MarioNovak wrote:

Alan B wrote:

MarioNovak wrote:Science shows that evolution can't create new genes

I see.

So, er, "Therefore, God?" Is that what you are suggesting?

I am suggesting what is logically necessary. If genes exist and observable processes cannot create them, then it logically follows: - new genes are the result of the "processes" science cannot observe.

jamest wrote:

Thomas Eshuis wrote:

jamest wrote:It is interesting to see that a particular organism did not create one single new gene after 60,000 generations.

Citations?

So you are disputing the facts of the experiment, I see.

jamest wrote:Well I didn't present those facts, so will leave it to MN to provide relevant citations.

jamest wrote:...so will leave it to MN to provide relevant citations.

Rachel Bronwyn wrote:I think I dated the OP.

kennyc wrote:

Rachel Bronwyn wrote:I think I dated the OP.

Did you collect DNA? Can it be eliminated from the gene pool?

Due to this reason the only real scientific test for the idea od evolution is this: can evolutionary processes produce a new or de novo genes? De novo genes are genes without homologues in genomes of other organisms.

The evolutionary origin of orphan genes

Nature Reviews Genetics 12, 692-702 (October 2011) | doi:10.1038/nrg3053

Diethard Tautz & Tomislav Domazet-Lošo

Abstract

Gene evolution has long been thought to be primarily driven by duplication and rearrangement mechanisms. However, every evolutionary lineage harbours orphan genes that lack homologues in other lineages and whose evolutionary origin is only poorly understood. Orphan genes might arise from duplication and rearrangement processes followed by fast divergence; however, de novo evolution out of non-coding genomic regions is emerging as an important additional mechanism. This process appears to provide raw material continuously for the evolution of new gene functions, which can become relevant for lineage-specific adaptations.

http://www.nature.com/nrg/journal/v12/n ... g3053.html

MarioNovak wrote:Since, by proponents of evolution, evolutionary processes created every level of biological organisation and since all living beings depend on genes, as they specify all proteins, functional RNA chains and hold the information to build and maintain an organism's cells, from the science perspective - evolution is natural process that produce a new genes. So, the real scientific question is this: is there a knowledge in biology, based on facts learned through experiments and observation which shows that processes of evolution can create new genes?

Abstract

In order to understand the evolution of enzyme reactions and to gain an overview of biological catalysis we have combined sequence and structural data to generate phylogenetic trees in an analysis of 276 structurally defined enzyme superfamilies, and used these to study how enzyme functions have evolved. We describe in detail the analysis of two superfamilies to illustrate different paradigms of enzyme evolution. Gathering together data from all the superfamilies supports and develops the observation that they have all evolved to act on a diverse set of substrates, whilst the evolution of new chemistry is much less common. Despite that, by bringing together so much data, we can provide a comprehensive overview of the most common and rare types of changes in function. Our analysis demonstrates on a larger scale than previously studied, that modifications in overall chemistry still occur, with all possible changes at the primary level of the Enzyme Commission (E.C.) classification observed to a greater or lesser extent. The phylogenetic trees map out the evolutionary route taken within a superfamily, as well as all the possible changes within a superfamily. This has been used to generate a matrix of observed exchanges from one enzyme function to another, revealing the scale and nature of enzyme evolution and that some types of exchanges between and within E.C. classes are more prevalent than others. Surprisingly a large proportion (71%) of all known enzyme functions are performed by this relatively small set of 276 superfamilies. This reinforces the hypothesis that relatively few ancient enzymatic domain superfamilies were progenitors for most of the chemistry required for life.

A significant proportion of the reactions required for life are performed by a relatively small number of superfamilies so it can be postulated that a few ancient enzymatic domain superfamilies were progenitors for most of the chemistry required for life, this considerably develops previous observations [37]. Using the phylogenetic trees to define the evolutionary route taken within a superfamily to change function, we were able to generate the E.C. change matrix. The large numbers of changes at the E.C. 4th level in the summary of E.C. changes in phylogentic trees compared to the low number of E.C. class changes indicates that changes in specificity occur mostly at the leaves of the trees, while more fundamental changes in chemistry occur at the root of the tree. Further work is required to ascertain when in evolution these changes occurred. Therefore a large amount of enzyme diversity occurs through evolution rather than de novo invention. Although, of course, new enzymes must have evolved at some stage, probably very early in the evolution of life. To identify the small number of ‘original’ enzyme progenitors requires more work and more experimental data.

Abstract

Gene duplications are believed to facilitate evolutionary innovation. However, the mechanisms shaping the fate of duplicated genes remain heavily debated because the molecular processes and evolutionary forces involved are difficult to reconstruct. Here, we study a large family of fungal glucosidase genes that underwent several duplication events. We reconstruct all key ancestral enzymes and show that the very first preduplication enzyme was primarily active on maltose-like substrates, with trace activity for isomaltose-like sugars. Structural analysis and activity measurements on resurrected and present-day enzymes suggest that both activities cannot be fully optimized in a single enzyme. However, gene duplications repeatedly spawned daughter genes in which mutations optimized either isomaltase or maltase activity. Interestingly, similar shifts in enzyme activity were reached multiple times via different evolutionary routes. Together, our results provide a detailed picture of the molecular mechanisms that drove divergence of these duplicated enzymes and show that whereas the classic models of dosage, sub-, and neofunctionalization are helpful to conceptualize the implications of gene duplication, the three mechanisms co-occur and intertwine.

Author Summary

Darwin's theory of evolution is one of gradual change, yet evolution sometimes takes remarkable leaps. Such evolutionary innovations are often linked to gene duplication through one of three basic scenarios: an extra copy can increase protein levels, different ancestral subfunctions can be split over the copies and evolve distinct regulation, or one of the duplicates can develop a novel function. Although there are numerous examples for all these trajectories, the underlying molecular mechanisms remain obscure, mostly because the preduplication genes and proteins no longer exist. Here, we study a family of fungal metabolic enzymes that hydrolyze disaccharides, and that all originated from the same ancestral gene through repeated duplications. By resurrecting the ancient genes and proteins using high-confidence predictions from many fungal genome sequences available, we show that the very first preduplication enzyme was promiscuous, preferring maltose-like substrates but also showing trace activity towards isomaltose-like sugars. After duplication, specific mutations near the active site of one copy optimized the minor activity at the expense of the major ancestral activity, while the other copy further specialized in maltose and lost the minor activity. Together, our results reveal how the three basic trajectories for gene duplicates cannot be separated easily, but instead intertwine into a complex evolutionary path that leads to innovation.

Figure 2. Duplication events and changes in specificity and activity in evolution of S. cerevisiae MalS enzymes.
The hydrolytic activity of all seven present-day alleles of Mal and Ima enzymes as well as key ancestral (anc) versions of these enzymes was measured for different α-glucosides. The width of the colored bands corresponds to kcat/Km of the enzyme for a specific substrate. Specific values can be found in Table S2. Note that in the case of present-day Ima5, we were not able to obtain active purified protein. Here, the width of the colored (open) bands represents relative enzyme activity in crude extracts derived from a yeast strain overexpressing IMA5 compared to an ima5 deletion mutant. While these values are a proxy for the relative activity of Ima5 towards each substrate, they can therefore not be directly compared to the other parts of the figure. For ancMalS and ancMal-Ima, activity is shown for the variant with the highest confidence (279G for ancMalS and 279A for ancMal-Ima). Activity for all variants can be found in Table S2.
doi:10.1371/journal.pbio.1001446.g002

MarioNovak wrote:Due to this reason the only real scientific test for the idea od evolution is this: can evolutionary processes produce a new or de novo genes? De novo genes are genes without homologues in genomes of other organisms. This question is especially important because comparative genome analyses indicate that every taxonomic group so far studied contains 10–20% of genes that lack recognizable homologs in other species. These genes are also called orphan genes. http://www.cell.com/trends/genetics/abs ... 68-9525(09)00145-0

MarioNovak wrote:For example this research identified a total of 60 protein-coding genes that originated de novo on the human lineage since divergence from chimpanzee - http://www.plosgenetics.org/article/inf ... en.1002379
The functionality of these genes is supported by both transcriptional and proteomic evidence. RNA–seq data indicate that these genes have their highest expression levels in the cerebral cortex and testes, which might suggest that these genes contribute to phenotypic traits that are unique to humans, such as improved cognitive ability.
Since the chimpanzees and humans shared a common ancestor 240,000 generations ago, this indicates that the rate of origin of de novo genes is 1 gen per 4,000 generations. Of course, this rate will grow with the future discovery of new unique genes.

So, what can empirical science say about the power of evolution to create a new genes?

Shrunk wrote:

The evolutionary origin of orphan genes

Nature Reviews Genetics 12, 692-702 (October 2011) | doi:10.1038/nrg3053

Diethard Tautz & Tomislav Domazet-Lošo

Abstract

Gene evolution has long been thought to be primarily driven by duplication and rearrangement mechanisms. However, every evolutionary lineage harbours orphan genes that lack homologues in other lineages and whose evolutionary origin is only poorly understood. Orphan genes might arise from duplication and rearrangement processes followed by fast divergence; however, de novo evolution out of non-coding genomic regions is emerging as an important additional mechanism. This process appears to provide raw material continuously for the evolution of new gene functions, which can become relevant for lineage-specific adaptations.

http://www.nature.com/nrg/journal/v12/n ... g3053.html

Just reading this now. So far, no mention of orphan genes being magically created by Jesus as a viable hypothesis, and from the title and the abstract I don't expect that to be included. But I'll let everyone know if it comes up...

jamest wrote:

MarioNovak wrote:
Well, the biggest scientific observations of evolution in action is E. coli evolution experiment. On February 24, 1988. Richard Lenski and his team at Michigan State University embarked on an ongoing long-term evolution experiment. He started 12 genetically identical lines from a single strain of E. coli. The bacteria reproduced every few hours. The populations reached the milestone of 50,000 generations in February 2010 and 60,000 in in April 2014.
So, what did Lenski experiment show? How many new genes evolutionary processes created after 60,000 generations?
Well, the answer is 0, - ZERO. Most of the changes in this experiment involved streamlining the genome, deleting genes no longer needed, or reducing protein expression.

Were the bacteria all maintained within the same unchanging environment?

Zachary Blount on “Ham on Nye” Debate, Follow-up #3
I’m very pleased to present this guest post written by Dr. Zachary Blount, aka Dr. Citrate, as an in-depth follow-up to the “Ham on Nye” science versus creation debate. Zack did his undergraduate studies at Georgia Tech, and then obtained a masters degree from the University of Cincinnati. After that, he came to MSU, where he completed his Ph.D. in 2011. With his doctoral work generating so many interesting results and new questions, Zack stayed on here as a postdoctoral researcher. His current research is funded by a grant from the John Templeton Foundation Program on Foundational Questions in Evolutionary Biology.

Zack has devoted years to studying the evolution of the ability to grow on citrate that occurred in one of the 12 populations from the long-term evolution experiment (LTEE) with E. coli. We still don’t fully understand all of the steps involved. But a simple “on/off” switch it is not!

However, even if it had been a single, simple mutation that allowed the cells to grow on citrate, that still would have been evolution … it still would have been a beneficial mutation in the context of the experiment … and it would still have demonstrated the acquisition of new information encoded in the genomes of the bacteria that fits them to their environment. Of course, if it were so easy as a single, simple mutation, then we would have seen that capability evolve in many or all of the populations. But after almost 60,000 generations to date, only one population has evolved that ability.

You can read about the technical details of our findings in two papers here and here, as well as in a recent paper from a team at the University of Texas, Austin.

In what follows, the nomenclature Cit+ refers to the bacteria that evolved the ability to grow on citrate in the presence of oxygen, while Cit– refers to the bacteria – their ancestors and other E. coli – that lack that ability.

— Richard Lenski

* * * * *

My work on the evolution of aerobic growth on citrate in one of the LTEE populations has received a fair amount of attention over the years. (Sometimes there is a bit of a dream-like quality to it all. I still have a hard time conceiving that people unknown to me know about what this here kid from north Georgia has done.) The attention is rather gratifying because I’ve spent many years and a great deal of effort in school and in the lab to become an evolutionary biologist. But why did I do all that in the first place? Because I find evolution to be endlessly fascinating, beautiful, and even inspiring.

It means a lot to know that the work I spent several thousands of hours toiling away on has made a contribution to science. Even more satisfying is that my work has come to be viewed as a go-to example of evolution in action that may, perhaps, inspire in others some of the same feelings that have motived me.

Of course, this attention has also been a bit troubling because it has led to repeated disparagement, dismissal, distortion, and misrepresentation of my work by both professional and amateur creationists. These creationists often get entirely wrong the work my colleagues and I toiled long and hard to do, likely because they haven’t bothered to read our papers, learn the details and methods, or think much about the results. (I suspect some duplicity is in there, too.) Reflexive, unthinking dismissal bothers me – maybe because my parents and devoutly Southern Baptist Granny told me when I was a child that this is something that civilized folk simply should not do.

This brings me to the recent debate between the legendary science educator Bill Nye and the legendary obfuscator and anti-science showman Ken Ham. It was the standard sort of set-up, with Nye defending evolution and science against creationism, and Ken Ham, well, doing what Ken Ham does.

Twice during the debate, Ham discussed my work with the LTEE population that evolved the capacity to grow aerobically on citrate. The first time was at about 44 minutes, and included a video clip of Dr. Andrew Fabich, a “Biblical creationist” microbiologist at Liberty University. [You can read the transcript here.]

The evolution of the new Cit+ function is, and has been discussed as, an instance of evolutionary innovation that arose in a controlled experiment in which we can drill down and figure out how it evolved. Ham and Fabich, however, dismissed Cit+ as an innovation or even an instance of evolution using two arguments suggesting that neither knows the work well at all and likely have not read our papers. (In Ham’s case, this wouldn’t be surprising, as he has been called “willfully ignorant” even by other creationists, which is a bit like being called unkempt by Pig-Pen or in need of a haircut by Cousin Itt. In Fabich’s case, however, it would betray a lack of professional courtesy, at best.)

First, Ham repeatedly said that some of the bacteria in the LTEE “seemed” to have developed the ability to grow on citrate. This wording suggests either stupidity or duplicity on our part, as though we either didn’t check or just lied, but the fact of the matter is that there is no “seem” about it. The Cit+ bacteria do grow on citrate, and they do so under conditions that E. coli normally does not. This ability is something that is easy to demonstrate, and which I and my colleagues – not only in the Lenski lab but also other labs that are now working with these bacteria – have documented. And it’s not as though we don’t have the evidence – as Rich has pointed out to another anti-evolution critic, we have many, many, many vials full of them in our freezers.

The second argument was more direct. Both Ham and Fabich asserted that the Cit+ function did not evolve because using citrate did not involve “any kind of new information … it’s just a switch that gets turned on and off.” (Fabich went on to state that this “switch” is what we reported. That is emphatically not true. It beggars belief that anyone, much less a trained microbiologist, could actually read our 2012 paper, where we reported the genetic basis of Cit+, and come away thinking this.) Variations on that wording are often used by creationists who discuss the citrate work because it implies that Cit+ arose because of a pre-existing regulatory switch and involved no evolution at all. But that simply is not the case – that wording, dare I say it, is a lie.

If you take E. coli from a medium in which it is growing on glucose, and move it into a medium where the only thing to eat is something else, like lactose, it turns off the expression of some genes specific to growth on glucose, and it turns on other genes necessary to grow on lactose. That is what is called gene regulation, and that is what biologists mean when they talk about switching functions on and off – existing genetic circuitry that allows an organism to respond to changes in the external and internal environment. If you transfer normal, Cit– E. coli from a glucose medium to a medium with only citrate to eat, they don’t grow. They just sit there and starve. Regular E. coli cells have no existing genetic regulatory circuitry that “flips a switch” to allow them to start growing on citrate in the presence of oxygen. On the other hand, if you do the same thing with the Cit+ cells that evolved in the long-term experiment, the Cit+ cells will start growing happily on citrate. This difference is not a matter of gene regulation, but an evolved difference between the ancestral strain and the Cit+ lineage that allows Cit+ cells to grow on citrate.

No, the ability to grow on citrate is not a matter of simply flipping a pre-existing regulatory switch. Continuing the electrical metaphor, the evolved Cit+ function is instead about rewiring. My dear little Cit+ cells gained their ability to partake of the previously forbidden citrate by a genetic duplication involving a gene, called citT, which encodes a transporter protein that is used during anaerobic growth on citrate.

This duplication did something very special. You see, one of the major aspects of gene regulation is that genes have associated regulatory DNA sequences, including what are called promoters that control when genes are expressed. The citT gene is normally controlled by a promoter that tells the cell to turn it on only when there is no oxygen present. As shown in the Figure below, the gene duplication put one copy of citT next to, and under the control of, a promoter that normally controls another gene called rnk. The rnk gene is normally turned on when oxygen is present. The new association between citT and the rnk promoter – what we call the rnk-citT regulatory module – turns citT on when oxygen is present, and allows Cit+ cells to use citrate under the conditions of the LTEE. (To really feast on the citrate involved additional evolutionary changes, both before and after this rewiring, but I’ll leave that point aside for this post.)

There is a very interesting consequence of how the rnk-citT module originated. While Ham did not make this argument, other creationists have asserted that Cit+ arose simply by a loss of gene regulation, because they have the notion that evolution can only break things. However, the duplication that gave rise to the rnk-citT module caused no such thing. There is still a copy of citT that is linked to the same adjacent DNA sequence as before, and there is still a copy of rnk that is under the control of its own promoter. In other words, the cell got something new without losing anything old.

When they actually bother to explain all of that, creationists still dismiss Cit+ as being an instance of evolutionary innovation because it involved the rearrangement of existing components. True, the duplication responsible for Cit+ did rearrange components that were already there, but that rearrangement generated a new association between components that did not previously exist, and it produced a new function that also did not previously exist. To argue that rearrangements cannot produce innovation is akin to arguing that a novelist has done nothing creative in writing her novels because she only used words that already existed.

Shrunk wrote:

The evolutionary origin of orphan genes

Nature Reviews Genetics 12, 692-702 (October 2011) | doi:10.1038/nrg3053

Diethard Tautz & Tomislav Domazet-Lošo

Abstract

Gene evolution has long been thought to be primarily driven by duplication and rearrangement mechanisms. However, every evolutionary lineage harbours orphan genes that lack homologues in other lineages and whose evolutionary origin is only poorly understood. Orphan genes might arise from duplication and rearrangement processes followed by fast divergence; however, de novo evolution out of non-coding genomic regions is emerging as an important additional mechanism. This process appears to provide raw material continuously for the evolution of new gene functions, which can become relevant for lineage-specific adaptations.

http://www.nature.com/nrg/journal/v12/n ... g3053.html

Just reading this now. So far, no mention of orphan genes being magically created by Jesus as a viable hypothesis, and from the title and the abstract I don't expect that to be included. But I'll let everyone know if it comes up...

Rumraket wrote:

jamest wrote:

MarioNovak wrote:
Well, the biggest scientific observations of evolution in action is E. coli evolution experiment. On February 24, 1988. Richard Lenski and his team at Michigan State University embarked on an ongoing long-term evolution experiment. He started 12 genetically identical lines from a single strain of E. coli. The bacteria reproduced every few hours. The populations reached the milestone of 50,000 generations in February 2010 and 60,000 in in April 2014.
So, what did Lenski experiment show? How many new genes evolutionary processes created after 60,000 generations?
Well, the answer is 0, - ZERO. Most of the changes in this experiment involved streamlining the genome, deleting genes no longer needed, or reducing protein expression.

Were the bacteria all maintained within the same unchanging environment?

Yes. In other words, everything they carried of genes to survive in their natural environment (the mammalian gut) was eventually discarded through the accumulation of mutational deletions, because the environment to which they were introduced and subsequently adapted never changed and only contained a select few nutrients. So they naturally lost all the additional capacities they had that were not related to doing well in this particular environment.

What happened was as expected, they became much, much better at working well in this new environment. For evolutionary novelty to happen there needs to be the opportunity for novelty. The environment must be changing and fluctuating, new types of nutrients must occasionally enter it and so on. None of these conditions were part of the experiment. So the Long term evolution experiment with E coli has so far basically been an experiment in the ability of natural selection to streamline a single organism to function extremely well under one single living condition.

Fenrir wrote:

MarioNovak wrote:...snipped some whimpering...
"Evolutionary book" will not change the results of experimental science which shows total impossibility of random mutation and natural selection to create a new genes.

That's all well and fine, now all you need to do is actually link some genuine experimental science which shows, or even suggests, any such thing.

I suspect I have quite a wait ahead of me.

jamest wrote:Makes you wonder why Lenski didn't extend his experiment accordingly.

MarioNovak wrote:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3461117/

Have you ever heard of the terms like logic or rational?

The evolutionary community get all excited when Lenski discovered changes that involved moving one pre-existing gene from one location to another. They refer this as a "key innovation", and a "fascinating case of evolution in action".

If moving one pre-existing gene from one location to another is "key innovation", in the longest evolution experiment, what can you rationally and logically conclude: did experiment produced new gene or not?