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:

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.

[QUOTE] 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.

The intriguing genome of the Trichoplax (Placozoa meaning flat animals):
Trichoplax Genome Sequenced: ‘Rosetta Stone’ For Understanding Evolution

Nice Pic

Place on the evolutionary tree

Currently there is only one named species in the phylum: Trichoplax adhaerens.

[QUOTE]It’s a flattened blob, a few millimeters across and made up of a few thousand cells. It’s main claim to fame is its remarkable simplicity: it is a multicellular animal that consists of only four apparent cell types, and the only obvious organization is into an upper and lower surface. The upper surface consists of a sheet of covering cells, while the lower surface contains two cell types: the gland cells that secrete digestive enzymes onto whatever the animal is sitting on, and the cylinder cells that absorb whatever nutrients are released. In between is a loose network of fiber cells that are responsible for the animal’s movement.
Nerves, sensory cells and muscle cells are absent.
Interestingly (from the link):

[QUOTE]One other strange thing: in culture, Trichoplax is consistently asexual and reproduces by fission, but older cultures at high density begin to produce small motile presumptive sperm cells, and as individual animals desintegrate, they spew out ova. The two have never been observed to come together, though, so there is no fertilization, and while the ova may divide a half dozen times, they all eventually die. It is possible that there is another stage in the life cycle that is not viable under laboratory conditions and has never been observed.
The genome of this critter is even more fascinating.
From the nature article:
The Trichoplax genome and the nature of placozoans

Table 1 | Developmental transcription factors in the Trichoplax genome
Homeobox (Hox genes)

[]A) ANTP-class: Trox-2 (Hox/ParaHox-like), Not, Dlx, Mnx, Hmx, Hex, Dbx and seven others.
]B) PRD-class (paired box and homeobox): PaxB, Pitx, Otp, Gsc and five others
[]C) POU-class(POU domain and homeobox): POU class 4 (Brn-3), one other
]D) LIM-class (LIM domain and homeobox): islet, apterous, Lhx1/5 and one other
[]E) SIX-class (sine oculis homeobox): Six3/6 and one other
]F) TALE-class: Pbx/Exd, Irx, Meis
[*]G) HNF-class: Hnf

Going down the list, what are the functions of these Hox genes?

  1. Trox-2 (Hox/ParaHox-like)
    Hox/paraHox-like genes are involved in axial patterning in bilaterarian organisms. Basically, they control the formation of the anterior–posterior (AP) axis. Function of Trox-2?

[QUOTE]We speculate that Trox-2 functions within a hitherto unrecognized population of possibly multipotential peripheral stem cells that contribute to differentiated cells at the epithelial boundary of Trichoplax.
2) Not
In mice, Not controls the development of the caudal notochord. What is the notochord?

[QUOTE]The notochord is a flexible, rod-shaped body found in embryos of all chordates. It is composed of cells derived from the mesoderm and defines the primitive axis of the embryo. In lower vertebrates, it persists throughout life as the main axial support of the body, while in higher vertebrates it is replaced by the vertebral column. The notochord is found on the ventral surface of the neural tube.
What does it do in this flat, simple organism?

[QUOTE]The homeobox gene Not is highly conserved in Xenopus, chicken and zebrafish with an apparent role in notochord formation, which inspired the name of this distinct subfamily. Interestingly, Not genes are also well conserved in animals without notochord such as sea urchins, Drosophila or even Hydra, but appear to be highly derived in mammals. A search for homeobox genes in the placozoan Trichoplax adhaerens, one of the simplest organisms available today, revealed only two homeobox genes: a Not homologue and the previously described gene Trox-2, which is most similar to the Gsx subfamily of the Hox/ParaHox cluster genes. Not has a unique expression profile in Trichoplax. It is highly expressed in folds of intact animals and in the wounds of regenerating animals. The dynamic expression pattern of Trichoplax Not is discussed in comparison with the invariable expression pattern of Trox-2 and the putative secreted protein Secp1. The high sequence conservation of Not from Trichoplax to lower vertebrates, but not to mammals, represents a rare example of an apparent gene decay in the lineage leading to humans.
Interesting preadaptations.

Next, a look at the other Hox genes in this organism and their functions in higher animals.
Dlx, Mnx, Hmx,Hex, Dbx etc…

Hox genes video
Nice overview of Hox genes.

More Trichoplax preadaptations:
The Dlx gene

What does it do (wiki)?

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?

[QUOTE]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: ClustalW - original settings).
What does Dlx 5 do?

[QUOTE]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: Swissmodel)

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.

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.

[QUOTE]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.

[QUOTE]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 :p.
So four genes played a role:
]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.

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)

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

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?

Question Of Chance In Evolution Addressed

[QUOTE]What is remarkable is that the molecular genealogy of the living species shows their origin only 15 million years ago, with the same trajectory as in the distant past! Evidence suggests that trajectory has occurred again and again in other groups. The authors argue that the original trajectory was highly contingent on a set of initial conditions, but that given the possibilities afforded by time, a genetic background would arise (like flipping a coin long enough to achieve 10 heads or tails in a row) that was visible to natural selection, most likely driven by predation. Acting together, the eventual realization of a particular genetic and developmental channel, and natural selection opened the way for an adaptive solution.
Replay the tape of life and similar outcomes should be inevitable. Now compare these results to some of our own designed evolutionary software (see Programmed Evolution…).

Do you drop these threads around in the manner of a dog peeing on lampposts?

Interesting article:
Protein Superfamily Evolution and the Last Universal Common Ancestor (LUCA)

[QUOTE]By exploiting three-dimensional structure comparison, which is more sensitive than conventional sequence-based methods for detecting remote homology, we have identified a set of 140 ancestral protein domains using very restrictive criteria to minimize the potential error introduced by horizontal gene transfer. These domains are highly likely to have been present in the Last Universal Common Ancestor (LUCA) based on their universality in almost all of 114 completed prokaryotic (Bacteria and Archaea) and eukaryotic genomes. Functional analysis of these ancestral domains reveals a genetically complex LUCA with practically all the essential functional systems present in extant organisms, supporting the theory that life achieved its modern cellular status much before the main kingdom separation (Doolittle 2000). In addition, we have calculated different estimations of the genetic and functional versatility of all the superfamilies and functional groups in the prokaryote subsample. These estimations reveal that some ancestral superfamilies have been more versatile than others during evolution allowing more genetic and functional variation. Furthermore, the differences in genetic versatility between protein families are more attributable to their functional nature rather than the time that they have been evolving. These differences in tolerance to mutation suggest that some protein families have eroded their phylogenetic signal faster than others, hiding in many cases, their ancestral origin and suggesting that the calculation of 140 ancestral domains is probably an underestimate.
Mmm, “Functional analysis of these ancestral domains reveals a genetically complex LUCA with practically all the essential functional systems present in extant organisms”

Let’s see what they found:
From the conclusion:

[QUOTE]From this annotation we know that the LUCA, or the primitive
community that constituted this entity, was functionally and genetically complex (Table 1, Fig. 1, Supplementary Table 3), supporting the theory that life achieved its modern cellular status long before the separation of the three kingdoms.
Contrary to analyses based purely on sequence conservation and universal ubiquity throughout all species, which suggested a simple LUCA with translation and few other genes (Koonin 2003), with the application of a more sensitive method to detect remote homology, we can affirm that the LUCA held representatives in practically all the essential functional niches currently present in extant organisms, with a metabolic complexity similar to translation in terms of domain variety.
What did this primitive clade of LUCAs have? What kind of machinery was present?

  1. Replication, transcription, and translation
  2. Repertoire of metabolic pathways coupled with the necessary machinery including;

[]a) the use of glucose and other sugars
]b) the assimilation of amino acids and nucleosides/ base
[]c) the synthesis of ATP both by substratelevel phosphorylation and through redox reactions coupled to membranes
]d) Signal transduction pathways controlling perception.
[]e) These pathways are linked to gene regulation and protein modification, protein signal recognition, transport, and secretion, protein folding assistance
]f) And then of course the self-replication machinery.

With all these present in the LUCA, all that is needed is a little time for functional diversification and genetic expansion. The inevitable and repeated emergence of eyes, body plans, toolkits for body plans etc. should not be a problem, even expected if the tape of life was to be replayed even if randomness was taken into consideration.

How deep does the rabbit hole go?

Time will tell I guess…

More interesting preadaptations:
This time sponges (wiki).

[QUOTE]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

[QUOTE]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.

[B]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.[/B]

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

[QUOTE]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

[QUOTE]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. Interesting…


Talk about an armoury of ruses.

I don’t know mate. With yet another person having problems with your “answers”, I’d be doing some introspection right about now.

Look, some of us have it easy, we don’t mind answering questions. We, after all, think that “I don’t know” is a perfectly reasonable answer to questions we do not know the answer to.

This is something you need to work at. You need to learn to accept “I don’t know” as answer and more important, learn to be able to give it.

Making up shit is never going to cut it for you. Not amongst rational, thinking uman beans it ain’t.

Mind giving an ACTUAL answer? For you for all to see… Here.

I really do not have the time or inclination to go into this with you.

I’d have considered going through some of these with you but now that I know this evasion pisses you off, I may just use the tactic more often.

And of course, the major reason is because I still don’t bow down to what you dictate to me to post and what not to post and never ever ever will

Fair enough. The “we don’t mind answering questions.” above just does not apply to you it seems ;). Who is this “we” you are refering to again?

More preadaptations:

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. More coming…

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:

[QUOTE]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:

[QUOTE]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:

[QUOTE]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

[QUOTE]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 before the emergence of neurons, eyes, body plans etc. continues…

Yawn “Well, I can’t explain it, therefore a greater intelligence must be at work.”

What a tired little joke.


Don’t worry, this wabbit can handle it…

Aaaanyway… more preadaptations ;D.

More about toolkits for eye development in animals with no eyes, present before the emergence of eyes… the Trichplax genome.
Six3 and Six6 activity is modulated by members of the groucho family.

[QUOTE]Six3 and Six6 are two genes required for the specification and proliferation of the eye field in vertebrate embryos, suggesting that they might be the functional counterparts of the Drosophila gene sine oculis (so). Phylogenetic and functional analysis have however challenged this idea, raising the possibility that the molecular network in which Six3 and Six6 act may be different from that described for SO. To address this, we have performed yeast two-hybrid screens, using either Six3 or Six6 as a bait. In this paper, we report the results of the latter screen that led to the identification of TLE1 (a transcriptional repressor of the groucho family) and AES (a potential dominant negative form of TLE proteins) as cofactors for both SIX6 and SIX3. Biochemical and mutational analysis shows that the Six domain of both SIX3 and SIX6 strongly interact with the QD domain of TLE1 and AES, but that SIX3 also interacts with TLE proteins via the WDR domain. Tle1 and Aes are expressed in the developing eye of medaka fish (Oryzias latipes) embryos, overlapping with the distribution of both Six3 and Six6. Gain-of-function studies in medaka show a clear synergistic activity between SIX3/SIX6 and TLE1, which, on its own, can expand the eye field. Conversely, AES alone decreases the eye size and abrogates the phenotypic consequences of SIX3/6 over-expression. These data indicate that both Tle1 and Aes participate in the molecular network that control eye development and are consistent with the view that both Six3 and Six6 act in combination with either Tle1 and/or Aes.
And toolkits for forebrain neuronal development?
The LIM-homeobox gene Islet-1 is required for the development of restricted forebrain cholinergic neurons.

[QUOTE]Forebrain cholinergic neurons modulate complex mammalian behaviors such as reward-related learning and cognitive functions. Although their dysfunction is implicated in various psychiatric and neurodegenerative diseases, the factors governing cholinergic neuron differentiation and diversity are mostly unknown. We tested the role of the LIM-homeobox gene Isl1 in the development of forebrain cholinergic neurons by conditionally deleting Isl1 using a Six3-cre transgene. A depletion of cholinergic interneurons in the dorsal and ventral striatum, and cholinergic projection neurons in the nucleus basalis is observed and is ascribed to an early and persistent defect in cholinergic neuron differentiation. Notably, cholinergic innervation to the neocortex is abolished, whereas that to the hippocampus is unaltered. The unique pattern of cholinergic hypoinnervation encountered is supported by the presence of cholinergic projection neurons in the medial septum, the magnocellular preoptic area, and the substantia innominata. Together, these results demonstrate the requirement for Isl1 in the development of restricted telencephalic cholinergic neurons and link the development of cholinergic neurons in anatomically disparate sites to Isl1 function.
Some of these sequences present in bacteria and archaea