens. The cells react in unison at the tissue or organ level under centralized control by neurons and chemical signals such as hormones. Homeostasis is most apparent in the exquisite mechanisms that mammals have for balancing temperature and blood and tissue chemistry.

As discussed earlier for unitary organisms (Chap. 5), the physiological and the genetic individual are the same entity. How well the entire corpus responds to diverse environmental stimuli determines whether the elephant is sick or robust, whether it dies young or as an old matriarch, and whether it will contribute significantly to the population gene pool. Being by far the largest land animal, the healthy adult elephant has no natural predators. Evidently the main environmental challenge it faces is to find food, a process that takes about three quarters of the animal’s time (Chap. 5 in Eltringham 1982). Each cell is a party to this venture and if the functional unit dies, all components die. In short, the animal as an integrated unit has a complex neural network with which it can modify its behavior to stimuli such as hunger, thirst, or temperature extremes to maintain homeostasis.

In contrast, while cells of an E. coli clone may occur in aggregates, each is relatively more exposed than is an elephant cell to oscillations in the external environment. Each responds, and lives or dies, largely as a physiological individual (though coordinated responses such as quorum-sensing are known among some bacteria; Miller and Bassler 2001). Serological, electrophoretic, and molecular typing reveals the population structure of this species and shows that resident E. coli strains may persist for weeks or longer in a healthy human or other host despite loss of cells en masse when the host defecates (Selander et al. 1987; Touchon et al. 2009). (Note we are considering here events on a relatively local scale; the widespread and in some cases global distribution of microbial clones has been discussed previously; see Chaps. 4 and 5.) There is also turnover and sporadic reappearance of strains, the inoculum originating from a few cells that evidently persist in protected intestinal sites. Intra- as well as inter-specific competition is presumably extreme.

The environment is highly variable from the bacterial cell’s perspective both in time and space. Koch (1971, 1987) postulates that this is a “feast and famine existence”—brief periods of glut alternating with chronic malnutrition. In spatial terms, the clone is subject to the environmental vagaries of, say, the colon as opposed to the ileum, the intestinal wall or the lumen, the intestinal milieu of different hosts, and possibly to sporadic doses of antibiotics (variation in time and space). Finally, there is life, albeit in a declining phase, outside the host associated with soil, water, plants, or feces. Savageau (1983; see also Gordon 2013) estimates roughly that an average E. coli cell spends about half its life in the intestine and about half on the surface of the earth, drastically different environments! It manages environmental challenges by metabolic versatility through vast, intricate systems of biochemical reactions and metabolic regulation to reach some overall optimal compromise between rapid growth when conditions permit and persistence when they do not. For E. coli, this coordinated biochemical network is the counterpart to the elephant’s neurological network which, through natural selection, bestows upon the bacterium an appearance of similar predictive behavior (Tagkopoulos et al. 2008).

Of course, size and complexity inevitably impose many differences. Environmental signals of interest to E. coli are obviously different from those important to the elephant. To the bacterium, gravity is of no consequence, but Brownian motion, Reynolds number, and molecular diffusion coefficients are important (Chap. 4). Natural selection will be primarily for growth rate. To grow in the highly competitive environment of the intestine means in part being able to remove nutrients, often at very low levels, before the host or competing microflora do, and to efficiently convert these metabolites into cellular macromolecules. Efficiency of nutrient removal (defined as the equivalent number of volumes of medium that can be cleared of nutrient by a unit volume of cytoplasm per unit time; Koch 1971) is increased within limits by a decrease in size, asymmetry in shape, increase in the number of transport units per unit membrane, and increase in the capability of the transport mechanism.

Transport systems in E. coli work typically at about 1000 times lower concentrations than do those of yeast, algae, and the epithelium of macroorganisms (Koch 1976). Koch calculates (1971) that E. coli could theoretically clear 2800 times its own volume per second in growth media at 37 °C. He observes that one reason, if the bacterial cell were elephant-sized, it would starve to death in the midst of plenty is because of its inability to take up nutrients fast enough. The transport mechanisms evidently have evolved to a peak where further refinements would be useless, because the bacterium is constrained by viscosity of the fecal environment, which limits diffusion rate and, in turn, growth (Koch 1971, 1976; also, recall from Chap. 4 that viscosity is the denominator in the equation for Reynolds number. Therefore, an increase in viscosity will cause a decrease in Reynolds number, i.e., reduction in relative velocity of cell movement).

Efficient conversion of nutrient to biomass depends in part on the processes of protein synthesis, that is, on the efficiencies of transcription and translation. As an example consider protein synthesis. The rate of protein synthesis is directly proportional to the number of ribosomes, and each ribosome functions at a constant biosynthetic rate, regardless of the nutrient environment (Koch 1971; Koch and Schaechter 1984). Thus, regardless of the rate of cell division, each ribosome will wait the same length of time for a mRNA strand and take the same time to add an amino acid. While the cost to E. coli is that there is an excess of poorly utilized or nonfunctional ribosomes in very slowly growing cells, the benefit is that the bacterium is well equipped with ribosome machinery to get a head start for fast growth when a pulse of nutrients appears (Koch 1971; Koch and Schaechter 1984). Generation time is inversely proportional to size and, for E. coli in its intestinal environment, is about 40 h (Savageau 1983; Hartl and Dykhuizen 1984), while for the African elephant it is about 1 generation per 12 years (birth to puberty; Chap. 4 in Eltringham 1982).

The preceding paragraphs consolidate to this: E. coli cannot control its environment, whereas an elephant, by virtue of its bulk and related complexity and homeostasis mechanisms, can modify its environment markedly (Smith 1954; Bonner 1965, pp. 194-198). However, the bacterium can much more rapidly accommodate to changing environments and natural selection has shaped it to do so extraordinarily well in its dynamic conditions. This tracking of environments entails many genotypic and phenotypic adjustments, including ultrastructural and morphological changes, enzyme inhibition or stimulation, and induction or repression of protein synthesis, metabolic adjustments that may affect entire pathways (Chap. 3 and Harder et al. 1984; Forage et al. 1985). So the issue of size as it relates to environment is in large part one of being either a well-buffered, homeostatic individual destined to change relatively slowly in the face of adversity, or being exposed and vulnerable but capable of fast adjustment.