Of course, the paper you link shows that some transcriptional activity from pseudogenes can often result in differentiation into cancer cells, which can definitely be argued to constitute a considerable design flaw.
To cite or not to cite? That is the question. Whether tis easier on the mind to be called out for misrepresentation, or for not providing references, is a personal choice - but both lead to a sea of troubles that will end him.
Yes, but from using a common descent model as a guide to understanding those systems. How do you know scientists won’t find other uses that benefit the organism in the future if they start using a common design model. Here is an example of what I mean:
“However, with a growing number of instances of pseudogene-annotated regions later found to exhibit biological function, there is an emerging risk that these regions of the genome are prematurely dismissed as pseudogenic and therefore regarded as void of function.”
Seth W. Cheetham, Geoffrey J. Faulkner, and Marcel E. Dinger, “Overcoming Challenges and Dogmas to Understand the Functions of Pseudogenes,” Nature Reviews Genetics 21 (March 2020): 191–201, doi:10.1038/s41576-019-0196-1.
What makes the common design model useless?
Can you please define what you mean by “useless” because I may not agree with how you are defining it since it is coming from a common descent perspective?
We don’t (and didn’t) need common descent to understand the consequences of having a GULO pseudogene. Its very simple to dig: those with GULOP suffer the terrifying symptoms of scurvy and die afterwards, unless they get vitamin C from external sources.
If there was a common designer, giving us GULOP was one of the biggest blunders it made. That falsifies your hypothesis.
It doesn’t matter whether we find some benefit associated with GULOP, what matters is that it’s current nonfunctionality in humans and some primates is extremely detrimental to them.
The part I boldened indicates why this paper is of no relevance to GULOP. If it still doesn’t make sense to you, read the following paragraphs slowly to understand why.
GULO is a gene that encodes for the protein GULO. GULO catalyzes the synthesis of a molecule called ascorbic acid, otherwise known as vitamin C.
In humans and several other animals, GULO no longer encodes for the GULO protein, because of several crippling mutations. This mutant, damaged form of GULO is called GULOP (GULO pseudogene). In some other animals like rats, GULO is not damaged, so with the aid of its gene product (GULO) they can make their own vitamin C, hence, preventing them from getting scurvy.
So we know what GULOP should do and the consequences of it not doing what it should: if GULOP wasn’t broken in humans, we would have being able to make our own vitamin C, but it is broken, so we must consume vitamin C from external sources to make up for its inactivity. GULOP is notable because not only is it inactive, its inactivity is harmful to organisms to have it. This has been tested in mice, whose functional GULO was inactivated with mutations: just like us, mice whose GULO is broken by the experimenter must be fed dietary vitamin C to keep it alive.
Under your common design hypothesis, GULOP is a design flaw, thus falsifying it.
What makes your version of the common design hypothesis test useless, is that it fails to properly distinguish what we would expect under common descent from common design.
For example, you said we would expect to see design flaws under common descent which is just ridiculous. How can there be design flaws in a process that happened without a mind behind it? More importantly, design flaws are not a prediction of common descent, because descendants get whatever their ancestors possessed: if an ancestral population had genes for something as cool as X-ray vision or bad as blindness the descendants will likely get it, no questions asked.
Another important problem for your test is that it operates on the premise that the designer did not use common descent to generate all extant biodiversity, so we have to ask how you know that premise is true?
As I said before, What looks like a flaw from the harmful effects of cancerous mutations in organisms is primarily a result of decay imposed by the second law of thermodynamics rather than poor design (Just ask for this reference). Of course, some might argue that an all-powerful all-knowing omnibenevolent common designer, whose purpose is to ensure species survive and reproduce under natural conditions, could have effectively designed living organisms in which these flaws would not occur at all . However, the second law of thermodynamics must exist in all possible worlds unlike other laws of nature because it pertains to quantum mechanics as well as general relativity (Abe & Okuyama, 2011). This means it would require the suspension of the second law (i.e., a miracle) to prevent them from occurring at all.
According to the theory, we would not expect a miracle or random event to happen based upon that designer’s personal nature that is similar to ours [ reference is at bottom]. More importantly, it appears as though this designer uses the laws of nature to eliminate these instances and chooses to remain consistent with them. This involves editing and limiting the harmful genetic changes (Just ask for this reference) and regulating harmful mutations that do arise in a way that preserves a balance between predator and prey populations because too many predators or prey can cause a collapse of the ecosystem (Just ask for this reference).
For instance, mitochondrial and chloroplast DNA are abundantly involved in apoptosis, which is the single most important feature of multicellularity because it ensures timely death of individual cells. Cancer may be the ecological equivalent of apoptosis, ensuring the timely death of individuals so that resources are available for the young.
In addition, there are examples of cancer cells developing through viral infection (Just ask for this reference)) and thus, as stated before, viruses are necessary evils. Further research might find more cases like these in other genetic diseases.
With that said, I admitted before that these explanations do not adequately explain why we see these occurrences in humans since we seem to be uniquely made in the image of this designer where we have the ability to recognize and manipulate digital information to our advantage, which we don’t definitively see in animals yet. For this reason, we would most likely expect this designer to want a special relationship with humans based on human experience.
“From an abstract, informational perspective, protein domains appear analogous to words in natural languages in which the rules of word association are dictated by linguistic rules, or grammar.”
Lijia Yu et al., “Grammar of Protein Domain Architectures,” Proceedings of the National Academy of Sciences, USA 116, no. 9 (February 26, 2019): 3636–45, doi:10.1073/pnas.1814684116.
Natural selection has been considered to be the blind watch maker by some because the designer is the mindless environment or natural law. This is what I meant.
I was just referencing Jerry Coyne’s book Why Evolution is True where he claims, “Imperfect design is the mark of evolution; in fact it’s precisely what we expect from evolution.” (Coyne, 2014, p. 81)
His prediction is based upon the observation that “[n]ew parts don’t evolve from old ones, and we have to work well with the parts that have already evolved. Because of this, we should expect compromises: some features that work pretty well, but some not as well as they might, or some features—like the kiwi wing—that don’t work at all, but are evolutionary leftovers.” (Coyne, 2014, p. 81)
So are you telling me Jerry Coyne is mistaken or maybe you just disagree?
Well first off, Common descent does not attempt to explain the origin of life or viruses from what I know. Second, under the common design model, the origin of life has to apparently be designed from scratch or in a top-down manner according to prebiotic in-vitro experiments. Moreover, viruses have only been shown to arise without a host from scientists who genetically or synthetically create viruses (Just ask for reference).
More importantly, Phage-assisted experiments highly suggests that the experimenter needs to intervene in the process to give viruses a boost in function and fitness in order to force bacteria to evolve. This is because the phages that are lacking the functional pIII protein are rapidly lost under continuous culture conditions because they have no ability to propagate (just ask for reference).
This statement indicates you most likely don’t know what the second law of thermodynamics means. However, what is intriguing is that you believe GULOP was a consequence of the second law of thermodynamics, explain? (Let’s see if you really know what the second law means).
GULOP doesn’t look “like a flaw”, it is a flaw and an expensive one. Your version of common design requires such things not be found in extant organisms, but they are found, falsifying it.
What the heck do you mean by “cancerous mutations”? There is nothing cancerous about the mutations which incapacitated GULO. Stop quoting irrelevant sections from ID sources as replies to objections, its beginning to irritate me. Do it again, and I won’t reply you on this topic anymore.
Baseless, ad hoc assertions.
You and your quote source are profoundly ignorant of cancer biology to even liken it to apoptosis. Clowns.
Viruses like HIV which can cause cancer are not necessary evils. Your profound ignorance is rearing it’s ugly head again. Clown.
Again these are baseless, ad hoc, assertions.
Oh great, your profound ignorance is shining for all to see again. Common descent is not natural selection and it can occur without natural selection.
You are just clueless, mindlessly quoting ridiculous material from only God knows where.
Dear ID and creationist lurkers, please before you attempt to criticize evolutionary theory make sure you understand what you are saying or risk showing your ignorance or misunderstanding like this fellow.
Jerry is speaking of evolution, not common descent. Common descent is not evolution. As a tinkerer, evolution is bound to produce suboptimal systems at times, so we expect things like GULOP to show up. In contrast, common descent is simply going from a single ancestral species to two or more descendant species. Common descent does not predict design flaws, descendants just get whatever they can from their ancestor be it beneficial, neutral or harmful.
I am telling you gravely misunderstood Jerry Coyne. I don’t expect less from someone who mindlessly quotes irrelevant or ridiculous material and has nigh zero understanding of basic evolutionary biology.
When did I argue such?
More irrelevant junk. I never argued about or mentioned the origin of life or virus, so you bringing it up is a failed attempt at distracting readers.
Stop quoting irrelevant material. This has nothing to do with common descent.
I know of an eight year old girl who will be dead from a brain tumor in less than a year. But hey, how lovely it is that your magical designer is implementing this sort of social Darwinism, or selective eugenics through the application of cancer and viral infections. I’m sorry but weren’t eugenics and social Darwinism supposed to be a bad thing in theism-land? Apparently now it is a good thing when God culls the old and weak through cancers and viruses so there’s more resources for then young. Too bad when the young some times get caught in the crossfire.
How in the world is the article you reference supposed, in any way, to support this claim? You’re blathering.
In his book Why Evolution is True , evolutionary biologist Jerry Coyne claims that " Imperfect design is the mark of evolution; in fact it’s precisely what we expect from evolution." (p. 81) He makes this prediction because "[n]ew parts don’t evolve from old ones, and we have to work well with the parts that have already evolved.
which is exactly what @Meerkat_SK5 wrote. @Meerkat_SK5 also gives the same potentially wrong page number as Luskin, the same “[n]ew” as Luskin, and the same two quotes split up in the same way as Luskin.
So once again @Meerkat_SK5 is trying to pass off IDer misrepresentations as the original text, and once again has cited the original source, and not Luskin’s article or wherever he actually got that quote from.
@Meerkat_SK5 is lying about his sources, and bears full responsibility for once again saying the exact opposite of his cited source. There is no reason to think @Meerkat_SK5 has read Coyne’s “Why Evolution is True”, he clearly doesn’t know or care whether his ‘quote’ is representative or accurate, he clearly hasn’t learnt anything from his earlier misrepresentation of Yockey, and any citations from him can be dismissed immediately as unreliable.
I know these predictions would not be considered specific enough under the standards of science, but this is the best I can do for now based on my limited knowledge on those fields of science.
UNIVERSAL COMMON DESIGN PREDICTIONS
The rest of the non-coding regions of the DNA should reveal real sequencing differences between apes and humans as well as between other animal species based on how they are expressed in the regulatory genes rather than the genes that are present.
We should find many more examples of species having similar features for similar purposes but be applied to different environments and ultimately be unrelated types of organisms from alleged suboptimal design flaws.
We should find function from vestigial features within species. it’s important to point out that the argument for function does not depend only on whether the organism would survive or not survive without this function but can still be useful in other ways that don’t involve life or death.
We should find many more examples of retroviruses or bacteria, which cause genetic or infectious diseases within animals and humans, being a product of harmful mutations and/or the random transmission of mobile genetic units under terrestrial conditions.
We should NOT find evidence of E.coli evolving biochemical machinery to metabolize citrate within Lenski’s experiment.
We should find more creatures experience enhanced survival capabilities when undergoing “nociceptive sensitization".