It isn’t my model. It is THE model. In THE model, a mixture of bird and mammal features would be a violation of the nested hierarchy. You are saying (at least for this moment in time) that there is no reason why separately created species could not have a mixture of bird and mammal features.
So we have two models. Common descent predicts a nested hierarchy. Separate creation does not. What do we see? A nested hierarchy.
A dependency graph is not a nested hierarchy. This was explained by Ewert over and over and over and over.
Fish and octopus share the same environment, and yet one has a forward facing retina and one has an inverted retina.
Based on what evidence???
So you don’t have a mechanism. All you have is bald assertions.
HOW???
CpG mutations are random mutations. You have yet to cite a single observation of a non-random mutation.
What about the rest of the genes? What about the rest of the exons and introns in that very gene?
Those are random mutations. That same process produces neutral and detrimental mutations. There is no guidance of the process towards specific mutations at specific bases in response to a specific stimulus from the environment.
Terrestrial, cold-blooded, inverted and everted retina - wolf spider[1]
If the difference between eye retinal arrangements is due to environmental design requirements and/or thermoregulation, why do spiders have both types? Does the top of their head inhabit a different environment to the side of their head? Is their head part warm-blooded and part cold-blooded?
@Meerkat_SK5 is thrashing around wildly because he has no responses available except to misinterpret the questions.
You are hopelessly confused. You claimed that the differences in the retinas of cephalopod and human eyes were due to the requirements of their different environments. @T_aquaticus pointed out that fish, which live in the same environment as cephalopods, have the same sort of eyes as humans, notably that inverted retina. Yet under your theory as expressed, we would expect fish eyes to be like cephalopod eyes. Instead, we see that eyes fit into a nested hierarchy, with vertebrate eyes being similar regardless of environment. Massive fail for common design.
No, not true. It contained some of the genes, not all of them. (I assume you meant to say “development” rather than “evolution”, since there are no genes that direct evolution.) But new genes arise all the time in evolution, and old genes are lost. No single-celled organism has even a single HOX cluster, for example, while every teleost has seven.
That potential seems minimal, since most 3rd position transitions do nothing, and most 2nd position transitions are selected against. Assuming you’re talking about protein evolution. I will point out that there is exactly zero evidence for this postulated “front-loading”.
Not a single one of them means what you imagine it does.
A citation must be sufficient to enable the reader to find the cited publication. I find it hard to believe that any of this is your own words too. I also find it hard to believe that any of those publications actually says what you claim it does.
That too doesn’t say what you think it does.
No. It’s your job to provide it. It’s also your job to show when you’re quoting. You’ve been called out on all this many times.
Thanks, God. But that’s nonsense. Cancer is the failure of apoptosis. Hey, what’s the divine function of river blindness?
So you can’t defend your claims. You should probably retract them.
You are confusing separate creation with common design. They are not the same thing. Here let me explain my model in more detail. But, as you read, don’t forget that HGT creates phylogenetic patterns as well:
3.8 billion years ago, there were viruses that contained all the genes to make certain evolutionary trajectories more likely for the formation of basic types.
Within the deep-sea hypothermal vents of the primitive earth, these viruses were naturally selected into different species of unicellular organisms, which underwent a heavy amount of HGT.
Then, the designer used HGT and cytosine deamination to develop basic types from different locations and times around the globe. These basic types would branch into diverse progeny to deliberately pioneer environments of the globe over long epochs of time
As a result, we would see biochemical and morphological similarities among all living things. More importantly, we would expect to see nested hierarchies extending back into the deep past.
Sorry for the confusion but I was not necessarily using or referring to Ewert’s specific model. Instead, I was more so using the rationale that he used to explain nested patterns. I was merely suggesting that the unity of nested patterns do not imply that organisms are related to other organisms. Instead, organisms are dependent on other organisms.
Based on this experiment showing how self-replicating RNA molecules could “evolve into complex living systems by expanding their information and functions open-endedly":
" As we have presented it here, the key distinction between the origin of life and other ‘emergent’ transitions is the onset of distributed information control, enabling context-dependent causation, where an abstract and non-physical systemic entity (algorithmic information) effectively becomes a causal agent capable of manipulating its material substrate "
…Purely analogue life forms could have existed in the past but are not likely to survive over geological timescales without acquiring explicitly digitized informational protocols. Therefore, life forms that ‘go digital’ may be the only systems that survive in the long-run and are thus the only remaining product of the processes that led to life. " [emphasis added]
What about them? I was just trying to provide an example that disproves your claim.
It is too technical for me to explain it in my own words. So here is Mike Gene:
"There are two primary points of focus where C-T transitions may exert their effect. The first revolves around genomic organization, as a drift in the C-to-T direction may play a role in modifying the genome’s system architecture.
The second design principle that may be involved focuses on the small-scale coding effects of C-T transitions. I count 37 different codons that contain cytosine. A single C-T transition expands this set to 48 codons (since some of the original codons had two or more C’s). Of the 48 substitutions, 17 are silent (not changing the amino acid sequence). Among the 31 changes, 4 introduce premature stop codons (nonsense mutations) and 27 result in amino acid changes (missense mutations). "
Here it is again, but with emphasis added:
"In conclusion, it appears that the mutational processes which drive evolution are not random, but rather are the result of properties of the DNA itself in combination with functional constraint at the protein level. "
“Our discovery yields a new account of the forces driving patterns of natural variation, challenging a long-standing paradigm regarding the randomness of mutation and inspiring future directions for theoretical and practical research on mutation in biology and evolution.”
"For over a century, the leading theory of evolution has been based on random mutations. The results show that the HbS mutation is not generated at random but instead originates preferentially in the gene and in the population where it is of adaptive significance,”
“Nevertheless, we show how an association of repair with transcription or chromatin-associated proteins could overcome the drift limit and lead to non-random hypomutation along the genome in most organisms.”
Mike Gene offers a reason for why C-T transition may be this way now:
"The ability for C-T transition to unmask front-loaded states may have long ceased to exist. Such a dynamic may have been crucial to some early events in evolution, yet given these states may have dissipated (the proximal objectives were reached), current mutations may no longer reflect any detectable design bias . In such a case, the current predominance of C-T transitions (involved in some disease states) may simply be a vestige of design .
Furthermore, I am not suggesting that C-T bias continues to happen frequently or after basic types were created. This may explain why they appear to be random these days. But the studies I just gave you on C-T do appear to suggest they are non-random. If somehow they are not, then the other studies showing non-randomness should suffice as evidence.
Nevertheless, this would not mean C-T bias cannot unpack buried design from this front-loaded state. Here is evidence suggesting that it does:
You guys are starting to get away from the original point that I made. When I said…Common design hypothesis suggests that the differences between a particular set of basic types that are similar in morphology and/or moleculars are due to the different design requirements that each of them will need for their environment.
This means that we would expect to find function much more frequently and similar basic types operating in different environments.
I, then, mentioned the human eye and the octopus’s eye to provide an example of this convergence.
Correct.
This study begs to differ:
"To date, the strongest evidence for the mutationist hypothesis is that pseudogenes in GC-rich isochores accumulate GC-biased base substitutions, while pseudogenes in AT-rich isochores accumulate AT-biased base substitutions.
This is an important observation, because pseudogenes have no known function. If GC-rich pseudogenes were maintained by negative selection acting on GC content, while AT-rich pseudogenes were subject to genetic drift, as has been proposed (Bernardi 2000), then base substitutions would be fixed at a lower rate in GC-rich than in AT-rich pseudogenes. The opposite was observed"
No, you’re just running away from the evidence that contradicts your point. Notice that you fail every time you try to get into the specifics of biology.
That study has nothing to do with front-loading.
No. I’m tired of it. Instead, try posting something relevant. You might even explain why it’s relevant. And think before you type.
That too was gibberish.
Not in the sense you imagine. Certainly not design.
Neither of them says what you think.
Pick any. Explain how you know it’s a basic type. Also explain what a basic type is, because I’m no longer sure what you mean by it. Apparently not what baraminologists mean by “holobaramin”.
ETA apologies for this. I check if pre-moderation applies before posting anything substantive and seem unable to delete it now. Mods feel free to delete.
Mike Gene was a contributor to a web site called Telic Thoughts from the early 2000s for a few years. I believe he was working in the biological sciences in some capacity but I don’t recall it ever being made clear. He self-published a book called The Design Matrix which proposed a methodology for detecting “Design”. I bought a copy. It is not an impressive work. Mike still blogs but is more interested in opposing the spread of LBGT across the US these days.
So why didn’t the basic types include a type that had a mixture of bird and mammal features?
So was I. Ewert stated that the majority of modules in a dependency graph will be non-taxonomic, which means they would be violations of a nested hierarchy.
Ewert said the opposite. He said that if the pattern of life was a tree then the dependency graph was falsified and common ancestry was supported.
Did this produce all of the genes seen in eukaryotes?
They produce the predicted divergent tree pattern. You claimed they would be convergent, and they aren’t.
It’s not too technical for me, and I can see it is nonsense.
But they are random, contrary to what the authors try to claim. These mutations produce beneficial, neutral, and detrimental effects. They are random with respect to fitness which is the only definition used in biology. These mechanisms can not produce a specific beneficial mutation at a specific base in response to a specific environmental stimulus. Therefore, they are random.
No, he doesn’t. It’s nonsense.
Then why are the octopus and fish eye different? Why are all of the inverted retinas associated with backbones while the forward facing retinas are not?
Normally we think of flipping a coin as “random;” 50/50, heads or tails. However coins actually usually have a 1 or 2% bias towards one side.
But it would be ridiculous to point to the coin flips and say “See? Since it’s not random, God must be guiding each flip.” A better explanation would be that coins aren’t perfect discs, and don’t have an exactly centered center of gravity. If you want to connect a non-random event to design, you have to prove its not just non-random, but non-statistical. Non-random does NOT mean non-statistical.
In the same way, mutations aren’t random, but they ARE statistical. This is perfectly in line with evolution; we would expect more essential genes (like developmental genes) to be more carefully conserved than less essential or completely vestigial genes (like non-coding DNA). Pointing out that the process isn’t 50/50 isn’t proof of divine guidance, because just like coins, there’s a coherent naturalistic explanation.
It’s also pretty simple to demonstrate that mutations aren’t guided. If a population is large enough, it reaches mutation saturation; where EVERY possible mutation is expressed by at least one individual, every generation. If mutation was guided, shouldn’t we never see that? Shouldn’t we see that some mutations occur consistently, while other mutations never occur, since they aren’t part of God’s plan?
That’s not at all what your sources are saying though. Your sources show that some loci are more susceptible to mutation than others, and some types of mutation are more common than others. What they don’t support is that these trends represent information; none of these studies are saying “the A in this sequence is non-randomly mutating into B, which is creating a new gene.” If you want to claim that God is inserting information into the genus through non-statistical mutations, you have to show that.
True, and bias does not mean non-random. For instance, a steady net flow across a pressure gradient is absolutely described by statistical mechanics which is biased but random with respect to the direction of a particular molecule. Same for free electrons in a length of copper wire; voltage differences introduce bias to random motion.
A better example is the game of craps where you sum two dice rolls. In this game, 7 is way more common than either 2 or 12. Does this mean the roll of the dice are nonrandom? No.
The way in which craps is random is that the outcome of the roll is not influenced by the bet the player makes. If a player puts his bet on the pass line (where an initial roll of 7 or 11 is an automatic winner) the odds of rolling a winning roll is not increased. The dice are blind to what the player needs. In the same way, mutations are blind to what the organism needs in a given environment.
That doesn’t make the results non-random, only unequally distributed.
‘Average’ dice (those numbered 2,3,3,4,4,5 instead of 1,2,3,4,5,6) still produce random numbers. They simply have a different range and distribution to normal dice. .
Careful… you can’t draw conclusions about the randomness of mutations by looking at genomes after selection has occurred.
He is someone who has made the front-loading hypothesis scientifically testable. So far, his prediction on it has been confirmed multiple times. It looks like a legit scientific hypothesis of Intelligent design that is even better than Winston’s dependency graph. I am using it because it fits quite nicely to my theory.
Can you please elaborate on why you say that?
I was referring to the first part of what you said in regards to natural selection playing the part rather than Cytosine Deanimation. As the study suggested, this is can’t be the case.
Let me provide evidence now for Mike Gene’s hypothesis according to him:
"…the case for front-loading would be stronger if the tyrosine kinases were much older and closer to the original cells. What’s more, way back in 2002, I predicted:
my working hypothesis (just recently being seriously entertained) is that the original cells were front-loaded to make it more likely that multicellular states would evolve. These leads me to predict that we will find remnants or “fossils” of such front-loaded distributed among protozoa. Specifically, we will find various pieces of information, necessary for multicellular life, not necessary for single-celled existence, yet still present in many single-celled organisms. {emphasis added)
So are the researchers correct in dating the origin of tyrosine kinases just prior to the split between choanoflagellates and metzoans? Or was yours truly correct in expecting them to be older, and thus more widely distributed?
Consider the findings of another research paper: Genome Analysis of the Unicellular Green Alga Chlamydomonas reinhardtii Indicates an Ancient Evolutionary Origin for Key Pattern Recognition and Cell-Signaling Protein Families, by Glen L. Wheeler, Diego Miranda-Saavedra and Geoffrey J. Barton. Genetics 179: 193–197 (May 2008).
Here is one finding:
Chlamydomonas therefore contains a full complement of the phosphotyrosine-signaling tool kit as found in metazoans and choanoflagellates (King et al. 2008). The discovery of TKs, SH2 domains, and PTPs in chlorophyte algae and land plants suggests that phosphotyrosine signaling mediated by TKs is of general importance in photosynthetic organisms and represents an ancestral mode of cellular signaling.
And
The identification of such a large family of putative TKs in Chlamydomonas supports the hypothesis that phosphotyrosine signaling appeared early in eukaryote evolution before the divergence of the Opisthokont lineage."
If you want to read more on this, then check here:
Breeds within a kind can reproduce with others of the same species and potentially hybridize with other breeds/species within a kind. Limited variation in surface features over time. This represents members of a single basic type and usually forms a clade. Example: Caucasians and Asians
Basic type
A recognizable base form and structure that does not change over time. They are separate and
unique (no common ancestors) - fully functional (no primitive ancestors) - similar in form/design due to similarity in function and common designer. It represents the entire group related by common ancestry, including past and present generations: Example: all of mankind.
Because a mix and match of characters like the example you gave would make it extremely problematic to objectively organize species into nested hierarchies.
I can’t speak for Winston, but what my model suggests is that the common descent interpretation of nested patterns is violated because we would see various types of convergence much more frequently at the biochemical level. But, the nested hierarchies themselves are not necessarily violated because the primary mechanism is HGT and non-random mutations.
Keep in mind, Winston’s model is not based on any comprehensive theory of intelligent design. For instance, it is not derived from a purported mechanism, identity of designer, or motives of this designer. It does not even incorporate Homoplasy. It’s simply a model of history or what happened. Just testable assertions and assumptions.
In contrast, my model flows from observations, experiments, and prior theories that are almost identical to mine. Thus, it does not have anything to do with my model.
No, just specific type of genes necessary to survive and reproduce in a particular environment.
I guess I got mixed up with the type of convergence you are talking about. Let me provide a different example later then:
Wrong. This is not the only definition of random in biology. There are 3 according to Ayala:
"The mutations that yield the hereditary variations available to natural selection arise at random. Mutations are random or chance events because (i) they are rare exceptions to the fidelity of the process of DNA replication and because (ii) there is no way of knowing which gene will mutate in a particular cell or in a particular individual.
However, the meaning of “random” that is most significant for understanding the evolutionary process is (iii) that mutations are unoriented with respect to adaptation; they occur independently of whether or not they are beneficial or harmful to the organisms. Some are beneficial, most are not, and only the beneficial ones become incorporated in the organisms" through natural selection."
The study you mentioned is referring to the definition of random that suggests they are rare exceptions to the fidelity of the process of DNA replication
For example, they hypothesized that the cell might make mistakes in copying repeated sequences during DNA replication. While the cell is “fixing the buttons,” the DNA has more time to mutate. Thus, these repeats influence the mutation rate, as mutations in the repeats on either side of the mutated DNA would abrogate protein function, preventing them from being eliminated and resulting in a mutational hot spot in between stable DNA sequences. Further, the authors found that 97% of the sites under positive selection, and 60% of all mutated sides were near repetitive sequences.
One of the study I provided suggested almost exactly what you just said here:
“Unlike other findings on mutation origination, this mutation-specific response to a specific environmental pressure cannot be explained by traditional theories. “We hypothesize that evolution is influenced by two sources of information: external information that is natural selection, and internal information that is accumulated in the genome through the generations and impacts the origination of mutations,” said Livnat.”
Well, I gave you the study that supports the mechanism that Mike Gene purported. So it does not matter. Just read the study instead if you want more insight into that mechanism.
You are confusing same habitats with same environments. They are not the same thing. “Habitat is the natural home of a plant, animal, or another organism. The environment is the state in which the organic, inorganic, and cultural elements interact to protect the birth, growth, existence, etc. of an organism.” What is the distinction between habitat and environment? - Science Query
Remember, the ecology criteria , i created, involves examining where each basic type lives and how each of them interacts with their environment, including other living things.
This criteria is a survey of 5 questions where each practical criterion is designated by a letter (A–E) and a title in the form of a question (shelter, prey, predators, trophic level, habitat).
In the case of fish and octopuses, if the answer to the question “Is there a substantial difference in habitat?” is ‘No’ or ‘TBD,’ a follow-up question is asked: “Do they respond differently in different habitats?” (this may require artificially planting them in different habitats for an answer).
If the answer to either question is ‘Yes,’ we can conclude that God constructed each basic type separately.
However, if the answer is ‘NO’ or ‘TBD’ to both questions, we must rely on other measures to make a confident conclusion. If most of the questions yield a ‘NO’ or ‘TBD’ answer, then the results are inconclusive.
Eehhhhh!!! Welcome back! Long time no see. You came just in time.
Anyhow, I can agree with what you said here to some extent. But, it can still be additional evidence for divine guidance. The acutal proof for divine guidance is based on the ENCODE results.
For instance, as Mattick and Dinger have pointed out:
“the argument of a largely non-functional genome is invoked by some evolutionary theorists in the debate against the proposition of intelligent design of life on earth, particularly with respect to the origin of humanity. In essence, the argument posits that the presence of non-protein coding or so-called ‘junk DNA’ that comprises > 90% of the human genome is evidence for the accumulation of evolutionary debris by blind Darwinian evolution, and argues against intelligent design, as an intelligent designer would presumably not fill the human genetic instruction set with meaningless information.
This argument is threatened in the face of growing functional indices of noncoding regions of the genome, with the latter reciprocally used in support of the notion of intelligent design and to challenge the conception that natural selection accounts for the existence of complex organisms."
John S. Mattick and Marcel E. Dinger, “The Extent of Functionality in the Human Genome,” The HUGO Journal 7, no. 2 (2013): doi:10.1186/1877-6566-7-2.
As suggested, the ENCODE project revealed that most, if not all, of these non-coding regions play an important role in the accurate functioning of the DNA (Pennisi, 2012). While these results apply only to the human genome, later studies discovered large portions of functional elements within animal and plant species as well (Burgess & Freeling, 2014; Bai et al., 2015). In fact, ever since the ENCODE results, there have been many more examples such as these, revealing specific functions for non-coding DNA:
It is noteworthy that there is controversy surrounding the ENCODE results (Eddy, 2012; Graur et al., 2013). One of the foremost criticisms relegated at ENCODE has to do with its use of a causal definition of function to determine gene functionality, and critics have suggested a more viable definition of function, called the “selection effect definition”, where sequences in genomes can be considered useful only if they evolved under evolutionary processes to perform a particular function.
However, Mattick & Dinger (2013) addressed these criticisms. They showed the many weaknesses in the selection effect definition and responded to the objections made against the definition used by ENCODE: “Assertions that the observed transcription represents random noise…is more opinion than fact and difficult to reconcile with the exquisite precision of differential cell- and tissue-specific transcription in human cells.”
Mpst of the studies I presented don’t show this. But, one of them does show it:
"Unlike other findings on mutation origination, this mutation-specific response to a specific environmental pressure cannot be explained by traditional theories. “We hypothesize that evolution is influenced by two sources of information: external information that is natural selection, and internal information that is accumulated in the genome through the generations and impacts the origination of mutations,” said Livnat."
By examining the de novo origination of HbS, Livnat was able to disentangle for the first time whether the malaria-protective mutation arises randomly and spread in Africa only because of selection pressure or instead whether it could actually be originatingde novo more frequently in sub-Saharan Africans – a group that has been subject to intense malarial selection pressure for many generations. If the mutation is random, then it should be equally likely to emerge in both geographical groups. However, if mutation is nonrandom, then perhaps it would actually emerge more frequently in Africans."
If you think I’m doing so, feel free to provide an example. Make sure you include details of what I have misunderstood.
I am confident that you will be unable to, partly because almost all of my replies to you have consisted entirely of highlighting where you have lied about your sources, and partly because you rarely understand or respond substantially to anything.
Here’s an illustrative example:
It should be obvious even to you that you have neither explained how you know mankind is a basic type, nor analyzed mankind with the ecology method.
No, it doesn’t. We don’t observe these processes producing what you claim.
I agree with everything Ayala describes. The mechanism of mutation you are describing is random by everything Ayala describes.
That would be included in the fidelity of the process of DNA replication. Replication has less fidelity in repeat regions. Just as Ayala states, mutations in these regions may be beneficial, neutral, or detrimental. There is also no way of predicting which replication will produce a mutation at a specific base in the repeated sequence. It fits all of the requirements Ayala sets out.
They would need to show that this same mechanism is not producing neutral and detrimental mutations elsewhere in the genome. Have they done that? They would also need to show some sort of mechanism that senses malaria in the environment which then causes the specific mutation, and they haven’t done that.
The mechanism is incapable of doing what Mike Gene claims.
Fish and octopus live right next to each other. How is that not the same habitat or environment?
On that topic, the form of citation you used for Mattick & Dinger’s HUGO article suggests your source was not their actual article, but the extract quoted by RtB here (or perhaps some other secondary source using or used by RtB).