Preadaptations

[Techne]

Preadaptations (aka exaptations) are features that perform a function but was not produced by natural selection for its current use. It could be argued that an exaptation forms as a result of co-option from a preadaptation, however Daniel Dennett denies exaptation differs from preadaptation. A simple example of a preadaptation is a feather that evolved (through natural selection) for warmth and was coopted into a new function, flight.

The genomes of various ancient organisms have been sequenced and it is interesting to view the presence of several preadaptations in the genomes of these creatures. The purpose of this thread is to highlight several of these interesting findings. If anyone come across any interesting findings, post it here .

Various trees of life exist. For example:
1
2
3
4
5
6
7

For the purpose of this thread, tree #2 (Dhushara, trevol.jpg) will be used as it is a nice representation of the evolution of animals (especially vertebrates). Horizontal gene transfer and endosymbiotic events are however not clear and tree #7 (Doolittle) is probably a better way of looking at evolution. Therefore keep #2 and #7 in mind and try and piece them together.

Preadaptations in the genome of the choanoflagellate, Monosiga brevicollis:
Choanoflagellates (link) are single-celled organisms thought to be most closely related to animals. The divergence time of this organism was about >600 million years ago (Link) (Blue circle in image).

Tyrosine Kinases are crucial for multicellular life to exist and play pivotal roles in diverse cellular activities including growth, differentiation, metabolism, adhesion, motility, death (link). More than 90 Protein Tyrosine Kinases (PTKs) have been found in the human genome. Interestingly Monosiga brevicollis has a tyrosine kinase signaling network more elaborate and diverse than found in any known metazoan.

Adherens junctions are also crucial components of multicellular life and function to communicate and adhere together in tissues. Even though Monosiga brevicollis are single-celled and do not form colonial assemblages, it is interesting to know they posses about 23 cadherins genes (Cadherins) usually associated with multicellular organisms.

Calcium signaling toolkits also play a crucial role in multicellular signaling. Calcium signaling plays a crucial part in contraction, metabolism, secretion, neuronal excitability, cell death, differentiation and proliferation. Thus, it is also interesting to note that Monosiga brevicollis has an extensive calcium signaling toolkit and emerged before the evolution of multicellular animals.

Tyrosine kinases, calcium signaling, and adherens junctions all play a part in neural signaling and other multecellular systems. Monosiga brevicollis does not have a nervous system. Thus it is also interesting to find the presence of the hedgehog gene in the genome of Monosiga brevicollis. Signaling by Sonic hedgehog (Shh) controls important
developmental processes, including neural stem cell proliferation. (Link).
Nice article:
Multigene Phylogeny of Choanozoa and the Origin of Animals
Compare the hedgehog gene of Monosiga brevicollis to that of humans.

Another interesting fact about the genome of the Monosiga brevicollis is noted in this article.

Interestingly, the choanoflagellate has nearly as many introns - non-coding regions once referred to as "junk" DNA - in its genes as humans do in their genes, and often in the same spots. Introns have to be snipped out before a gene can be used as a blueprint for a protein and have been associated mostly with higher organisms.

The choanoflagellate genome, like the genomes of many seemingly simple organisms sequenced in recent years, shows a surprising degree of complexity, King said. Many genes involved in the central nervous system of higher organisms, for example, have been found in simple organisms that lack a centralized nervous system.

Likewise, choanoflagellates have five immunoglobulin domains, though they have no immune system; collagen, integrin and cadherin domains, though they have no skeleton or matrix binding cells together; and proteins called tyrosine kinases that are a key part of signaling between cells, even though Monosiga is not known to communicate, or at least does not form colonies.

(Emphasis mine)


Fascinating multicellular preadaptations very early on in the evolution of single-celled organisms.

 

[Techne]

Interesting article about amoebas from 2005 (University of California):
Biologists determine genetic blueprint of social amoeba

An international team that includes biologists at the University of California, San Diego has determined the complete genetic blueprint of Dictyostelium discoideum, a simple social amoeba long used by researchers as a model genetic system, much like fruit flies and laboratory mice, to gain a better understanding of human diseases.

The scientific details of this seven-year-long genetic sequencing effort, which involved 97 scientists from 22 institutions in five countries, are contained in a paper featured on the cover of the May 5 issue of the journal Nature.

The international team's achievement will have an immediate application for biomedical researchers, who can now mine the Dictyostelium genome for a host of genes that cause human disease, thus gaining a new and efficient way to study those human diseases with a simple organism in their laboratories.

For evolutionary biologists, the genetic blueprint of Dictyostelium, the first amoeba genome to be sequenced, has clarified the place that Dictyostelium occupies in the hierarchy of life.

"It is more closely related to fungi and animals than we had previously thought," says Adam Kuspa, a professor of biochemistry and molecular biology at Baylor College of Medicine in Houston and a senior author of the Nature paper.

The discovery will also improve geneticists' understanding of how the genes from Dictyostelium and other genetic model organisms have been conserved or adapted through evolution in humans and other organisms.

"The cells which gave rise to plants and animals had more types of genes available to them than are presently found in either plants or animals," explains William Loomis, a professor of biology at UCSD and one of the key members of the international sequencing effort. "Specialization appears to lead to loss of genes as well as the modification of copies of old genes. As each new genome is sequenced, we learn more about the history and physiology of the progenitors and gain insight into the function of human genes."

In 1989, Loomis and Kuspa, then a postdoctoral fellow in Loomis' laboratory, initiated a critical portion of the effort when they began the arduous task of constructing a physical map of the genes located on the six chromosomes of Dictyostelium.

The scientists mapped the location of several hundred genes on those chromosomes based on landmarks that had been discovered over the years, then created a set of 5,000 large DNA clones, each about 200,000 nucleotide bases long, that proved useful for other researchers in assembling the genetic sequences of Dictyostelium's genome. Another UCSD biologist involved in the genome effort, Christophe Anjard, an assistant project scientist in Loomis' laboratory, analyzed families of Dictyostelium genes and uncovered relationships with these genes in both animals and plants.

Dictyostelium is used as a model organism for studying cell polarity, how cells move and the differentiation of tissues. It also exhibits many of the properties of white blood cells.

Three years ago, another team of UCSD biologists discovered that two genes that are used by Dictyostelium to guide the organism to food sources are also used to guide human white blood cells to the sites of infections and play a role in the spread of cancer. (see: http://ucsdnews.ucsd.edu/newsrel/science/mcchemo.htm)

Dictyostelium usually exists as a single cell organism that inhabits forest soil, consuming bacteria and yeast. When starved, however, the single cells come together, differentiate into tissues and become a true multicellular organism with a fruiting body composed of a stalk with spores poised on top. This increases its utility in a variety of studies.

"An organism's relationship to humans depends on how related the proteins are that are found in the two cell types," says Kuspa. "You can make direct analogies, or you could learn general principles about how cells regulate their behavior. Both things will apply in the studies we do."

He and the other members of the international sequencing team found that there are more protein coding genes in the organism than they had thought and nearly twice as many as there are in fungi. Their unraveling of the genome also allowed Rolf Olsen, a postdoctoral fellow working in Loomis' laboratory, to generate a tree of life and show that amoebozoa, the group to which Dictyostelium belongs, evolved from the common ancestor of eukaryotes (the group of organisms that contain all animals, plants, algae, protozoa, slime mold and fungi) before fungi. Dictyostelium has about 12,000 genes that produce a greater variety of proteins than the approximately 6,000 found in fungi. And its genes are more closely related to human genes than are the genes from fungi.

"That really speaks to how much we will relate the gene function information we find to humans," Kuspa says. "It makes Dictyostelium a better model for looking for targets against which drugs can act."

Key collaborators in the project at Baylor included Richard Gibbs and George Weinstock, co-directors of Baylor's Human Genome Sequencing Center, and Richard Sucgang, an assistant professor of biochemistry. Baylor performed about one half of the sequencing work.

Phylogenetic analysis suggest Dictyostelium discoideum diverged after plants and before metazoa.

Any idea how many preadaptations for multi-cellularity existed? E.g.: Unicellular programmed cell death (autophagic, apoptotic metabolic catastrophe and necrotic processes), differentiation, adhesion, calcium toolkits, tyrosine kinase signaling cascades?

 

[Techne]

More interesting preadaptations:
This time sponges (wiki).

Sponges are among the simplest animals. They lack gastrulated embryos, extracellular digestive cavities, nerves, muscles, tissues, and obvious sensory structures, features possessed by all other animals.

Nice site about sponges.

Evolutionary history of sponges (Sponges = light blue, Divergence time = yellow)​

Choanoflagellates had a lot of the toolkits necessary to develop a nervous system as well as multi-cellularity, even though they are simple uni-cellular organisms that do not form colonial assemblages.

Now the Origin of Nerves are Traced to Sponges

Sponges are very primitive animals. They don't have nerves cells (nor muscles nor eyes nor a lot of other things we commonly associate with animals). So scientists figured sponges split from the tree of life before nerves evolved.

A new study has surprised researchers, however.

"We are pretty confident it was after the sponges split from trunk of the tree of life and sponges went one way and animals developed from the other, that nerves started to form," said Bernie Degnan of the University of Queensland. "What we found in sponges though were the building blocks for nerves, something we never expected to find."

In humans and other animals, nerves deliver messages to and from the brain and all the parts of a body.

Degnan and colleagues studied a sea sponge called Amphimedon queenslandica. "What we have done is try to find the molecular building blocks of nerves, or what may be called the nerve's ancestor the proto-neuron," Degnan said. They found sets of these genes in sponges.

Nice .
Free, online peer-reviewed article:
A Post-Synaptic Scaffold at the Origin of the Animal Kingdom


There are even more fascinating findings from the genome of the sponge.

"But what was really cool," he said, "is we took some of these genes and expressed them in frogs and flies and the sponge gene became functional — the sponge gene directed the formation of nerves in these more complex animals.

The research, announced this month, was published in the journal Current Biology.

Article with the details:
Article abstract:
Sponge Genes Provide New Insight into the Evolutionary Origin of the Neurogenic Circuit

The nerve cell is a eumetazoan (cnidarians and bilaterians) synapomorphy [1]; this cell type is absent in sponges, a more ancient phyletic lineage. Here, we demonstrate that despite lacking neurons, the sponge Amphimedon queenslandica expresses the Notch-Delta signaling system and a proneural basic helix loop helix (bHLH) gene in a manner that resembles the conserved molecular mechanisms of primary neurogenesis in bilaterians. During Amphimedon development, a field of subepithelial cells expresses the Notch receptor, its ligand Delta, and a sponge bHLH gene, AmqbHLH1. Cells that migrate out of this field express AmqDelta1 and give rise to putative sensory cells that populate the larval epithelium. Phylogenetic analysis suggests that AmqbHLH1 is descendent from a single ancestral bHLH gene that later duplicated to produce the atonal/neurogenin-related bHLH gene families, which include most bilaterian proneural genes [2]. By way of functional studies in Xenopus and Drosophila, we demonstrate that AmqbHLH1 has a strong proneural activity in both species with properties displayed by both neurogenin and atonal genes. From these results, we infer that the bilaterian neurogenic circuit, comprising proneural atonal-related bHLH genes coupled with Notch-Delta signaling, was functional in the very first metazoans and was used to generate an ancient sensory cell type.

Whole parts of the nervous system were present in animals that do not have a nervous system, yet these parts are interchangeable and function just like they should in animals that do have a nervous system.

 

[Techne]

The sea urchin is another interesting creature (Green circle, yellow circle = divergence time):

It provides valuable knowledge for cancer, Alzheimer's and infertility research:

Sea Urchins' Genetics Add To Knowledge Of Cancer, Alzheimer's And Infertility


What is even more interesting is what lurks in its genome. According to present models, they originated at least 450 million years ago. These organisms have no eyes, ears or a nose, yet they have the genes humans have for vision, hearing and smelling (see above link). They also have a surprisingly complex immune system, which surpasses the human one by far.

Now the genes in the genetic toolkit (nice video) in animals responsible for assigning specific properties of the various body parts are known as Hox genes. Here is a nice overview of Hox genes. A great deal of Hox genes are found in the sea urchin, the pattern of gene expression just differs, resulting in a different body plan.

Right at the base of the animal tree, a sundry of genes necessary for sight, smell, hearing as well as the various body plans were present in the genome of the common ancestor.

The Trichoplax adhaerens genome is equally intriguing.

 

[Techne]

A Trichoplax preadaptation:

The Dlx gene​

What does it do (wiki)?

• Dlx genes are required for the tangential migration of interneurons from the subpallium to the pallium during vertebrate brain development [3].
  
• It has been suggested that Dlx promotes the migration of interneurons by repressing a set of proteins that are normally expressed in terminally differentiated neurons and act to promote the outgrowth of dendrites and axons [4]. Mice lacking Dlx1 exhibit electrophysiological and histological evidence consistent with delayed-onset epilepsy [5].
  
• Dlx2 has been associated with a number of areas including development of the zona limitans intrathalamica and the prethalamus.
  
• Dlx5/6 expression is necessary for normal lower jaw patterning in vertebrates [6].
  
• Dlx7 is expressed in bone marrow

A quick BLAST of the sequence reveals it is closely related to human Dlx1, as well as Dlx1 in other vertebrates (including Zebrafish, the mouse, rat opossum, dog etc.)

More specifically, what does Dlx1 do?
Pubmed

This gene encodes a member of a homeobox transcription factor gene family similiar to the Drosophila distal-less gene. The encoded protein is localized to the nucleus where it may function as a transcriptional regulator of signals from multiple TGF-{beta} superfamily members. The encoded protein may play a role in the control of craniofacial patterning and the differentiation and survival of inhibitory neurons in the forebrain. This gene is located in a tail-to-tail configuration with another member of the family on the long arm of chromosome 2. Alternatively spliced transcript variants encoding different isoforms have been described.

It is possible to create a homology of this protein to look at its possible structure. The closest match is the human Dlx 5 protein structure. Sequence alignment places the Dlx sequence of Trichoplax closer to human Dlx5 than to human Dlx1 (Figure 1)

Figure 1: ClustalW - original settings​

What does Dlx 5 do?
Pubmed:

This gene encodes a member of a homeobox transcription factor gene family similar to the Drosophila distal-less gene. The encoded protein may play a role in bone development and fracture healing. Mutation in this gene, which is located in a tail-to-tail configuration with another member of the family on the long arm of chromosome 7, may be associated with split-hand/split-foot malformation.

The homology model of the protein:
A good quality protein was generated (Figure 2).

Figure 2: Swissmodel of Trichoplax Dlx protein (2djn.pdb as template)​

So, a Hox gene responsible for a sundry of neurologically associated developmental processes present in an organism with no nerve, sensory or bone cells at the base of the evolutionary tree. Awesome .​

 

[iceaura]

So, a Hox gene responsible for a sundry of neurologically associated developmental processes present in an organism with no nerve, sensory or bone cells at the base of the evolutionary tree. Awesome

I'm not following your argument, exactly.

Did you disagree with Dennett's analysis of these vocabularies? His view, shared by most evolutionary theorists and structurally fundamental to Darwinian theory, seems persuasive.

 

[Techne]

I agree, and think that preadaptation does not differ from exaptation.

 

[Techne]

More fascinating preadaptations from the Trichoplax:

The Mnx (aka HB9) gene​

The Trichoplax Mnx sequence: ABC86118
Comparison of this sequence with a few others: Cladogram

The human Mnx1 gene.
The fly Mnx gene (exex)
The Zebrafish Mnx gene

What does it do?
It is involved in the development of the pancreas and motor neurons.
1) Zebrafish mnx genes in endocrine and exocrine pancreas formation.
2) The Mnx homeobox gene class defined by HB9, MNR2 and amphioxus AmphiMnx.

The HB9 homeobox gene has been cloned from several vertebrates and is implicated in motor neuron differentiation. In the chick, a related gene, MNR2, acts upstream of HB9 in this process. Here we report an amphioxus homologue of these genes and show that it diverged before the gene duplication yielding HB9 and MNR2. AmphiMnx RNA is detected in two irregular punctate stripes along the developing neural tube, comparable to the distribution of 'dorsal compartment' motor neurons, and also in dorsal endoderm and posterior mesoderm. We propose a new homeobox class, Mnx, to include AmphiMnx, HB9, MNR2 and their Drosophila and echinoderm orthologues; we suggest that vertebrate HB9 is renamed Mnx1 and MNR2 be renamed Mnx2.

Interesting research:​

Directed Evolution of Motor Neurons from Genetically Engineered Neural Precursors.

Stem cell-based therapies hold therapeutic promise for degenerative motor neuron diseases such as amyotrophic lateral sclerosis and for spinal cord injury. Fetal neural progenitors present less risk of tumor formation than embryonic stem (ES) cells but inefficiently differentiate into motor neurons, in line with their low expression of motor neuron-specific transcription factors and poor response to soluble external factors. To overcome this limitation, we genetically engineered fetal rat spinal cord neurospheres to express the transcription factors HB9, Nkx6.1 and Ngn2. Enforced expression of the three factors rendered neural precursors responsive to sonic hedgehog and retinoic acid and directed their differentiation into cholinergic motor neurons that projected axons and formed contacts with co-cultured myotubes. When transplanted in the injured adult rat spinal cord, a model of acute motor neuron degeneration, the engineered precursors transiently proliferated, colonized the ventral horn, expressed motor neuron-specific differentiation markers and projected cholinergic axons in the ventral root. We conclude that genetic engineering can drive the differentiation of fetal neural precursors into motor neurons which efficiently engraft in the spinal cord. The strategy thus holds promise for cell replacement in motor neuron and related diseases.

What did these guys do? They enforced the expression of 3 genes associated with neuronal development in order to direct the development of motor neurons. Sonic hedgehog also played a role .
So four genes played a role:

1. HB9
2. Nkx6.1
3. Ngn2
4. Sonic hedgehog

Are similar genes present in the Trichoplax genome?
1. HB9 (mnx)
Yes (see above).

2. Nkx6.1
Here is the human Nk6 gene
And here is the Trichoplax version

3. Ngn2
Here is the human neurogenin 2 (ngn2) gene
And here is the Trichoplax version.
A quick BLAST (blastp) the human genome shows this sequence to be closely related to ngn2 (E-value = 3^-8).

4. Sonic hedgehog (shh)
Here is the human shh gene
This gene seems to absent in from the Trichoplax genome, however, the presence of shh in Monosiga brevicollis (unicellular eukaryote that diverged before Trichoplax) suggest the possibility of gene loss in this lineage.

Wonder what will happen if shh is co-expressed and together with mnx, Nk6 and ngn2 in Trichoplax, or whether these genes will function like their counterparts in higher animals.

A complex array of neurologically associated developmental pathways present in this eumetazoan that has no nerves, sensory cells and muscle cells, and there is more .​

 

[Harro]

Hi Techne, thanks for the heads up.

Preadaption sounds very plausable. If you think about it some mutations could change the DNA but not be harmfull to the organism but not advantageous iether. So it remains in the gene pool. This could explain alot of the junk DNA I hear biology articles talk about. Now if there is a shift in the environment where the organism have the preadaption that is actually benificial to the organism that genetic preadaption could become the dominate genes.

 

[Techne]

Hi Harro,

Junk DNA seems like a myth...
'Junk' DNA proves functional

On the development of eyes​

Several types of eyes exist and these include the camera-type eye, the compound eye, and the mirror eye (Figure 1). Ernst Mayr proposed that eyes evolved in all animal phyla 40 to 60 times independently.
A monophyletic program governing the development of the different eye types is proposed and the Pax6 gene is posited to be the master control gene. The Pax6 gene also plays a part in controlling the development of the nose, ears and parts of the brain.

What is needed for the developmental program of eyes?
A few core genes include:
Pax6 (eyeless [eye]) in Drosophila)
Six-type genes (E.g. Six3)
Sox-type genes (E.g. Sox2)
atonal ( E.g. Atoh7)
Retinoid receptors
Fox transcription factors (E.g. FoxN4)
Pitx

Fascinating experiments have been conducted by shuffling around the genetic program architecture of genes associated with eye development in various animals.
For example in Drosophila:
Ectopic eye structures are able to be induced on the antennae, legs, and wings of fruit flies. This is done by targeted expression of the eyeless gene (Pax6 Drosophila homologue) (Figure 2). The Pax6 gene from the mouse is able to do the same job as the Drosophila version (Figure 3). And in Xenopus embryos, ectopic eye structures in can also be induced by the Drosophila eyeless (Pax6) version (Figure 4).

What about the Trichoplax adhaerens genome? Any genes for eye development?
It seems quite a chunk of the circuitry needed for eye development is present. (From table 1)
PaxB (eyeless?)
Six genes
Sox gene
Atonal gene
Retinoid X Receptor
Fox transcription factors
Pitx

All that is missing seems to be crystalins (plays a part in lens formation). However, Darwin posited that "The simplest organ which can be called an eye consists of an optic nerve, surrounded by pigment-cells and covered by translucent skin, but without any lens or other refractive body." Thus large chunks of the circuitry for eye development in Trichoplax is present but no eyes!

Now compare the developmental program to evolution.
Here is an interesting article that shows the parallels between evolution and development.

For development:
Primordial germ cells (PGC) are prevented from entering the somatic program and are demethylated (genome-wide erasure of existing epigenetic modifications). Then the gametes are imprinted (targeted DNA methylation) during gametogenesis, only to be demethylated again after fertilization. Then during development, DNA is methylated again, causing totipotential cells to become pluripotent. X-inactivation and reactivation (of the paternal gamete I think) also occurs. The whole process is governed by the genetic (and epigenetic?) program. During the unfolding of this somatic program, random variation and selection occur, ultimately leading to just a few endpoints, every time it is successful. The process is constrained (few end points) as a result of pre-existing information that is set up during the inititiation of the process. All this is controlled by information in the genome.

For evolution:
There also seems to be only a few endpoints (small subset, limited variation) out of all the possible endpoints.
In the article:
An End to Endless Forms: Epistasis, Phenotype Distribution Bias, and Nonuniform Evolution
It is argued to be as a result of genetic instructions dating earlier in evolutionary time. Preadaptations...

As already seen in the evolution of eyes, as soon as these sets of genes were formed (E.g. Pax genes), through whatever mechanism), evolution seemed to have been biased to a few end points, and these few endpoints arose 40-60 times, independently, as a result of pre-existing (preadaptations) information in the case of eyes.

What other "biased" end points can there be? Nervous systems, smell, hearing? And why would evolution be biased, as in development, to only reach a few end points over and over?

Seeing that evolution is biased towards a few endpoints which is partly due to the massive amounts of preadaptations in organisms at the base of the evolutionary tree. Now evolution seems to learn....

Facilitated Variation: How Evolution Learns from Past Environments To Generalize to New Environments
Abstract:

One of the striking features of evolution is the appearance of novel structures in organisms. Recently, Kirschner and Gerhart have integrated discoveries in evolution, genetics, and developmental biology to form a theory of facilitated variation (FV). The key observation is that organisms are designed such that random genetic changes are channeled in phenotypic directions that are potentially useful. An open question is how FV spontaneously emerges during evolution. Here, we address this by means of computer simulations of two well-studied model systems, logic circuits and RNA secondary structure. We find that evolution of FV is enhanced in environments that change from time to time in a systematic way: the varying environments are made of the same set of subgoals but in different combinations. We find that organisms that evolve under such varying goals not only remember their history but also generalize to future environments, exhibiting high adaptability to novel goals. Rapid adaptation is seen to goals composed of the same subgoals in novel combinations, and to goals where one of the subgoals was never seen in the history of the organism. The mechanisms for such enhanced generation of novelty (generalization) are analyzed, as is the way that organisms store information in their genomes about their past environments. Elements of facilitated variation theory, such as weak regulatory linkage, modularity, and reduced pleiotropy of mutations, evolve spontaneously under these conditions. Thus, environments that change in a systematic, modular fashion seem to promote facilitated variation and allow evolution to generalize to novel conditions.

Biased evolution towards a few endpoints under intrinsic control.

And now proteins that control evolution...

Evolution's new wrinkle: Proteins with cruise control provide new perspective

Related articles: Number 1
Mutagenic Evidence for the Optimal Control of Evolutionary Dynamics

Elucidating the fitness measures optimized during the evolution of complex biological systems is a major challenge in evolutionary theory. We present experimental evidence and an analytical framework demonstrating how [biochemical networks exploit optimal control strategies in their evolutionary dynamics. Optimal control theory explains a striking pattern of extremization in the redox potentials of electron transport proteins, assuming only that their fitness measure is a control objective functional with bounded controls.

Evolution is guided by the optimization of fitness measures that balance functionally beneficial properties.

Fitness functions actually guiding evolution?


Number 2:
Optimal control of evolutionary dynamics

From the conclusion:

The observation that coevolving biopolymer sequences may optimally control each other’s evolution raises the prospect of artificial optimal control of evolutionary dynamics. Possible applications include the control of replication fidelity in nucleic acid amplification reactions and the design of therapeutics that dynamically regulate the evolution of viral populations.

And again from this article:

The authors sought to identify the underlying cause for this self-correcting behavior in the observed protein chains. Standard evolutionary theory offered no clues. Applying the concepts of control theory, a body of knowledge that deals with the behavior of dynamical systems..., .

the researchers concluded that this self-correcting behavior could only be possible if, during the early stages of evolution, the proteins had developed a self-regulating mechanism, analogous to a car's cruise control or a home's thermostat, allowing them to fine-tune and control their subsequent evolution.

Self-regulating systems biasing future evolutionary trajectories towards a few outcomes?

 

[Walter L. Wagner]

Very interesting. It would appear that genes now used for specific higher functions were present for lower functions, then slightly modified when circumstances arose to allow the higher functions. It really goes to show the 'plasticity' of genes and their morphological expression. We had a thread about primate/human chromosome number, showing that the Homo lineage has two chromosomes joined into one, which in all other primates remain as two chromosomes. As expected, the chromosomes are joined at the telomeres, and one of the two centromeres is now non-functional. I wonder if perhaps the joining of those two chromosomes somehow activated additional gene functions that might have earlier been suppressed?

 

[Techne]

Very interesting. It would appear that genes now used for specific higher functions were present for lower functions, then slightly modified when circumstances arose to allow the higher functions. It really goes to show the 'plasticity' of genes and their morphological expression. We had a thread about primate/human chromosome number, showing that the Homo lineage has two chromosomes joined into one, which in all other primates remain as two chromosomes. As expected, the chromosomes are joined at the telomeres, and one of the two centromeres is now non-functional. I wonder if perhaps the joining of those two chromosomes somehow activated additional gene functions that might have earlier been suppressed?

Goes to show you, genomes seem to be prepared/preadapted for evolutionary processes.


More preadaptations from Trichoplax:

The Hex Homeobox gene​

Its function?
Critical element in the development of the liver:
The role of Hex in hemangioblast and hematopoietic development.
The homeoprotein Hex is required for hemangioblast differentiation.
The homeobox gene HEX regulates proliferation and differentiation of hemangioblasts and endothelial cells during ES cell differentiation.

Detoxification of free radicals and damaging molecules play a crucial part in cellular homeostasis as well as systems homeostasis. The liver is mainly responsible for system homeostasis as it contains the highest concentration cells (hepatocytes do the heavy lifting) capable of detoxification, modification and excretion of hazardous molecules. It would be interesting to see what a gene that is associated with the development of the liver is doing in this simple organism at the base of the eumetazoan tree.

http://www.nature.com/nature/journal/v454/n7207/fig_tab/nature07191_T1.html​

http://www.nature.com/nature/journal/v454/n7207/fig_tab/nature07191_T1.html

And the Dbx gene?​

The trend of neurologically associated homeobox genes continues.
Regulation and function of Dbx genes in the zebrafish spinal cord.

Dbx homeodomain proteins are important for spinal cord dorsal/ventral patterning and the production of multiple spinal cord cell types. We have examined the regulation and function of Dbx genes in the zebrafish. We report that Hedgehog signaling is not required for the induction or maintenance of these genes; in the absence of Hedgehog signaling, dbx1a/1b/2 are expanded ventrally with concomitant increases in postmitotic neurons that differentiate from this domain. Also, we find that retinoic acid signaling is not required for the induction of Dbx expression. Furthermore, we are the first to report that knockdown of Dbx1 function causes a dorsal expansion of nkx6.2, which is thought to be the cross-repressive partner of Dbx1 in mouse. Our data confirm that the dbx1a/1b/2 domain in zebrafish spinal cord development behaves similarly to amniotes, while extending knowledge of Dbx1 function in spinal cord patterning. 2007 Wiley-Liss, Inc

Pitx: Another neurologically associated Hox gene present in the Trichplax genome.​

The various versions:
Trichoplax. Function unknown at present. Would be interesting to find out what it is.
Human Pitx1 Its function:

This gene encodes a member of the RIEG/PITX homeobox family, which is in the bicoid class of homeodomain proteins. Members of this family are involved in organ development and left-right asymmetry. This protein acts as a transcriptional regulator involved in basal and hormone-regulated activity of prolactin.

Human Pitx2 Its function:

This gene encodes a member of the RIEG/PITX homeobox family, which is in the bicoid class of homeodomain proteins. The encoded protein acts as a transcription factor and regulates procollagen lysyl hydroxylase gene expression. This protein plays a role in the terminal differentiation of somatotroph and lactotroph cell phenotypes, is involved in the development of the eye, tooth and abdominal organs, and acts as a transcriptional regulator involved in basal and hormone-regulated activity of prolactin. Mutations in this gene are associated with Axenfeld-Rieger syndrome, iridogoniodysgenesis syndrome, and sporadic cases of Peters anomaly. A similar protein in other vertebrates is involved in the determination of left-right asymmetry during development. Alternatively spliced transcript variants encoding distinct isoforms have been described

Human Pitx3 Its function:

This gene encodes a member of the RIEG/PITX homeobox family, which is in the bicoid class of homeodomain proteins. Members of this family act as transcription factors. This protein is involved in lens formation during eye development. Mutations of this gene have been associated with anterior segment mesenchymal dysgenesis and congenital cataracts.

Zebrafish Pitx1
Zebrafish Pitx2
Zebrafish Pitx3
Drosophila Ptx1 (fruitfly)

More interesting facts about Pitx:
The Pitx homeobox gene in Bombyx mori: Regulation of DH-PBAN europeptide hormone gene expression

The diapause hormone-pheromone biosynthesis activating neuropeptide gene, DH-PBAN, is expressed exclusively in seven pairs of DH-PBAN-producing neurosecretory cells (DHPCs) on the terminally differentiated processes of the subesophageal ganglion (SG). To help reveal the regulatory mechanisms of cell-specific DH-PBAN expression, we identified a cis-regulatory element that regulates expression in DHPCs using the recombinant AcNPV-mediated gene transfer system and a gel-mobility shift assay. Bombyx mori Pitx (BmPitx), a bicoid-like homeobox transcription factor, binds this element and activates DH-PBAN expression. The BmPitx was expressed in various tissues, including DHPCs in the SG. Suppression of DH-PBAN expression by silencing of the BmPitx successfully induced non-diapaused eggs from a diapause egg producer. To the best of our knowledge, this report is the first to identify a neuropeptide-encoding gene as a target of the Pitx transcriptional regulator in invertebrates. Thus, it is tempting to speculate that functional conservation of Pitx family members on neuropeptide gene expression occurs through a "combinational code mechanism" in both vertebrate and invertebrate in neuroendocrine systems.

PITX genes are required for cell survival and Lhx3 activation
Zebrafish pitx3 is necessary for normal lens and retinal development.

And the trend of neurologically associated genes present in this basal eumetazoan continues...

Otp: The trend of neurolically associated developmental genes in the genome of the Trichoplax continues...​

The various versions:
Trichoplax: Function unknown at present. Interested in its function in a basal eumetazoan.
Human otp. Its function:
The role of Otx and Otp genes in brain development.

Over the last ten years, many genes involved in the induction, specification and regionalization of the brain have been identified and characterized at the functional level through a series of animal models. Among these genes, both Otx1 and Otx2, two murine homologues of the Drosophila orthodenticle (otd) gene which encode transcription factors, play a pivotal role in the morphogenesis of the rostral brain. Classical knock-out studies have revealed that Otx2 is fundamental for the early specification and subsequent maintenance of the anterior neural plate, whereas Otx1 is mainly necessary for both normal corticogenesis and sense organ development. A minimal threshold of both gene products is required for correct patterning of the fore-midbrain and positioning of the isthmic organizer. A third gene, Orthopedia (Otp) is a key element of the genetic pathway controlling development of the neuroendocrine hypothalamus. This review deals with a comprehensive analysis of the Otx1, Otx2 and Otp functions, and with the possible evolutionary implications suggested by the models in which the Otx genes are reciprocally replaced or substituted by the Drosophila homologue, otd.

The same for mice:
The murine Otp homeobox gene plays an essential role in the specification of neuronal cell lineages in the developing hypothalamus.

Hypothalamic nuclei, including the anterior periventricular (aPV), paraventricular (PVN), and supraoptic (SON) nuclei strongly express the homeobox gene Orthopedia (Otp) during embryogenesis. Targeted inactivation of Otp in the mouse results in the loss of these nuclei in the homozygous null neonates. The Otp null hypothalamus fails to secrete neuropeptides somatostatin, arginine vasopressin, oxytocin, corticotropin-releasing hormone, and thyrotropin-releasing hormone in an appropriate spatial and temporal fashion, and leads to the death of Otp null pups shortly after birth. Failure to produce these neuropeptide hormones is evident prior to E15.5, indicating a failure in terminal differentiation of the aPV/PVN/SON neurons. Absence of elevated apoptotic activity, but reduced cell proliferation together with the ectopic activation of Six3 expression in the presumptive PVN, indicates a critical role for Otp in terminal differentiation and maturation of these neuroendocrine cell lineages. Otp employs distinct regulatory mechanisms to modulate the expression of specific molecular markers in the developing hypothalamus. At early embryonic stages, expression of Sim2 is immediately downregulated as a result of the absence of Otp, indicating a potential role for Otp as an upstream regulator of Sim2. In contrast, the regulation of Brn4 which is also expressed in the SON and PVN is independent of Otp function. Hence no strong evidence links Otp and Brn4 in the same regulatory pathway. The involvement of Otp and Sim1 in specifying specific hypothalamic neurosecretory cell lineages is shown to operate via distinct signaling pathways that partially overlap with Brn2.

The Zebrafish version. Its function: More of the same.
Differential regulation of the zebrafish orthopedia1 gene during fate determination of diencephalic neurons

The homeodomain transcription factor Orthopedia (Otp) is essential in restricting the fate of multiple classes of secreting neurons in the neuroendocrine hypothalamus of vertebrates. However, there is little information on the intercellular factors that regulate Otp expression during development

In the sea urchin.
Evolution of OTP-independent larval skeleton patterning in the direct-developing sea urchin, Heliocidaris erythrogramma.

The Orthopedia gene (Otp) encodes a homeodomain transcription factor crucial in patterning the larval skeleton of indirect-developing sea urchins.

A clear example of a cooption, whereby the same gene plays a role in neurological development in vertebrates and skeletal development in the sea urchin. Recycling of pre-existing genes for various, distinct, developmental processes.​

 

[Walter L. Wagner]

Still even more interesting.

I read an article yesterday [not at my fingertips - I'll get it this afternoon and provide more detail later] in which a retrovirus gene, inserted in the distant past into the genome as part of the 'junk' DNA, is now used in uterine functions. I'll look for the article [seen on a college hall's wall] and give its cite later.

As we know, retroviruses simply cause disease of an organism. Those that survive an attack by a retrovirus of the germ cells, survive with the DNA inserted into the germ line, where they can become fixed in the gene pool of that species after the passage of many generations. They are typically inactivated thereafter. The one referenced above later found use in another function. It is not known when it was inserted, and I'm not certain if it is present in non-mammalian vertebrates.

It's almost like Lincoln Logs. All the pieces are there waiting to make appropriate proteins when activated by a mutation that might have a use when an evolutionary niche arrives.

 

[Techne]

Still even more interesting.

I read an article yesterday [not at my fingertips - I'll get it this afternoon and provide more detail later] in which a retrovirus gene, inserted in the distant past into the genome as part of the 'junk' DNA, is now used in uterine functions. I'll look for the article [seen on a college hall's wall] and give its cite later.

As we know, retroviruses simply cause disease of an organism. Those that survive an attack by a retrovirus of the germ cells, survive with the DNA inserted into the germ line, where they can become fixed in the gene pool of that species after the passage of many generations. They are typically inactivated thereafter. The one referenced above later found use in another function. It is not known when it was inserted, and I'm not certain if it is present in non-mammalian vertebrates.

It's almost like Lincoln Logs. All the pieces are there waiting to make appropriate proteins when activated by a mutation that might have a use when an evolutionary niche arrives.

Yeah, biomolecular machinery, a reasonably optimal genetic code, optimized for evolution, preadaptation etc. Cells seem prepared for the future .

Well, it is not a fact that retroviruses are the origin of diseases. They might act as regulatory elements in the immune system and a fault in the system might cause it it to look like erv's are the cause. It would be interesting to learn about the mechanism of how an ERV causes a disease. But, a faulty p53 gene is also the cause of many cancers, yet it is crucial in many functions in normal cells.

Also, ERVs and LTR elements do play a crucial role in many cellular processes.
E.g.

Today, it is commonly believed that ERVs are just junk elements that randomly integrated into genomes and caused havoc in the past, then these shared errors were propagated in future generations. As research progresses in this area, it is becoming more and more apparent that some of these elements bare some functionality (believed to be co-opted) and are actually crucial for certain processes. ERV research at present is rich with speculations and it is a fertile ground for new and exciting ideas regarding their importance. Confirmed importance of ERV elements in various species include:

1) Independent envelope genes from unrelated ERV families regulate trophoblast differentiation and syncytia formation during synepitheliochorial placentation. Are there examples of Eutheria that are capable of reproduction without ERVs?
Humans (primates): HERV-W and HERV-FRD Read up on this one it is really interesting
Mice (Rodentia): Syncytin-A and -B
Sheep (Artiodactyla): enJSRV


2) Retroelement formatting of the genome [[7]].
System architectures formatting by retroelements and other repeat elements possibly have an effect on morphological, physiological and reproductive function.

3) LTRs play a fundamental role in gene expression (This is also fascinating)
Independently acquired LTRs have assumed regulatory roles for orthologous genes [[8]].
An LTR is the dominant promoter in the colon, indicating that this ancient retroviral element has a major impact on gene expression [[9]].
LTR class I endogenous retrovirus (ERV) retroelements impact considerably on the transcriptional network of human tumor suppressor protein p53 (guardian of the genome) [[10]].

4) Role in autoimmunity [[11]].
Disease associations have been established, however there is as yet no proven definite causative association between HERVs and disease.
a) Human endogenous retroviruses can encode superantigenic activity
b) Transcriptional activation. HERVs may act as insertional mutagens or cis-regulatory elements causing activation, inhibition, or alternative splicing of cellular genes involved in immune function.
c) Molecular mimicry. Production of neo-antigens by modification of cellular components.
d) Epitope spreading.
e) Activation of innate immunity through pattern recognition receptors.

More and more functions are being found for ERV elements and LTRs. It may very well turn out that ERV elements are the crucial elements that make us human.

Refs:
[7] von Sternberg R, Shapiro JA. How repeated retroelements format genome function. Cytogenet Genome Res. 2005;110(1-4):108-116.

[8] Romanish MT, Lock WM, van de Lagemaat LN, Dunn CA, et al. Repeated recruitment of LTR retrotransposons as promoters by the anti-apoptotic locus NAIP during mammalian evolution. PLoS Genet. 2007 Jan 12;3(1):e10.

[9] Dunn CA, Medstrand P, Mager DL. An endogenous retroviral long terminal repeat is the dominant promoter for human beta1,3-galactosyltransferase 5 in the colon. Proc Natl Acad Sci U S A. 2003 Oct 28;100(22):12841-12846.

[10] Wang T, Zeng J, Lowe CB, Sellers RG, Salama SR, Yang M, et al. Species-specific endogenous retroviruses shape the transcriptional network of the human tumor suppressor protein p53. Proc Natl Acad Sci U S A. 2007 Nov 20;104(47):18613-18618.

[11] Colmegna I, Garry RF. Abstract Role of endogenous retroviruses in autoimmune diseases. Infect Dis Clin North Am. 2006 Dec;20(4):913-929.

 

[Walter L. Wagner]

Sorry for the delay in getting that article.

It was from David Brown of the Washington Post, reproduced in the Daily Herald on September 2, 2008. He references that a few HERVs [Human Endogenous Retro Viruses] that have been incorporated into the human genome, but then took on new roles [other than viral infection and disease of the host]. "For example, a protein called syncytin, which helps cells fuse together in the placenta, is actually the evelope gene from a HERV." He likely means the HERV gene incorporated into the genome produces a protein called syncytin, and not that the gene is the protein.

More about this at:

http://jvi.asm.org/cgi/content/abstract/75/23/11709

In another study, 10 versions of HERV-K viruses, incorporated in various parts of the genome but with varying disabling mutations, were examined and the original virus deduced. It was replicated and tested in the laboratory, and found capable of infecting host cells.

Here's the link to the original newspaper article: http://www.heraldextra.com/content/view/278932/36/

 

[Techne]

It is indeed striking how Horizontal Gene Transfer aided in the development of reproduction in eutheria.

More about Placozoa and predaptations.
That old tree of life gets uprooted so often it is not even funny. So much for the predictive value of evolutionary science. This time it hits an interesting turn.
Concatenated Analysis Sheds Light on Early Metazoan Evolution and Fuels a Modern ‘‘Urmetazoon’’ Hypothesis


This time that interesting little animal with only four cell types but also genetic tool kits for eyes, ears, nerves, bone formation and body plans gets placed at the based of the metazoan tree. See figure:

From the article:

Following one of the basic principles in evolutionary biology that complex life forms derive from more primitive ancestors, it has long been believed that the higher animals, the Bilateria, arose from simpler (diploblastic) organisms such as the cnidarians (corals, polyps, and jellyfishes). A large number of studies, using different datasets and different methods, have tried to determine the most ancestral animal group as well as the ancestor of the higher animals. Here, we use ‘‘total evidence’’ analysis, which incorporates all available data (including morphology, genome, and gene expression data) and come to a surprising conclusion. The Bilateria and Cnidaria (together with the other diploblastic animals) are in fact sister groups: that is, they evolved in parallel from a very simple common ancestor. We conclude that the higher animals (Bilateria) and lower animals (diploblasts), probably separated very early, at the very beginning of metazoan animal evolution and independently evolved their complex body plans, including body axes, nervous system, sensory organs, and other characteristics. The striking similarities in several complex characters (such as the eyes) resulted from both lineages using the same basic genetic tool kit, which was already present in the common ancestor. The study identifies Placozoa as the most basal diploblast group and thus a living fossil genome that nicely demonstrates, not only that complex genetic tool kits arise before morphological complexity, but also that these kits may form similar morphological structures in parallel.

More:

According to the placula hypothesis, we suggest that the placula already had the genetic capability and basic building blocks to build a nervous system, and that from here, the final build-up of the nervous system developed via independent, but parallel, pathways in diploblasts and Bilateria. The genome of the placozoan Trichoplax adhaerens indeed delivers some notable evidence that the genetic inventory may precede morphological manifestation of organs [23]. For example, the placozoan genome harbors representatives of all major genes that are involved in neurogenesis in higher animals, whereas placozoans show not the slightest morphological hint of nerve or sensory cells.

Genetic tool kits present for the development of neurological organs before they evolve...
Play the tape of life again and it should unfold in a similar fashion.

 

[Walter L. Wagner]

Well, that makes sense. If both groupings had the same 'genetic tool kit' already present, then they could both end up relying on that tool kit to engage in parallel evolutionary strategies, independently of each other.

So what were these 'genetic tool kits' doing in the precursor organisms? For the retrovirus I cited, the one tool-kit that was adapted for helping cells fuse together in the placenta was previously used for the viral envelope of the retrovirus that had invaded a precursor organism.

Lots more questions every time we look deeper!

 

[Techne]

Consider Hox-genes.
A brief overview of Hox genes

Basically these genes control the formation of body plans and how they unfold and emerge during development.
Now consider the following article:
Homeodomain proteins belong to the ancestral molecular toolkit of Eukaryotes
Abstract:

Multicellular organization arose several times by convergence during the evolution of eukaryotes (e.g., in terrestrial plants, several lineages of "algae," fungi, and metazoans). To reconstruct the evolutionary transitions between unicellularity and multicellularity, we need a proper understanding of the origin and diversification of regulatory molecules governing the construction of a multicellular organism in these various lineages. Homeodomain (HD) proteins offer a paradigm for studying such issues, because in multicellular eukaryotes, like animals, fungi and plants, these transcription factors are extensively used in fundamental developmental processes and are highly diversified. A number of large eukaryote lineages are exclusively unicellular, however, and it remains unclear to what extent this condition reflects their primitive lack of "good building blocks" such as the HD proteins. Taking advantage from the recent burst of sequence data from a wide variety of eukaryote taxa, we show here that HD-containing transcription factors were already existing and diversified (in at least two main classes) in the last common eukaryote ancestor. Although the family was retained and independently expanded in the multicellular taxa, it was lost in several lineages of unicellular parasites or intracellular symbionts. Our findings are consistent with the idea that the common ancestor of eukaryotes was complex in molecular terms, and already possessed many of the regulatory molecules, which later favored the multiple convergent acquisition of multicellularity.

So, the findings that genes controlling the emergence of body plans were present waaaay before multicellular organisms were even on the cards. Same can be said for a whole lot of other tool kits for multicellularity.

The article continues:

All model organisms for which HD proteins have been characterized and functionally studied belong to eukaryotic lineages that developed multicellularity. Their specific involvement in developmental functions suggests that HD-containing transcription factors belong to the ‘‘good building blocks’’ (King 2004) that allowed some of the eukaryotes to achieve multicellularity and complex organization. During eukaryote evolution, multicellularity was acquired many times independently, but only within four of the main eukaryotic taxa, which for that reason have been considered ‘‘enriched for multicellularity’’ (King 2004). These are the Hetero****a (containing the multicellular brown algae, in addition to many unicellular lineages), the Plantae (with several independent acquisitions of multicellularity, e.g., within red algae, in several lineages of green algae, and in the terrestrial plants or Embryophyta), the Opistho****a (of which a number of fungal lineages, some choanoflagellates, and the Metazoa are multicellular), and the Amoebozoa (mostly unicellular, but comprising the multicellular myxomycetes and dictyostelids).

Also:

The results of character optimization (Fig. 1) show that, instead of being a derived character of ‘‘higher’’ eukaryotes lineages enriched for multicellularity, the HD existed in the last common ancestor of all living eukaryotes. Although the HD occurs in all lineages containing multicellular organisms (animals, fungi, plants, amoebozoans, and hetero****s), this is nothing more than the retention of a eukaryotic plesiomorphy. This conclusion applies for both rooting hypotheses, under the assumption that convergent acquisitions of the HD did not occur (see figure legend for details). Exclusion of convergence events seems justified here by the conservation in length and primary sequence, besides similarity of three-dimensional architecture, strongly arguing in favor of the homology of all eukaryote HDs

And Figure 1:

Fig. 1. Mapping of homeodomain (HD) presence/absence onto the phylogenetic tree of eukaryotes. Trees to the left and to the right are identical in their topology, but they differ by their rooting (to the left: opistho****s1amoeobozans vs. bi****s; to the right: rooting on excavates). Squares indicate observed character states in terminal taxa (black square: presence of HD; white square: absence of HD). The symbol indicates multicellular taxa. The maximal known number of HDs is given for each taxon (with symbol when this number comes from EST or partial genome data). Note that these numbers may not reflect the full complement of homeobox genes in that taxa. s: symbiotic taxa (either parasitic or symbiotic in the strict sense). Black branches: unambiguous presence of HD; white branches: unambiguous absence of HD; gray branches: presence and absence of HD are equiparsimonious, but absence would require convergent acquisitions. With root 1, parsimony favors a unique acquisition of the HD in the common branch of eukaryotes, followed by two to four independent losses (in Guillardia nucleomorph, apicomplexans, kinetoplastids, and Giardia). The maximal number of four convergent losses is obtained if the (unlikely) event of a de novo reacquisition of HD in hetero****s and Trichomonas is excluded. With root 2, the same statement (no de novo or convergent acquisitions) implies a similar evolutionary scenario, with acquisition of HD in an ancestor of all eukaryotes, followed by four independent losses.

So, the data STRONGLY suggest that the information needed for body plans were present waaaay before body plans were present.

It continues.

All investigated eukaryote taxa possess either both groups of HDs or no HD at all, which we consider an intriguing observation, because after duplication, one duplicate is commonly lost in some branches of the phylogenetic tree (Force et al. 1999). Although this pattern may have occurred by chance, it may instead result from evolutionary forces acting on the genome for conservation of both of these functional categories of HDs. Possibly, they complement for the function of the ancestral HD (before the duplication) (Force et al. 1999; see also discussions about the functional significance of ancient dichotomy between TALE and non-TALE in Bu¨ rglin 1995, 1998, 2005). Relaxing the constraint, under conditions where these functions are not needed, may result in the loss of both HD categories, as observed for example in apicomplexans and kinetoplastids. A better understanding of the functional integration of TALE and non-TALE HD proteins in gene networks of the ancestral eukaryotic cell may help to test this hypothesis in the future.

Natural selection as an evolutionary force is a vacuous concept.
Will Provine in his book:
The Origins of Theoretical Population Genetics
From page 199 (see above link):

As John Endler has argued eloquently in Natural Selection in The Wild (1968), natural selection is not a mechanism. Natural selection does not act on anything, nor does it select (for or against), force, maximize, create, modify, shape, operate, drive, favor, maintain, push or adjust. Natural selection does nothing. Natural selection as a natural force belongs in the insubstantial category already populated by the Becker/Stahl phlogiston (Endler 1986) or Newton's "ether".
Natural selection is the necessary outcome of discernible and often quantifiable causes.

Natural selection DOES NOTHING, it is not an evolutionary force.

The finding that the Ur-eukaryote was quite complex and had the necessary tool kits to bias evolutionary directions toward multicellularity and organisms with body plans over and over provides a keen insight into the nature of evolutionary processes over deep time.

Article continues:

The pattern of HD evolution recovered in this study is consistent with the view that ‘‘Ur-eukaryota’’ was a complex organism, from a molecular point of view (Forterre and Philippe 1999; Bapteste and Gribaldo 2003; Roy and Gilbert 2005), in contrast with more traditional conceptions assuming a progressive evolution toward increased complexity

Anyone want to guess what the old view was?

Ur-eukaryota probably possessed many of the good building blocks, which were subsequently recruited, by convergence in several lineages, to perform the functions required for development of multicellular organisms. In other terms, we suggest that the eukaryotes as a whole are preadapted for multicellularity, which only means that the ancestral complexity of the eukaryote genome and cell biology facilitated multiple acquisitions of multicellularity.

Preadapted FOR multicellularity. Mmmmmm. Sound familiar?

So, evolution seems to be biased towards multicellularity. Replay that tape of life and we should get a similar result .

 

[Walter L. Wagner]

Again, very interesting. And, it makes sense that if the various branches of multicellular eukaryotes [green algae, brown algae, red algae, animals, etc.] already had the genetic kits included in their unicellular ancestors, that they could then all rely on those kits in subsequent evolution to independently obtain multicellularity [as a form of 'convergent evolution'].

So, what functions did those genetic kits [that later served to allow multicellularity] serve in our common unicellular ancestor to all of our multicellular cousins?

 

[Techne]

Again, very interesting. And, it makes sense that if the various branches of multicellular eukaryotes [green algae, brown algae, red algae, animals, etc.] already had the genetic kits included in their unicellular ancestors, that they could then all rely on those kits in subsequent evolution to independently obtain multicellularity [as a form of 'convergent evolution'].

That is indeed an interesting view of evolution.
The similarities between evolution and development are striking.

So, what functions did those genetic kits [that later served to allow multicellularity] serve in our common unicellular ancestor to all of our multicellular cousins?

Interesting question. I am sure we will find out.

Interesting finding:
Billions Of Years Ago, Microbes Were Key In Developing Modern Nitrogen Cycle

ScienceDaily (Mar. 3, 2009) — As the world marks the 200th anniversary of Charles Darwin's birth, there is much focus on evolution in animals and plants. But new research shows that for the countless billions of tiniest creatures – microbes – large-scale evolution was completed 2.5 billion years ago.