…increases in cellular sizes roughly coincide with the alleviation of at least one environmental constraint, namely low atmospheric oxygen pressure. The origin of body plans (±0.6 bya) also seem to coincide with an increase in atmospheric pressure.

Those two points in time are remarkable and seem to suggest Mike's 4th expectation of FLE. It would seem to me that the task of reverse-engineering how the biodiversity of life came to be is way more complex than it ever was as it now appear that the environment affects biological entities, and vice-versa.

3) Why did all the toolkit parts for the hh-pathway converge on a single sterolation pathway when so many other possibilities are available? Or is it the optimal possibility and random variation and selection processes used by life hit a global optimum?

This seems to correlate (somewhat) to my post on Probabilistic Design. Were the initial conditions set so that the first life forms (single-celled organisms) could not only evolve using stochastic evolutionary mechanisms, but participate in terraforming the environment so that more complex forms could evolve in a more favourable setting. It would be interesting to see an in-depth analysis of this.

Some "priveleged planet" implications immediately come to mind. Namely that an oxygen rich atmosphere can only be expected to stabilize on a "Goldilocks" planet roughly the mass of Earth – not too small or too big.

http://researchpages.net/media/resources/2007/11/05/goldblatt_draft02_ wsed.pdf

Thanks for the interesting article. From the article:

ConclusionIn this study, we have shown that transmembrane proteins can be divided into two groups according to their oxygen content. Independent topology prediction reveals these same two groups. We have shown that the proportion of receptors to channels increases over time and coincides with a change in cellular organization. In addition, older proteomes contain less oxygen per residue and produce fewer high-oxygen proteins. Taken together, this suggests that oxygen use was selected against in these proteomes. This constraint lessened over time as the concentration of atmospheric oxygen increased, which resulted in the extracellular domains of transmembrane proteins increasing in size over time faster than the internal domains. Consequently, we propose the following hypothetical mechanism: atmospheric oxygen concentration constrained the topology of ancient transmembrane proteins by limiting the number and size of external domains that could be formed. Any mechanistic explanation of how atmospheric oxygen concentration limited the number and size of external domains is necessarily speculative. One possibility is that it was simply futile to exude large, oxygen-rich domains in a reducing atmosphere where oxidized amino acids could have been rapidly reduced. In this case, the use of oxygen-rich amino acids would have been selected against by natural selection because protein structure would have been more robust when fewer oxidized residues were exuded.

Stated differently, eukaryotic proteomes were more receptive and robust in accepting oxygen-rich amino acids.

Linking this to the timing of appearance of eukaryotic cells implies that the oxygen content is preferentially increased in receptors, and that this increase affects receptor function. This makes intuitive sense because the external domains of receptors required for communication have specific secondary and tertiary structures, many of which have some minimum size [23]. This is consistent with the bias we found towards having both longer and more oxygen-dense external domains in receptors relative to channels, and with the fact that eukaryotic genomes encode more and larger receptors than do prokaryotes. This suggests that protein oxygen content itself is important, rather than being a proxy for some other property.

Thus, it seems reasonable to argue that eukaryote proteomes were more receptive of oxygen-rich amino acids, and this in turn aided in the development of secondary and tertiary structures needed for communication. A pre-existing property of eukaryotes was able to take more advantage of the change in atmospheric oxygen pressure. This lead to the unfolding of toolkits for multicellular body plans.

1) Why does an increase in atmospheric oxygen seem to have the effect of driving eukaryotic multilcellular life but not bacteria and archaea? Is an intrinsic and latent property present in this domain?

The article cites a paper that discusses one possible effect: the rising oxygen levels brought selection pressure in bacteria and archaea for transmembrane proteins which did not exclude oxygen:

Acquisti C, J Kleffe & S Collins (2007). Oxygen content of transmembrane proteins over macroevolutionary time scales. Nature 445: 47-52

From the abstract:

We observe that the time of appearance of cellular compartmentalization correlates with atmospheric oxygen concentration. To explore this correlation, we predict and characterize the topology of all transmembrane proteins in 19 taxa and correlate differences in topology with historical atmospheric oxygen concentrations. Here we show that transmembrane proteins, individually and as a group, were probably selectively excluding oxygen in ancient ancestral taxa, and that this constraint decreased over time when atmospheric oxygen levels rose. As this constraint decreased, the size and number of communication-related transmembrane proteins increased. We suggest the hypothesis that atmospheric oxygen concentrations affected the timing of the evolution of cellular compartmentalization by constraining the size of domains necessary for communication across membranes.

KC

But I suspect it has also affected prokaryotes a lot, albeit in a less obviously visible way.

Any suggestions on how to quantify this effect. Or is this an untestable hunch?

Peace

Nice quote. Guess if you are not a crackpot, you are not good at what you do.

Hi Raevmo,

Raevmo: Who says there was no effect on non-eukaryotes?

It didn't. From:
Rokas A. The origins of multicellularity and the early history of the genetic toolkit for animal development. Annu Rev Genet. 2008; 42: 235-251.

Organism vs Cell type number:
Actinobacteria 3
Cyanobacteria 3
Myxobacteria 3
Cellular slime molds 3
Animals 3–122
Fungi 3–9
Volvocine green algae 2
Plants 5–44
I suspect archaea do not consist of more than 3 types.

Also no body plans in bacteria or archaea.