Curious about Neo-Darwinian theory

[Muttaru]

So as many of us agree on, the Cambrian explosion was when most of the body forms we see today existed.

I guess my question is, how does it suppose that the supporting brain functions for the body functions simultaneously evolved.

If Neo-Darwinian theory is true, does this imply that were there a bunch of organisms with floppy appendages that didn't do anything? Or perhaps nervous systems that were linked to nothing? Is this wrong, and why? If it instead happened more incrementally, would these give enough selective advantage at each step to keep progressing, and why is this mathematically the most plausible answer?

I mean, if you need a series of mutations to get from A to B and C to D (probably way more than these in actuality), with C and D being required for the new organism there would be many more with only a B or only a D than both a B and a D.

If you get one mutation "out of sync" with the others, do they still work together enough to cohesively provide a benefit? Is there enough survival advantage from the one trait to actually be survival of the fittest? Or is there just some kind of genetic drift, and why would this be?

Maybe this would be better phrased, why do Neo-Darwinian theorists think that their mechanism is the best one to explain this phenomena?
Survival of the fittest doesn't seem to necessarily have the best answers to explain arrival of the fittest.


My personal viewpoint is that when God made a new organism, he made them from something already existing, and "rigged" the dice, so to speak.


Trying to think of what Neo-Darwinian theory has as it's strongest supports as opposed to any other form of evolution...

Convergence
Some transitional forms
Microevolution
Vestigial parts (Does this get close to being anti-Lamarck theory? Neutral selective pressure vs negative selective pressure?)

Looking forward to hearing .

[godslanguage]

Curious about Neo-Darwinian theory?

So am I!

Please get back to me when you find evidence for it beyond the micro-level where even in micro-context insignificant changes have been observed not likely to produce anything else beyond extinction via accumulation of random mutations overtime.

According to Darwinian evolution, you are right, we should be nothing more then blobs of goo composed of many blobs of goo. The Darwinists somehow adapted this idea to information processing systems when DNA was first discovered where it had absolutely zero compatibility. Nothing especially from that point on made any sense in light of Darwins theory. It has little explanatory power when we discuss complex digital codes that are processed in such ways such as the case with the Von Neumann stored program architecture.

Darwinian theory is good if we discuss play doh, you can mold it and shape it, it will adapt to the surrounding environment. The rounder a play doh the better chance it has of rolling down a hill and the better chance of it getting under a rock before it starts raining which would otherwise melt it. The other play dohs, oh..., sadly, they won't make it, they just weren't round enough So goes the Darwinian explanation of complex specified information...

All your questions are good, btw, but unfortunately if you are like me you will find disappointing answers.

[BGoodForGoodSake]

The brain is composed of nerve tissues which in turn are composed of nerve cells, also called neurons.

A good place to start would be to look for the simplest organism which has neurons.
Lets take a look at Cnidarians [ni daria], or more specifically jellyfish.

These organisms don't have a central nervous system like we do. They have something called a nerve net.
The nerve net is a loose web of nerves found on the skin of the jellyfish.

When an organism develops it starts from a single cell which then multiplies.
Each cell looks just like the next one. So at some point you have a nice ball of cells which are all alike.
Somewhere along the line each cell differentiates from the others to become a specific kind of cell.

So in the jellyfish some cells "decide" to become neurons (nerve cells). A signal sets off a reaction to turn some of the cells located on the outside to become neurons.

When the signal goes off some genes are expressed. This means that a gene is turned on. Even though all the cells in the jellyfish have the genes to turn them into neurons only some of these cells use the genes to become nerve cells.

Now lets take a look at sponges. Sponges are the simplest of all animals. They do not have neurons. But when we look at their genes we find that they too have the genes to make neurons. So at some point these genes which had one purpose in sponges began to be used to make nerve cells. I do not know what their purpose in sponges is, but we are sure to have an answer for that in the near future.

Stay tuned.

[godslanguage]

Now lets take a look at sponges. Sponges are the simplest of all animals. They do not have neurons. But when we look at their genes we find that they too have the genes to make neurons. So at some point these genes which had one purpose in sponges began to be used to make nerve cells. I do not know what their purpose in sponges is, but we are sure to have an answer for that in the near future.

Thanks for bringing this up Bgood.

See this is the problem, genes which have no adaptive significance whatsoever in the earliest of life forms, functions that we have supposedly "evolved" via Darwinian Evolution were already there from the beginning. This gets to the core of topics such as front-loading which are circulating not only the web sphere but scientific circles. Bgood ofcourse, will tell you that "we will know in the future", but they can't know because it wasn't part of the problem, it was already a built-in solution.

[BGoodForGoodSake]

Thanks for bringing this up Bgood.

See this is the problem, genes which have no adaptive significance whatsoever in the earliest of life forms, functions that we have supposedly "evolved" via Darwinian Evolution were already there from the beginning. This gets to the core of topics such as front-loading which are circulating not only the web sphere but scientific circles. Bgood ofcourse, will tell you that "we will know in the future", but they can't know because it wasn't part of the problem, it was already a built-in solution.

Just out of curiosity do you have any examples of genes which have no adaptive significance in earlier lifeforms?

[godslanguage]

Thanks for bringing this up Bgood.

See this is the problem, genes which have no adaptive significance whatsoever in the earliest of life forms, functions that we have supposedly "evolved" via Darwinian Evolution were already there from the beginning. This gets to the core of topics such as front-loading which are circulating not only the web sphere but scientific circles. Bgood ofcourse, will tell you that "we will know in the future", but they can't know because it wasn't part of the problem, it was already a built-in solution.

Just out of curiosity do you have any examples of genes which have no adaptive significance in earlier lifeforms?

Nice try . Genes which simply booted almost analogous to how BIOS asks CMOS to load the OS from the master
boot record on the target drive. ie: a targeted search. What I mean with no adaptive significance are genes
which were not the product of a gradual processes. Genes could very well be adaptive to certain niches, but those genes were already inherent (demonstrating contigency) and modules would simply dynamically express them given that niche or environmental context (you may call that "adaptation" if you like). This is not a process that is driven by chance via natural selection. Now, I will pose the question: do you have evidence for those nerve genes or any gene for that matter being the product of gradualist process accumulated via simply adaptation and natural selection? Genes of course, are sub sequences of DNA in the chromosome which encode particular features. Earliest and most important genes such as those that build the proteins for ATP synthase would be a start. Nerve genes are another bigger issue.

[BGoodForGoodSake]

Just out of curiosity do you have any examples of genes which have no adaptive significance in earlier lifeforms?

Nice try . Genes which simply booted almost analogous to how BIOS asks CMOS to load the OS from the master
boot record on the target drive. ie: a targeted search. What I mean with no adaptive significance are genes
which were not the product of a gradual processes. Genes could very well be adaptive to certain niches, but those genes were inherent with the pre-existing modules simply dynamically expressed them given that niche or environmental context (you may call that "adaptation" if you like).

Very well then, given your definition of "no adaptive significance above" do you have any examples of such genes in earlier lifeforms?

[godslanguage]

For starters:

Trichoplax adhaerens barely qualifies as an animal. About 1 millimeter long and covered with cilia, this flat marine organism lacks a stomach, muscles, nerves, and gonads, even a head. It glides along like an amoeba, its lower layer of cells releasing enzymes that digest algae beneath its ever-changing body, and it reproduces by splitting or budding off progeny. Yet this animal's genome looks surprisingly like ours, says Daniel Rokhsar, an evolutionary biologist at the University of California, Berkeley (UCB) and the U.S. Department of Energy Joint Genome Institute in Walnut Creek, California. Its 98 million DNA base pairs include many of the genes responsible for guiding the development of other animals' complex shapes and organs, he and his colleagues report in the 21 August issue of Nature.

Biologists had once assumed that complicated body plans and complex genomes went hand in hand. But T. adhaerens's genome, following on the heels of the discovery of a similarly sophisticated genome in a sea anemone (Science, 6 July 2007, p. 86), “highlights a disconnect between molecular and morphological complexity,” says Mark Martindale, an experimental embryologist at the University of Hawaii, Honolulu. Adds Casey Dunn, an evolutionary biologist at Brown University, “It is now completely clear that genomic complexity was present very early on” in animal evolution.

Science 22 August 2008:
Vol. 321. no. 5892, pp. 1028 - 1029
DOI: 10.1126/science.321.5892.1028b

GENOMICS: 'Simple' Animal's Genome Proves Unexpectedly Complex

[hopefulcynic]

For starters:

Trichoplax adhaerens barely qualifies as an animal. About 1 millimeter long and covered with cilia, this flat marine organism lacks a stomach, muscles, nerves, and gonads, even a head. It glides along like an amoeba, its lower layer of cells releasing enzymes that digest algae beneath its ever-changing body, and it reproduces by splitting or budding off progeny. Yet this animal's genome looks surprisingly like ours, says Daniel Rokhsar, an evolutionary biologist at the University of California, Berkeley (UCB) and the U.S. Department of Energy Joint Genome Institute in Walnut Creek, California. Its 98 million DNA base pairs include many of the genes responsible for guiding the development of other animals' complex shapes and organs, he and his colleagues report in the 21 August issue of Nature.

Biologists had once assumed that complicated body plans and complex genomes went hand in hand. But T. adhaerens's genome, following on the heels of the discovery of a similarly sophisticated genome in a sea anemone (Science, 6 July 2007, p. 86), “highlights a disconnect between molecular and morphological complexity,” says Mark Martindale, an experimental embryologist at the University of Hawaii, Honolulu. Adds Casey Dunn, an evolutionary biologist at Brown University, “It is now completely clear that genomic complexity was present very early on” in animal evolution.

Science 22 August 2008:
Vol. 321. no. 5892, pp. 1028 - 1029
DOI: 10.1126/science.321.5892.1028b

GENOMICS: 'Simple' Animal's Genome Proves Unexpectedly Complex

There are three possibilities here:
1.Trichoplax is secondarily simple. In other words, its ancestors possessed a more complex body plan, but these features were lost in the lineage which gave rise to Trichoplax. The developmental genes however were retained, in either functional or nonfunctional form.
2.Trichoplax has an as yet undiscovered part of its life cycle. The developmental genes are specific to a specific part of the life cycle.
3.The developmental genes exist for no reason, and do not provide any selective advantage to the host organism.

Let's go through these possibilities one by one.

1.This would not be unprecedented. Blind cave fish possess non-functional genes which would normally code for eyes. These fish are descendants of fish which possessed functional eyes. At some point in their evolution, blind cave fish lost the ability to develop eyes, but they have retained the genes to do so.

Something similar may be going on with Trichoplax. But in my opinion, it seems as if the amount of structures that would need to be lost is simply too much. However, nature continues to surprise me, so you never know.

2. The second possibility is more interesting. Many organisms have life cycles in which juveniles and adults are radically different. Frogs and tadpoles come to mind. Frogs possess genes for making fins and gills, but these structures are absent in the adult form.

Trichoplax has never been studied in the wild, and very little is known about its native environment. It is entirely possible that the relatively simple body plan is only one part of the organism's life cycle. Presumably then, the developmental genes found in the organism's genome are needed by the other stages of the life cycle.

Is there any evidence to support this hypothesis? Yes. Researchers have found that Trichoplax is capable of sexual reproduction- analysis of the genome indicates genetic recombination occurs on occasion. However, the known form of Trichoplax lacks the means to reproduce sexually. In fact, it has only been observed to reproduce asexually. Maybe, an as yet undiscovered form of Trichoplax possesses a more complex body plan and is capable of sexual reproduction.

3. If I'm not mistaken, you are advocating the third hypothesis: the developmental genes are useless to Trichoplax. If this is the case, then we can make a simple prediction and test it against the evidence. If the genes really are useless, then mutations within them will not affect the organism. Thus, mutations will accumulate at a predictable rate. This rate will be equivalent, or nearly so, to the background mutation rate of the organism. Is this the case? In the article you cited, did the researchers find that the developmental genes were all broken? What was the ratio of synonymous to non-synonymous mutations?

[BGoodForGoodSake]

For starters:

Trichoplax adhaerens barely qualifies as an animal. About 1 millimeter long and covered with cilia, this flat marine organism lacks a stomach, muscles, nerves, and gonads, even a head. It glides along like an amoeba, its lower layer of cells releasing enzymes that digest algae beneath its ever-changing body, and it reproduces by splitting or budding off progeny. Yet this animal's genome looks surprisingly like ours, says Daniel Rokhsar, an evolutionary biologist at the University of California, Berkeley (UCB) and the U.S. Department of Energy Joint Genome Institute in Walnut Creek, California. Its 98 million DNA base pairs include many of the genes responsible for guiding the development of other animals' complex shapes and organs, he and his colleagues report in the 21 August issue of Nature.

Biologists had once assumed that complicated body plans and complex genomes went hand in hand. But T. adhaerens's genome, following on the heels of the discovery of a similarly sophisticated genome in a sea anemone (Science, 6 July 2007, p. 86), “highlights a disconnect between molecular and morphological complexity,” says Mark Martindale, an experimental embryologist at the University of Hawaii, Honolulu. Adds Casey Dunn, an evolutionary biologist at Brown University, “It is now completely clear that genomic complexity was present very early on” in animal evolution.

Science 22 August 2008:
Vol. 321. no. 5892, pp. 1028 - 1029
DOI: 10.1126/science.321.5892.1028b

GENOMICS: 'Simple' Animal's Genome Proves Unexpectedly Complex

It's interesting you bring this up as an example.

I believe that what you are trying to imply here is that these genes which "include many of the genes responsible for guiding the development of other animals" has no use in this particular organism.
OR
That these genes are identical to the genes in other "higher organisms"

They are in fact not. What the scientist means in his quote is that there are analogous genes in higher organisms.
Meaning that these genes are identifiable because they are similar to genes in higher animals.

I think an analogy can be helpful here.
The gene in question is Trox-2 which is this animals version of a Hox gene in mammals. This gene plays a vital role in cellular organization in development. Note that the genes are not identical but that this is this particular animals version.

Imagine a world where every cell is out for themselves and does not communicate with other cells.
This is the world before multi-cellular animals came into existence.

Now comes along a foreman who can direct these cells to work together.
The foreman in our analogy is the Trox-2 gene.

Now at first this foreman can only make simple organizations.

But after many generations of foremen the organizational skills become increasingly elaborate. Thus leading to the formation of organs and such.

Thus the HOX genes found in higher animals. It is interesting to note that the number of HOX genes also increases as we get to more complicated animals. The assumption then is that as animals evolved, the number of HOX genes increased allowing them to differentiate and mutate, leading to more complex organisms.

So as you can see, right in front of us we see that HOX genes responsible for animal development do have humble beginnings.

Things to note. The genome of a Trichoplax is relatively small, it is only about 10 times larger than that of E-coli a bacteria found in animal guts.

Now for your other question.

do you have evidence for those nerve genes or any gene for that matter being the product of gradualist process accumulated via simply adaptation and natural selection?

Interestingly enough the Trichoplax has genes similar to those responsible for nerve cells expressed in the mature adult. Obviously these animals do not possess nerve cells, but the expressed genes give the animal the ability to propagates stimulus from one end of the animal to the other. If this isn't a proto nerve I don't know what is.

[godslanguage]

I think Bgood, you are putting words in the authors mouth.
ie:

What the scientist means in his quote is that there are analogous genes in higher organisms

Even so, if they are mearly "analagous" there is no way for you to show that as opposed to the same pattern genes utilized later on.

Here is what the author adds:

Despite being developmentally simple—with no organs or many specialized cells—the placozoan has counterparts of the transcription factors that more complex organisms need to make their many body parts and tissues. It also has genes for many of the proteins, such as membrane proteins, needed for specialized cells to coordinate their function. “Many genes viewed as having particular 'functions' in bilaterians or mammals turn out to have much deeper evolutionary history than expected, raising questions about why they evolved,”

What adaptive significance do genes which code for complex protein stuctures have? How exactly did NS
source them this early on?
If those genes have underlying critical function that could easily be tested by knockout experiments. If the organism is indistinguishable then those genes can't be explained by NS. In software engineering we inject code almost (one could say) unecessarily to make the chores of the program bullet proof. This code just lies around until its absolutely required, examples include recovery and error handling code. The necessary toolkit is built-in to the program so that its populated with the essentials to adapt to new expected and unexpected "future" context. Intelligence seems to best explain this "anticipating" control code that triggers these genes. So the developmental toolkit is not only the pattern genes themselves that code for complex protein structures but control code that works in parallel to make sure that happens. The problem here does not merely limit itself to the genes themesleves in terms of ratio of the genome size (as you pointed out) but control code (and probably other code) which has potential to exponentially increase functional complexity without any continous trace.

Here is another LINK

A few quotes of relevance:

The paper, "An autopodial-like pattern of Hox expression in the fins of a basal actinopterygian fish," shows that the genetic and developmental toolkit that builds limbs with fingers and toes was around long before the acquisition of limbs, according to the scientists, and that this toolkit exists in some primitive form in a living primitive bony fish, the paddlefish.

This is the first molecular support for the theory that the genes to help make fingers and toes have been around for a long time—well before the 375-million-year-old Tiktaalik roseae, the newly found species discovered in 2004 by Shubin and colleagues. Tiktaalik provided a missing evolutionary link between fish and tetrapods and was among the first creatures that walked out of water onto land.

What Tiktaalik revealed morphologically, Shubin, Davis and Dahn have proven genetically.

"This report provides important new information about the evolution of hands and feet in vertebrate animals," said Lance Grande, PhD, head of collections and research at the Field Museum.

Another paper supporting front-loading: LINK

"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."

Another paper supports evolutionary jumps "in two discrete episodes" and not without a prexisting potential (again supporting front-loading hypothesis):

LINK

"Approximately 3/4 of
the 16-orders-of-magnitude increase in maximum size occurred
in 2 discrete episodes. The first size jump required the
evolution of the eukaryotic cell, and the second required
eukaryotic multicellularity. The size increases appear to have
occurred when ambient oxygen concentrations reached sufficient
concentrations for clades to realize preexisting evolutionary
potential, highlighting the long-term dependence of
macroevolutionary pattern on both biological potential and
environmental opportunity."

But surely, as always, there is some neo-Darwinian explanation for all of this...

[hopefulcynic]

If those genes have underlying critical function that could easily be tested by knockout experiments.

No it can't, and here's why. When cells are grown in the lab, they are grown under optimum conditions. This is unavoidable, because there is no way to simulate all of the stresses that an organism in the wild would encounter. If a gene is involved in some type of stress response, or metabolism of an unusual food source, then deletion of that gene may not give a phenotype in the lab. This does not imply that the gene is useless.

PS Please read over my earlier post in this thread. It should answer many of your questions regarding Trichoplax.

[godslanguage]

because there is no way to simulate all of the stresses that an organism in the wild would encounter

If a gene is involved in some type of stress response, or metabolism of an unusual food source, then deletion of that gene may not give a phenotype in the lab. This does not imply that the gene is useless.

I agree that putting this type of animal back to its "optimum" habitat would be unrealistic after a knockout experiment has been performed. But more realistic studies with Mice have shown exactly this, large regions of coding genes (which had other coding potential) were removed, tests were performed including tests you alluded too and practically nothing about them could be differentiated.

In a knockout experiment, an organism is engineered to lack the expression and activity of one or more genes. This is done through genetic manipulation, using snipping enzymes, crossover activity, or binding to either eliminate the specific gene sequence or make it unusable. Once the extracellular DNA is changed, it is reintroduced into embryonic stem cells, where the engineered copy is encouraged to replace the organism's own gene. The infected stem cells are injected into blastocysts which are implanted in surrogate mothers.

Knockout experiments are often performed in order to determine the functional role of a specific gene in the organism by studying the defects caused by the resulting mutation. Knockout experiments are especially useful for understanding the genes that code for the protein parts essential for the functioning of molecular machines.

The opposite experiment to a knockout experiment is the Gain of Function experiment, in which the targeted gene is enhanced either by the addition of more copies of that gene on the DNA or through methods to enhance the frequency of its transcription. With knockout experiments combined with Gain of Function experiments, a fuller range of gene function can be assessed.

[hopefulcynic]

I agree that putting this type of animal back to its "optimum" habitat would be unrealistic after a knockout experiment has been performed. But more realistic studies with Mice have shown exactly this, large regions of coding genes (which had other coding potential) were removed, tests were performed including tests you alluded too and practically nothing about them could be differentiated.

References? I seriously doubt that they could account for all possible scenarios.

[godslanguage]

I agree that putting this type of animal back to its "optimum" habitat would be unrealistic after a knockout experiment has been performed. But more realistic studies with Mice have shown exactly this, large regions of coding genes (which had other coding potential) were removed, tests were performed including tests you alluded too and practically nothing about them could be differentiated.

References? I seriously doubt that they could account for all possible scenarios.

Here is abstract:

Ultraconserved elements have been suggested to retain extended perfect sequence identity between the human, mouse, and rat genomes due to essential functional properties. To investigate the necessities of these elements in vivo, we removed four noncoding ultraconserved elements (ranging in length from 222 to 731 base pairs) from the mouse genome. To maximize the likelihood of observing a phenotype, we chose to delete elements that function as enhancers in a mouse transgenic assay and that are near genes that exhibit marked phenotypes both when completely inactivated in the mouse and when their expression is altered due to other genomic modifications. Remarkably, all four resulting lines of mice lacking these ultraconserved elements were viable and fertile, and failed to reveal any critical abnormalities when assayed for a variety of phenotypes including growth, longevity, pathology, and metabolism. In addition, more targeted screens, informed by the abnormalities observed in mice in which genes in proximity to the investigated elements had been altered, also failed to reveal notable abnormalities. These results, while not inclusive of all the possible phenotypic impact of the deleted sequences, indicate that extreme sequence constraint does not necessarily reflect crucial functions required for viability.

Here is the paper:
LINK