“Our experiments show how biological complexity can evolve though simple, high-probability genetic paths,” said Thornton, who served as co-senior author. “Before the last common ancestor of all animals, when only single-celled organisms existed on Earth, just one tiny change in DNA sequence caused a protein to switch from its primordial role as an enzyme to a new function that became essential to organize multicellular structures.”
Let’s hope filling this gap creates two more, either side of it!
Posting in bad faith is not against the rules, Phoodoo.
The OP has nothing to say of relevance to intelligent design. Is there somewhere hidden in all the snark in this thread a comment that discusses the OP and it’s relevance to intelligent design?
I’d hate to think someone was posting in good faith and I missed it.
Of course it does. The claim of ID in general is that the evolution of biological complexity is beyond the reach of naturalistic and unintelligent processes.
In fact your yourself have stated that you believe evolution is statistically impossible.
But if said biological complexity is actually the result of highly probable, simple genetic changes, that has implications for the anti-naturalist claims of ID.
In this respect the OP is evidence against that particular prong of the case for ID. It does not disprove that there was never any ID anywhere, rather it is evidence against the idea that ID is required.
And you took that literally. 🙂
How much complexity was added?
Another vindication of Behe. Could have been ripped right from the pages of DBB. And that was twenty years ago. Such progress.
It turns out, for one specific function at least, it most likely came down to dumb luck.
Got to love a theory that’s based on “dumb luck.” Modern science at it’s finest. It just happened, that’s all. The anti-ID crowd believes in the power of dumb luck, and that’s for some reason I’ve yet to fathom more reasonable than intelligent design.
Yes. that’s the sound of snickering you hear.
Do you have good intuitive measure? A new function evolved, the mutation conferred a capacity the cells did not have before. Quantify that however you want, just make sure you apply that measure consistently across all of biology.
You’re the one who started blathering about a book you hadn’t read to try to support your claim, but I congratulate you on your maturity here. Not many peolple would have had the courage to concede like you did.
Bingo.
Powerball.
What claim of Behe’s do you think is vindicated specifically?
Nobody actually believes “it just happened” without any preceding physical causes, this is a caricature you’re now inserting for rethorical reasons to try and downplay the results. But a caricature it is.
Are you denying that it is the case that single mutation could radically alter the function of the protein in question? If that’s not lucky, then what is it? Do you believe the world has been somehow set up such that at some point in the future, that mutation would have this particular effect in this particular protein?
Through “molecular time travel” experiments, they not only deciphered the sequence of the ancestral gene for this protein, they resurrected it in the laboratory to study how it functioned roughly one billion years ago.
What’s next then, wormholes? Why not.
The study, published in the journal eLife on January 7, 2016, is the first to experimentally describe a molecular mechanism involved in the evolution of multicellularity, and establishes a paradigm for research in evolutionary cell biology and the origins of complex life.
The first. I see a Nobel Prize coming.
What do you mean? Your question makes no sense in the context of what you quote.
Virtually nothing is known concerning the mechanisms and dynamics by which fundamentally novel protein functions evolve.
Doug Axe vindicated.
Are you all sure this paper is anti-ID?
Mung,
‘Cos he aims to keep it that way!.
Mung,
I don’t think defeating ID was its motivation, no. But a single residue change, on a reconstruction based entirely on conventional evolutionary assumptions, that leads to a complete and significant change of function – doesn’t really fit with the general run of ID expectations, if we discount the hopelessly vague (there’s got to be something left!).
Well, Allan, if you’re satisfied with a sample size of one, I am certainly not one to argue.
I haven’t completed reading the paper. It’s long and, for me, complicated. Did they actually evolve a protein? I think I recall reading something about cultures and choanoflagellates and flies.
From the hype:
How do they know that this is what actually took place?
Are people here satisfied with the “it could have happened therefore it did happen” sort of “logic” that seems to permeate evolutionary “reasoning”?
You have to understand what ancestral sequence reconstruction actually is. That’s how you know. I also recommend you read the paper, because they speak about the undertainty of the results and the work they do to ensure it’s not just some kind of fluke.
Mung:
Are people here satisfied with Mung’s “I don’t understand this stuff but I’ll bet it’s wrong” approach to science?
No, they didn’t actually evolve a protein. They reconstructed an ancestral protein from which extant proteins evolved. This is what ancestral sequence reconstruction is. The math is quite complicated and I can’t tell you in detail how it works (maye somebody like John Harshman or Joe Felsenstein is your best bet around here), but at a basic level they compare the sequences of extant proteins and use statistics to try to infer what the most probable ancestral state of the protein must have been, using maximum likelihood phylogenetic trees.
In this way, they can reconstruct the evolutionary history of the protein further and further back in time, mutation by mutation. When they have reconstructed these sequences in software, they then go into a lab and synthesize them biochemically, and then do various chemical assays to see if they actually work and how they work. When they do this, they are actually empirically testing the evolutionary postulate, that the extant proteins even DO have an evolutionary history, that they DID have ancestors and that those ancestral proteins had modified or different functions.
If they find that their reconstructed protein actually functions at all, and if they find that the further back in time the reconstructed state, the more altered the function, that is a good indication that these proteins really did actually evolve in the way they have reconstructed, because there’d be no a priori expectation you can use a statistical method to determine historical mutational states through sequence comparisons and just so happen to produce a functional protein with gradually more altered functions, using basic assumptions about how evolution proceeds at the molecular level (least character state changes).
No, if that was REALLY how they thought, I would not be satisfied with it. But that is emphatically NOT how they work.
Mung,
Dumb luck appears to largely govern precisely which two organisms mate, which determines the genetic combinations that they produce on meiosis, which can have a significant effect on evolution. It also causes one neutral allele among N to become fixed, despite no selection operating.
Now, one could say that intelligent design is a superior explanation, in which case every mating is written in the stars, and every neutral fixation was not neutral at all – the entire allele’s progress (which superficially appears to involve a lot of chance events) was guided. A lot of intelligent tinkering to achieve something that would happen anyway.
So I don’t see any fundamental reason, given that probabilistically something must happen, to say that what did happen was intelligently caused. YMMV, but I hope this helps you to fathom one of the the reasons, using non-selective, non-mutational scenarios as an example.
Mung,
No indeed, you seem very satisifed with Axe’s handful of negative results on the opposite tack.
They took modern proteins assumed to be commonly descended, and used an algorithmic method to reconstruct the assumed common ancestor protein. It was a matter of ‘reversing’ evolution back to the node.
Mung,
They inferred the ancestral sequence from the modern sequences. They might have got it wrong, but it’s unlikely to be something completely different. All the clues in modern proteins restrict the set of possible (rather, likely) ancestral sequences. It’s not a conjuring trick, and it’s not design.
Mung,
More like “You say that it could not have happened; here is some evidence that it could”. One can attempt to reconstruct history and reduce the set of things that could have happened to those that can reasonably be inferred to have happened if only certain causes were in operation.
There is some confusion between history and future in a lot of criticism. It’s impossible to tell where the drunkard will go next, but he may leave clues as to where he’s been, and restrict the entire space of prior possibility.
I would go further than that. In the case of ancestor reconstructions, they’re evidence that they DID happen.
I don’t know if this is a lot to ask, but I wonder if some of the in-the-know people around here(Harshman, Felsenstein?) could be bothered to explain with the simplest possible example, how an ancestral node in a tree with three branches, is inferred? How does the logic work? What is the reasoning employed?
Say we have three sequences: A, B and C
A: TTTTTATTCCCG
B: TTTTTTTTCCCG
C: AATTTTTTCCGG
I don’t know if these sequences could be used, I made them up such that A and B are supposed to be more closely related to each other than they are to C. Use a better example as you wish of course, I’d be interested in understanding the method better myself.
Perhaps Mung can tell us if he knows who his real parents are and how he knows.
First, you need a model of evolution, i.e. what the probability is of transformation from A to G, A to C, etc. per unit time. From this you can determine the likelihood of seeing the data you have at each site, given any particular set of branch lengths and any particular base at that site in the internal node. You pick the set of branch lengths (in units of probability of change) and the sequence at the internal node that maximizes that likelihood. If that internal sequence gives the observed sequence much higher probability than any other internal sequence, you can be reasonably confident in the inference. (A likelihood is a conditional probability, in this case the probability of observing the data given the model, including branch lengths and internal states.)
In the particular set of sequences you provide, I imagine that most models would determine the sequence at the internal node to be TTTTTTTTCCCG with a much greater likelihood than anything else.
I failed to notice that you consider the tree to be rooted. That gives us two internal nodes. I don’t think there is a way to estimate the sequence at the root node (the ancestor of all three species) without using a model that assumes a molecular clock, or assumes some of the branch lengths a priori. But with the usual models you can estimate the sequence at the A, B node in the same way I explained above. The usual models consider reversible evolution — that is, the probability of changing from A to T is the same as the probability of changing from T to A — and thus there is no arrow of time and all trees are considered unrooted. The root can be located on a particular branch, but there’s no way to decide where on that branch it lies.
Thanks a lot John that clarified it a bit, still not something that’s easy to really get a good intuitive grasp of I would say. I suspected the bit I take to be about substitution models (that is what you mean by “probability of transformation”, right?) would be part of it, otherwise I couldn’t see how it would be possible to infer what positions are more likely to have changed than others.
This sentence is almost opaque to me:
Can you clarify?
That remains to be seen. But I’ll try. What we’re trying to compute is the conditional probability of observing the data we do given a particular sequence at the internal node, the lengths of the three branches, and the substitution model. That conditional probability (likelihood) can be compared among internal sequences, etc. We prefer the internal sequence that gives the observed data the highest likelihood. (For any given internal sequence there is one combination of branch lengths that produces the highest likelihood, and that’s the only one we consider; and let’s think of the substitution model as fixed, so the internal sequence is the only variable.) If that internal sequence gives the data a much, much higher likelihood than any other, then we prefer it a lot and can consider a good estimate of the true ancestral sequence.
Was that better?
Much, already at the first sentence. Thank you.
It’s amazing how much one can learn just by asking, instead of trolling and saying “designdidit” and then thinking to yourself that disagreement is because your interlocutor secretly hates god.
That is known as Gish’s law, after Duane Gish.
Same way as most people, by faith. I rely on the testimony of others. I assume they are honest.
Mung,
23andMe allows you to trust, but verify. My folks are my folks, but we found out something interesting about my paternal grandfather’s parents.
Faith isn’t reliance on testimony.
Personally I have evidence that my parents are my parents. We clearly have physical and behavioral traits in common. In addition to the fact that they tell me I am their parents. None of this is faith. I also have evidence that my parents are generally honest, so I don’t have to assume they are.
I ask about parents because genetic testing reveals that a surprising percentage of parents lie.
Actually, DNA surprises don’t necessarily indicate infidelity. People are finding out about secret adoptions, out-of-wedlock births, and such. I suspect that as the ancestry databases accumulate genetic data, most people will find a surprise, if they go back six or eight generations.
So?
So your statement seems to contain a contradiction.
Unicellular and multicellular Organisms are best explained through design
http://reasonandscience.heavenforum.org/t2010-unicellular-and-multicellular-organisms-are-best-explained-through-design
Proponents of evolution claim like a mantra, that micro evolution leads to macro evolution, and no barrier exists which hinders the transition from one to the other, which last not least explains our biodiversity today.
The emergence of multicellularity was supposedly, a major evolutionary leap. Indeed, most biologists consider it one of the most significant transitions in the evolutionary history of Earth’s inhabitants. “How a single cell made the leap to a complex organism is however one of life’s great mysteries.”
Macro evolutionary scenarios and changes include major transitions , that is from LUCA, the last common universal ancestor, to the congregation to yield the first prokaryotic cells, the associations of prokaryotic cells to create eukaryotic cells with organelles such as chloroplasts and mitochondria, and the establishment of cooperative societies composed of discrete multi-cellular individuals. Or in other words : The current hierarchical organization of life reflects a series of transitions in the units of evolution, such as from genes to chromosomes, from prokaryotic to eukaryotic cells, from unicellular to multi cellular individuals, and from multi-cellular organisms to societies. Each of these steps requires the overcome of huge hurdles and increase of complexity , which can only be appreciated by the ones, that have spend time to educate themselves, and gained insight of the extraordinarily complex and manifold mechanisms involved. The emergence of multi-cellularity was ostensibly a major evolutionary leap.
The switch from single-celled organisms to ones made up of many cells have supposedly evolved independently more than two dozen times. Evolution requires more than a mere augmentation of an existing system for co-ordinated multicellularity to evolve; it requires the ex nihilo creation of an entirely new system of organisation to co-ordinate cells appropriately to form a multicellular individual.
There is a level of structure found only in multi-cellular organisms: intercellular co-ordination. The organism has strategies for arranging and differentiating its cells for survival and reproduction. With this comes a communication network between the cells that regulates the positioning and abundance of each cell type for the benefit of the whole organism. A fundamental part of this organisation is cellular differentiation, which is ubiquitous in multicellular organisms. This level cannot be explained by the sum of the parts, cells, and requires co-ordination from an organisational level above what exists in individual cells. There is a 4-level hierarchy of control in multicellular organisms that constitutes a gene regulatory network. This gene regulatory network is essential for the development of the single cell zygote into a full-fledged multicellular individual.
If evolution and transition from unicellular to multi cellular life is exceedingly complex, the chance that it happened once is also exceedingly small. That it happened multiple times separately, becomes even more remotely possible. Convergent evolution of similar traits is evidence against , not for evolution. In order to infer that a proposition is true, these nuances are important to observed. The key is in the details. As Behe states : In order to say that some function is understood, every relevant step in the process must be elucidated. The relevant steps in biological processes occur ultimately at the molecular level, so a satisfactory explanation of a biological phenomenon such as the de novo make of cell communication and cell junction proteins essential for multi-cellular life must include a molecular explanation.
The cells had not only to hold together, but important mechanisms to stick the cells together had to emerge, that is, the ability of individual cells to associate in precise patterns to form tissues, organs, and organ systems requires that individual cells be able to recognize, adhere to, and communicate with each other.
Of all the social interactions between cells in a multicellular organism, the most fundamental are those that hold the cells together. The apparatus of cell junctions and the extracellular matrix is critical for every aspect of the organization, function, and dynamics of multicellular structures. Animal cells use specialized adhesion receptors to attach to one another. Many of these adhesion proteins are transmembrane proteins, which means the extracellular portion of these proteins can interact with the extracellular portion of similar proteins on the surface of a neighboring cell. Although diagrams of adhesive structures may suggest that they are static once assembled, they are anything but. Cells can dynamically assemble and disassemble adhesions in response to a variety of events. This seems to be a essential requirement for function right from the beginning of multicellularity. Many adhesion proteins are continuously recycled: Protein at the cell surface is internalized by endocytosis, and new protein is deposited at the surface via exocytosis. The molecular machines to exercise these functions therefore had to emerge together with adhesion proteins. Furthermore, cell adhesion is coordinated with other major processes, including
1.cell signaling,
2.cell movement,
3.cell proliferation, and
4.cell survival.
We now know that cell-cell adhesion receptors fall into a relatively small number of classes. They include
1.immunoglobulin superfamily (IgSF) proteins,
2.cadherins,
3.selectins, and, in a few cases,
4.integrins
In order to explain multicellularity, its origin must be explained .
http://reasonandscience.heavenforum.org/t2187-cell-junctions-and-the-extracellular-matrix
Thus, the apparatus of cell junctions and the extracellular matrix is critical for every aspect of the organization, function, and dynamics of multi cellular structures. The arise of adhesive junctions, tight junctions and gap junctions, and how they emerged is therefor a key factor to explain multi-cellular life. The cells of multi-cellular organisms detect and respond to countless internal and extracellular signals that control their growth, division, and differentiation during development, as well as their behavior in adult tissues. At the heart of all these communication systems are regulatory proteins that produce chemical signals, which are sent from one place to another in the body or within a cell, usually being processed along the way and integrated with other signals to provide clear and effective communication. The arise of these communication channels had to arise together with junction mechanisms in order to establish successful multi cellular organisms. One feature without the other would not have provided success and advantage of survival.
The ability of cells to receive and act on signals from beyond the plasma membrane is fundamental to life. This conversion of information into a chemical change, signal transduction, is a universal property of living cells. Signal transductions are remarkably specific and exquisitely sensitive. Specificity is achieved by precise molecular complementarity between the signal and receptor molecules.
Question : signal transduction had to be present in the first living cells. How could the specificity of the signal molecule , and the precise fit on its complementary receptor have evolved ? or the Amplification, or the desensitization/adaptation, where the receptor activation triggers a feedback circuit that shuts off the receptor or removes it from the cell surface, once the signal got trough ?
Three factors account for the extraordinary sensitivity of signal transducers: the high affinity of receptors for signal molecules, cooperativity (often but not always) in the ligand-receptor interaction, and amplification of the signal by enzyme cascades. The trigger for each system is different, but the general features of signal transduction are common to all: a signal interacts with a receptor; the activated receptor interacts with cellular machinery, producing a second signal or a change in the activity of a cellular protein; the metabolic activity of the target cell undergoes a change; and finally, the transduction event ends. This seems to be a irreducible system, requiring high content of pre-programming and advanced coding.
http://reasonandscience.heavenforum.org/t2181-cell-communication-and-signalling-evidence-of-design
Question : how did the high affinity, cooperativity and amplification have emerged ? Is a preestablished convention not necessary, and so a mental process to yield the function ? Is trial and error or evolution not a completely incapable mechanism to get this functional information system ?
This is a important, essential and fundamental macro evolutionary change, and the explanation of macro-evolution must account for these changes, and provide feasible possible and likely ways through mutation and natural selection. Beside this, a shift on several levels of biological organization had to occur, providing a considerable advantage of survival, considering that for example one of the first cooperative steps required for the evolution of multicellularity in the volvocine algae was the development of the extracellular cell matrix from cell wall components, which can be metabolically costly to produce. But much more is required.
Ann Gauger: New genes and proteins must be invented. The cytoskeleton, Hox genes, desmosomes, cell adhesion molecules, growth factors, microtubules, microfilaments, neurotransmitters, whatever it takes to get cells to stick together, form different shapes, specialize, and communicate must all come from somewhere. Regulatory proteins and RNAs must be made to control the expression in time and space of these new proteins so that they all work together with existing pathways.In fact, in order for development to proceed in any organism, a whole cascade of coordinated genetic and biochemical events is necessary so that cells divide, change shape, migrate, and finally differentiate into many cell types, all in the right sequence at the right time and place. These cascades and the resulting cell divisions, shape changes, etc., are mutually interdependent. Interrupting one disrupts the others.
And last not least:
Like engineers carefully blowing up a bridge, cells have intricate, programmed suicide mechanisms. Without apoptosis, all multicellular life would be impossible. Good luck to proponents of evolution to explain how it emerged……..
http://reasonandscience.heavenforum.org/t2193-apoptosis-cell-s-essential-mechanism-of-programmed-suicide-points-to-design