Moderator’s remark: this post is long enough to need a “more” tag. But the wordpress editor will only allow me to add that at the very beginning or the very end. So here it is at the very beginning.
- “Nested hierarchies” or “cladistic analysis” or “consilience of independent phylogenies” is often offered as support for Darwinist evolution. This is the idea that the “tree of life” classification of organisms is somehow objective despite being a creation of very zealous “evolution” advocates. The three basic assumptions of cladistics models are: a) Any group of organisms are related by descent from a common ancestor (UCD – universal common descent); b) There is a bifurcating pattern of cladogenesis; c) Change in characteristics occurs in lineages over time. Although not explicit, UCD (“descent from a common ancestor”) here means by a Darwinian “natural selection mechanism” and not by a process generated by a designer that also happens to make use of biologic reproduction.
- No assumption can be tested by the model that uses them. That is why they’re called ‘assumptions’ and not ‘conclusions’. Instead, assumptions have to be tested independently through an entirely separated method or be accepted as axioms. An UCD “mechanism” has never been observed or proved elsewhere and is not “self-evidently true”, therefore not a valid axiom. Because UCD is an assumption in “cladistic analysis”, it cannot be logically also a conclusion of any such analysis. Furthermore the conclusions of any “cladistic analysis” will always and trivially be compatible with the UCD assumption in that model.
- Hypothesis testing requires an alternative (null) hypothesis and a procedure that demonstrates how the data available is compatible with the successful hypothesis and at the same time is statistically incompatible with the alternative hypothesis. In the “cladistic analysis” case, the alternative hypothesis to UCD is “common design”, and of course UCD cannot be an assumption of such an analysis. However this rule is violated twice, first by the use of an assumption also presented as conclusion, and second by the prejudiced rejection of the alternative “common design” hypothesis before analysis. This clearly demonstrates that “cladistic analysis” can never be logically used as proof of UCD. What “cladistic analysis” is instead is ‘curve fitting’ where the cladistics model is best fitted to certain (conveniently selected!) morphologic/biochemical/genetic biologic data points.
- The ‘designer’ hypothesis cannot fail against the ‘no designer’ (Darwinist evolution) alternative in a biologic comparative analysis as designers have maximum flexibility. This is not surprising as designers are free to incorporate whatever mechanism they want, including intelligent “selection” (human breeders do!) and “common descent” (human breeders do!) if they so desire.
- The claim that cars and other entities cannot be uniquely and objectively classified (“nested hierarchy”), while organisms can, is false. On one hand, we do know the history of the automobile, so a proper classification must be able to reconstruct their unique “evolution”. Yes, vehicle share parts, so to get to the actual development tree, we must group them differently than organisms since mass production works differently than biologic reproduction. On the other hand, organisms may not be uniquely classified as demonstrated by the numerous revisions and exceptions to the “tree of life”, and in any case, “uniquely classified” is an absolute claim that can never be proven since it is impossible to compare the infinity of possible organism classifications.
- The claim that the “tree of life” based on anatomy is validated by the match with the tree based on biochemistry fails. Anatomy is not independent of biochemistry. Also, the oldest DNA ever found was 700k years old therefore any match between the independent trees is limited. This is not to say that the fossil record is complete, or that fossils can be positively linked to one another and the living without – once again – presupposing UCD. The claim that “there is no known biological reason, besides common descent, to suppose that similar morphologies must have similar biochemistry” is false as the ‘designer’ hypothesis produces the same result when one designer creates all morphologies, and furthermore “I cannot think of an alternative reason why…” is not a valid argument.
- A “tree of life” is an artificial human construct as organisms do not come labeled with their position in a cladistics hierarchical structure. To decide the position of a certain organism, the human creators of the “tree” have to decide which morphologic/biochemical/genetic characteristics to include and what weight to attach to each of those measures. This further supports the claim that “cladistic analysis” is ‘curve fitting’ rather than ‘hypothesis testing’ – if a tree must be built, a tree will be built as in this example: “The close relationship between animals and fungi was suggested by Thomas Cavalier-Smith in 1987, […] and was supported by later genetic studies. Early phylogenies placed fungi near the plants and other groups that have mitochondria with flat cristae, but this character varies. More recently, it has been said that holozoa (animals) and holomycota (fungi) are much more closely related to each other than either is to plants […].”
1. False. They’re both fake trees aka “best fit”, not “independent”. Fake cannot prove fake.
2. This is too retard again. Fossils can only be linked if one presupposes descent. Even between living, one has to presuppose descent or else it’s doppelgänger or whatever coincidence.
Yes, stats do not apply because not essential to the methodology: http://www.ucmp.berkeley.edu/clad/clad2.html – do a search for “statistic”. What are you, some kind of lawyer?
Methodology of a Cladistic Analysis
HOW TO CONSTRUCT CLADOGRAMS
Here is an outline of the steps necessary for completing a cladistic analysis. Don’t be fooled, however, by the simplicity of these steps. Seeing a real cladistic analysis out to fruition can be a difficult and time consuming task.
Choose the taxa whose evoutionary relationships interest you. These taxa must be clades if you hope to come up with plausible results.
Determine the characters (features of the organisms) and examine each taxon to determine the character states (decide whether each taxon does or does not have each character). All taxa must be unique.
Determine the polarity of characters (whether each character state is original or derived in each taxon). Note that this step is not absolutely necessary in some computer algorithms. Examining the character states in outgroups to the taxa you are considering helps you determine the polarity.
Group taxa by synapomorphies (shared derived characteristics) not plesiomorphies (original, or “primitive”, characteristics).
Work out conflicts that arise by some clearly stated method, usually parsimony (minimizing the number of conflicts).
Build your cladogram, which is NOT an evolutionary tree, following these rules:
All taxa go on the endpoints of the cladogram, never at nodes.
All cladogram nodes must have a list of synapomorphies which are common to all taxa above the node (unless the character is later modified).
All synapomorphies appear on the cladogram only once unless the character state was derived separately by evolutionary parallelism.
No, “these Darwinistas are particularly stupid” is the right answer. We’re not dealing with a generic curve fitting in cladistics, but this is too hard to understand for some.
Moved a couple of posts to guano
1. Are you trying to get me with “hybrids”? Nice try. Maybe when you explain to me what a “species” and “speciation” is.
2. I don’t pretend to know how biologic creation happened, but if it’s anything like human creation, we sometimes take one thing and modify it into another. We don’t always create from scratch.
3. I follow them very well, but – let me repeat because you didn’t see this: “you are stuck in the wrong frame of mind and can’t get out therefore keep asking senseless questions”
4. I am asking a hypothetical situation – how can this be senseless? How can you be SURE cats won’t be born from dogs EVER? Don’t you trust Science? More likely you’re afraid to answer.
Your answer is childish. You can’t define as you please what happened.
The question remains: “why one”?!? Why would all others dies? Why not “four or five” of them?!? Darwin let it slip.
Which he has carefully avoided linking to. Wouldn’t want to be seen as doing his job, I guess.
Interested readers can find the comments here. They’re from Nonlin.org.
Jock, you crack me up.
Sorry to clip your wings, but just about anyone can draw trees.
1. This is too retard. An admission of failure and an attempt to sweep it under the rug. Yes orbits can be observed – all you do is measure positions over a few cycles.
2. This is too retard. The whole exercise is very subjective.
3. There is no “proper statistical support”. UCD is an assumption
4. They don’t say anything about “better statistical procedures”. It’s just another subjective decision. And they don’t call the previous decision a “mistake” for the same reason – one subjective decision replaces another. And for the little fishes that keeps forgetting, not hypothesis but curve fitting.
He means the ‘Design’ hypothesis. We, humans, predict Design based on the evidence.
One thing is clear, “evolution” is an impossibility. Darwinism and its neo fails all tests:
Gradualism fails – http://nonlin.org/gradualism/
Natural selection fails – http://nonlin.org/natural-selection/
Divergence of character fails – http://nonlin.org/evotest/
Speciation fails – http://nonlin.org/speciation-problems/
DNA “essence of life” fails – http://nonlin.org/dna-not-essence-of-life/
Randomness fails – http://nonlin.org/random-abuse/
Abiogenesis fails – http://nonlin.org/warmpond/
Science against Religion fails – http://nonlin.org/philosophy-religion-and-science/
And let’s test it again and make sure it fails again and again: http://nonlin.org/evotest/
You don’t know it’s “junk” meaning “it has never served any purpose”. Because we, the designers, do sometimes leave what looks like junk in our products but in fact that “junk” has had a purpose sometimes during manufacturing. Makes sense?
I don’t even know that the technology is there to eliminate chunks of “junk DNA” from zygotes and confirm no negative effects. Do you?
What’s going? Am I intruding on a conversation? 😀
So, to paraphrase, you’re saying that you don’t know what analogies are.
Sorry, but that’s clueless again. The equilibrium population of genes is around 20,000, but many more than that come and go during phylogeny. In other words, there’s lots of gene turnover. Your “calculation” has nothing to do with any real numbers.
Gene duplication is one major thing you have forgotten. Most of the time, when a gene is duplicated, one copy ends up being superfluous and ends up being deactivated by deletion, stop codon, or whatever, after which it eventually suffers death by deletion, and the genome doesn’t care.
This is you having no idea what’s being discussed here.
You misread the quote. It’s only a few bits of the genome that are more closely related between orangutans and humans than either to chimps. A few more bits have chimps closer to orangutans than humans. But it’s a tiny percentage in each case. That results from incomplete lineage sorting, a well-known and inevitable phenomenon. You should learn something about the science you ridicule; save embarrassment, assuming you’re capable of embarrassment.
Why is this important to the calculation?
I can recognize poor ones.
John, none of you points make any sense. Lets take a break on this one.
I see you don’t know what unintentional irony is either.
The point is that if there’s constant gene turnover, the size of the standing population of genes is irrelevant to the number of gene losses.
How much turnover? What percentage of genes are involved in the turnover? Is their evidence that supports this?
Lots. Don’t know. Yes; pseudogenes, for example. Most genes don’t just disappear all at once, you know. They get inactivated and start accumulating deletions.
Grammatically, it means that a a gene family belongs in only one module. That doesn’t mean that each module has only one gene family Bill.
Scientifically, it means that the author doesn’t know much about modules, since genes in the same family can participate in different processes, thus different “modules.” However, again, they might be using the words differently to the way evolutionary biologists and genomicists do.
There’s a thing called copy number variation, for example. Due to that phenomenon, regions of chromosomes vary in, ahem, copy numbers among individuals of a single species. Quite often, these regions contain genes, thus the genes get to be in multiple copies, then reduced to a few copies, then all copies might be deleted, etc, etc. There’s plenty of evidence for this. As sequencing is becoming cheaper, more specific studies are been published. For example, a few ones have shown that copy number variation can happen among the cells of a single individual.
This is but an example. John might know of other phenomena besides CNV. I still hope this helps.
You are acting a bit paranoid here, don’t you agree? No, I was not going to mention hybrids. If you must know: I just want to make sure that at the end of the day, you are not going to change lions into domestic cats because, hey, “it’s just like tanning”. Can we now please agree that the variations within Felidae are true breeding? No strings attached.
Ahhhh, you named the M-word. Was it necessary that the modifications were introduced at once, or could they have been added piecemeal?
And … you … dodged the question … again. Are all Felidae related OR were the variations created de novo, using some generic cat as a template? Can you even tell the difference between these two scenarios?
I did read that, but – let me repeat my answer because you seem to have trouble getting this: “Just because you have a hard time answering my questions doesn’t make them senseless.”
And you DO have a hard time answering them, don’t you, mister I-don’t-pretend-to-know-how-biologic-creation-happened?
It is a senseless question because it is getting us nowhere. Yes, I am sure cats won’t be born from dogs, because that doesn’t comport with what we know about reproduction. Yes, I trust science (no need for capitalization, you can stop kneeling too). Now, what were you trying to accomplish with that question?
Nobody is doing that. It is possible that the LUCA never existed. Fact is: if you ask why there can’t be multiple LUCA’s you make yourself look silly. just sayin’
You see what I see. What I see is variations around a fixed theme. ONE theme. All life is one.
What have your links to do with falsifying “Design”? I suggest you try a statement along the lines of “Design theory predicts that we will observe A or that we will not observe B.”
nonlin.org should just relax a little and try to figure out what a comment is saying before dramatically replying to it. Here’s what happened in this case:
1. John Harshman wondered aloud whether there was anything that Design would not predict.
2. I said, in reply to John, maybe junk DNA, because the Design people get upset at the thought that it was there.
Note that I wasn’t answering anything by nonlin.org. Nor was I, in that comment, arguing for the existence of junk DNA. Just commenting on what Design advocates get upset by.
Nevertheless nonlin.org refuted me by … (wait for it) … getting upset at the thought that junk DNA was there.
When I was working in Aarhus, I attended a talk by Mikkel about his research on primate genomes. As John correctly surmised, he showed the regions discordant with the species tree to be the result of incomplete lineage sorting (In fact, that was when I learned the term).
That is impossible, because evolution conclusively shows that we are most closely related to bananas. Better watch out for those Orang Utans…
One more example of nonlin.org misreading comments and dramatically replying, without bothering to figure out what was going on. Just a lighthearted exchange between me and keiths about “curvy” trees, followed by keiths bringing up trees drawn in a circular layout, and noting that Denyse O’Leary had failed to understand those, followed by me saying I had talked about how to draw those circular diagrams in my book.
We’re talking about how you draw pictures of the tree, once you have inferred it. Inferring trees is not easy, and actually neither is drawing good and clear pictures of them.
How justifiable is the term “junk DNA”? It means noncoding DNA, right? But is it non-functional? Is it non-functional in the sense that it has no function whatsoever or in the sense that we have not found the function yet?
Does “junk DNA” entail no adaptive advantage? Perhaps there’s even disadvantage? If there is no selective or adaptive advantage, then how to explain the existence of junk DNA from the evolutionary point of view?
But if it has some function, then why keep calling it junk?
Junk DNA is non-functional, by definition. Non-coding DNA is DNA that does not code for a protein, but plenty of non-coding sequences are known to be functional (e.g. ribosomal RNA). If a sequence has a function that has not been found yet, it is not Junk DNA.
You are correct that Junk DNA entails no adaptive advantage. Junk DNA can still be accommodated by evolutionary theory however, because, with the notable exception of natural selection, evolutionary mechanisms do not require any (adaptive) function (mutation, migration, genetic drift).
Oh and, never, ever, post something like this on Larry Moran’s Sandwalk blog.
Is that the voice of personal experience speaking? 🙂
Absolutely, although it was John Harshman, not Larry, that corrected me on this 🙂
This is a fine question. As others have already said it’s a good idea to drop by Larry Moran’s blog. See this link for an overview of important literature on the topic: Required reading for the junk DNA debate.
With regards to how evolution can explain it’s continued existence if it is deleterious, this video touches on that subject(though it’s about other things too but i recomment watching all of it): Evolutionary Cell Biology: Two Origins, One Objective – Michael Lynch
It basically has to do with the interplay of the forces of genetic drift and natural selection, which in turn are significantly affected by the effective population sizes of the relevant species. At very large population sizes (like bacteria) natural selection is a very strong force and has the power to remove excess nonfunctional DNA because it has a bioenergentic cost (it takes energy to copy it). But in large multicellular eukaryotes effective population sizes are several orders of magnitude smaller so genetic drift becomes a more significant force, preventing the same level of selection that is possible in prokaryotes.
That’s why he’s here. 🙂
Genetic drift is whatever ends up in the offspring from the parents. Natural selection is the differential survival. Neither of them is a force by any stretch of the imagination or by any torture of logic. They are outcomes of a bunch of factors where chance plays a significant role.
But thanks for the references. I guess I will give the lecture a try.
If we look at figure 9 it looks like what you say is partially true. A gene family can be assigned to a single module or part of a larger module with other gene families. The family can appear in different modules on the dependency graph. Thanks for the discussion this is helpful.
Lots of assumptions here.
None of what John mentioned are assumptions. Besides being obviously expected phenomena, there’s plenty of documentation on “eroded” genes. We just talked about the pseudogene for vitamin C biosynthesis, remember? That’s an example of what John mentioned.
Neither of those statements is true. That makes you 0 for 6 on this subject. Can’t you draw some kind of lesson about your reading comprehension skills from that?
Yes, I remember. This is a piece of evidence for common descent if the gene turns out to truly be without function. How is it verified that the identified gene is without function?
There is also evidence against common descent and Johns comments are full of assumptions. One of those being that common descent is true. Another one that is almost certainly false is that there are lots of gene turnover as we see lots of gene preservation over time. He may make a reasonable point if he can quantify “lots”.
Darwin’s boys are so certain that 90% of human genome may as well not be there, as they view it as useless junk, that they are willing to put their own careers and lives on line…
Larry Moran of sandwalkblogpost.com for example is writing a book that will apparently solidify the junk 90% junk DNA dogma once and for all…
I hope Larry Moran can do some “junk DNA” knockout studies on his “relatives” to experimentally prove his faith…
Until then, the 90% human junk DNA dogma will remain in the realm of science-fiction or wishful thinking by evolutionists… just as where the evolution theory itself remains…
I clearly missed the relationship between gene families and modules and Entropy was kind enough to work me through this.
Do you want to continue your juvenile “put down” or are we done at this point?
No, he didn’t work you through it. You showed by your response to him that you didn’t understand what he told you, because you made two more similar mistakes. I just want you to realize that you are not understanding some very simple things. And you should use that as a clue that you may not understand some more complex things.
I told you I had rudimentary understanding of the paper. My purpose of discussing the paper is to understand it better. During our discussions in the past you have made errors also. I don’t believe you would make the claim that you have not made any errors.
There are many “complex things” I don’t understand as there are many “complex things” you don’t understand.
What I do understand is you are trying your best to argue from authority which is an indication that your position is weak.
What percentage of junk DNA do you think would be consistent with intentional design?
You can’t survive for an extended period of time without eating vitamin c.
Looking at the gene sequence, several exons are completely missing, one of them has a frameshift mutation leading to a premature stop codon, and IIRC the rest of the remaining exons have several mutations.
You can of course just decide to believe, for no good reason, that the gene still has some other undiscovered function. But what would that be based on other than a desperate excuse to deny common descent? Please notice how you are coming up with rationalizations, as in after-the-fact excuses to avoid this piece of evidence. Rather than just accept the evidence as-is, you rationalize it away with excuses.
No all of those have been observed. You keep ignoring when I point this out.
Bill, once again, there isn’t any mechanism postulated to account for the patterns seen in comparative genetics, that hasn’t been observed to also take place in the present.
It would be evidence for common descent whether it is functionless or not.
It is the particular patterns in the distribution of mutations in the pseudogene across a multitude of species that is evidence for common descent, not the mere fact that it is functionless.
It is the fact that the characteristics of those species already testify to their shared genealogical relationship, and that this particular gene mirrors that particular relationship in the mutations that affect it.
It is not just the fact that the gene is shared across species, but the particular patterns in the deactivating mutations yield the same branching relationship you get from thousands of other genetic loci, or from comparative anatomy.
This is one of those facts you have not been able to really get for a long time. That we are not just talking about the gene being merely similar in several species, but the patterns in the similarities. And that those same patterns in the similarities, are also reflected by many other genetic loci (among them many other pseudogenes).
No, there isn’t any evidence against common descent. There are genetic loci that can’t be used to infer common descent, and therefore aren’t evidence for common descent. But there are none which are evidence against common descent.
This is another in a long list of concepts you have a problem with. You don’t understand what evidence even is. What it means to say that a piece of data is evidence for, or against, or neutral with respect to a particular hypothesis.
No, that’s an evidentially derived conclusion. The evidence lead to common descent, and no evidence against it has been found.
Those two are not mutually contradictory. The fact that SOME fraction of genes are preserved doesn’t mean THE REST has to be. There’s zero conflict there. It isn’t even implied. Once again your objection fails outright at the level of reason. We don’t even get to discuss the actual evidence as your ability to even think about what that evidence could imply is lacking.
It is extremely difficult and tiresome to have these conversations with you when you are so bad at relatively straightforward logical reasoning. You are so obviously seeking to support a particular conclusion and it is affecting your ability to think rationally.
The mechanism being functionally observed and it accounting for the pattern are two very different things.
How long does it take for two mutations accounting for an adaption to get fixed in a population? Michael Lynch attempted to answer this. How long would it take two broken genes to be deleted and fixed in a population?
I am asking this rhetorically only.
True, but if it turned out to be a regulatory gene in embryo development it would also be evidence for common design.
Both hypothesis win hands down over the null hypothesis.
This shows a lack of objectivity. Convergent evolution among other things is evidence against all organisms being linked together only by reproduction.
This is a straw-man.
I will admit that I don’t remember any. Remind me.
If you think I’m making an argument from authority, you don’t understand either what my argument is or what an argument from authority is. The problem isn’t that you don’t understand complex things; it’s that you don’t understand the simplest things, as shown by your inability to read Figure 9. Stop being so defensive and admit it to yourself.