I'm perplexed to note that pasting material that actually answers your questions is considered "spam" by you. I'm nevertheless going to continue.

From this paper:
http://cshperspectives.cshlp.org/content/6/6/a016071.full.pdf+html
Origin of Spliceosomal Introns and Alternative Splicing
Manuel Irimia and Scott William Roy

ORIGIN AND ESTABLISHMENT OF THE SPLICEOSOMAL SYSTEM DURING EUKARYOGENESIS

In this section, we discuss the major steps leading to the origin and establishment of the spliceosomal system in eukaryotes. Despite the persistence of disagreement on some important aspects, there is a general consensus about how this process may have unfolded (Fig. 2). According to this general model, spliceosomal introns evolved from invading group II introns, perhaps derived from the early mitochondrion (thought to be descended from an engulfed member of the a-proteobacteria, whose modern members contain group II introns). For some reason(s), these introns then proliferated to an unprecedented level in the host genome. Over time, the self-splicing activities of these many intron copies degenerated, which was associated with the increase of trans-encoded RNAs and proteins that promoted efficient intron splicing, setting the basis of the protospliceosomal machinery, and further releasing selective pressure on cisintronic splicing elements. As this protospliceosomal machinery recruited more proteins and became more efficient, introns became increasingly reliant on the emerging spliceosome for proper splicing.

The funny thing is, I reasoned just above that this is pretty much what must have happened simply by understanding the basics of catalyzed RNA hydrolysis and ligation. That you start with self-splicing RNA introns and then gradually build the more complex protein-dependent versions on top.

Turns out that this somewhat ad-hoc rationalization of mine (which would seem to predict that more complex protein-dependent intron splicing evolved from self-splicing RNA's) actually has strong empirical support from phylogenetics(from the same paper):

Transfer of Group II Introns to the Host Genome

Structural and functional evidence suggests that spliceosomal and group II self-splicing introns are evolutionarily related. Both types of introns are spliced through a similar two-step catalytic reaction that relies on an endogenous adenosine (the BP), and releases the excised intron as a lariat structure. The two intron types have similar boundary sequences (GT-AY in group II introns and usually GT-AG in spliceosomal introns, although some U12 introns are AT-AC) (Lambowitz and Zimmerly 2011), and there are striking structural similarities between key regions of group II intron domains and spliceosomal snRNAs (Lambowitz and Zimmerly 2011). These include at least (i) domain DV and U6 snRNA, with divalent metal-ion binding sites involved in catalysis and similar base-pairing interactions (Jarrell et al. 1988; Peebles et al. 1995; Yu et al. 1995; Abramovitz et al. 1996; Konforti et al. 1998; Yean et al. 2000; Shukla and Padgett 2002), further supported by crystal structure (Toor et al. 2008; Keating et al. 2010); (ii) ID3 subdomain and d –d0 motifs and U5 snRNA stem loop, involved in the recognition of 50 and 30 exons (Hetzer et al. 1997); and (iii) DVI and the U2-intron pairing that include the BP adenosine (Schmelzer and Schweyen 1986; Parker et al. 1987; Li et al. 2011). In addition, it
has also been shown that extracts of snRNAs can catalyze both splicing reactions without proteins in vitro (Valadkhan et al. 2007, 2009), in a similar manner to complete group II introns. Whereas it is theoretically possible that group II introns evolved from spliceosomal introns (or that both share a distinct common ancestor [Vesteg et al. 2012]), it seems much more likely that group II introns gave rise to spliceosomal introns (Cech 1986). The presence of spliceosomal introns in all extant eukaryotic supergroups indicates that this transformation occurred before LECA.

Understanding the basics implies(predicts it), phylogenetics supports it. Sorry, game over.

@Rumraket
Thank you for showing me complexity related group of constructions or answers, but that's not what I asked. I asked you to demonstrate how to build a construction that matches exactly with the constructions drawings you never saw or how to answer the question you never saw?

But of course, if you keep asking random people on the internet for ever-increasing technical details, then you will reach a point they can't easily explain something to you and at that point you can crow "Gotcha, you can't explain it, nahnahnanahnah! Goddunit."

MarioNovak wrote:@Rumraket
Thank you for showing me complexity related group of constructions or answers, but that's not what I asked. I asked you to demonstrate how to build a construction that matches exactly with the constructions drawings you never saw or how to answer the question you never saw?

I'm afraid you don't actually understand my answer. We can explain the general concepts if we bother to understand the basic underlying mechanisms.

If we understand, for example, how molecules bind to each other, we can use this knowledge to explain how a piece of RNA can find a sequence and cut itself out.

You're not going to get a different answer, because that is the answer your question. Insisting I haven't answered entails that you either didn't understand it, or that you're obfuscating to avoid admitting it. My answer isn't going to change, so have fun with that.

Rumraket wrote:

MarioNovak wrote:@Rumraket
Thank you for showing me complexity related group of constructions or answers, but that's not what I asked. I asked you to demonstrate how to build a construction that matches exactly with the constructions drawings you never saw or how to answer the question you never saw?

I'm afraid you don't actually understand my answer. We can explain the general concepts if we bother to understand the basic underlying mechanisms.

If we understand, for example, how molecules bind to each other, we can use this knowledge to explain how a piece of RNA can find a sequence and cut itself out.

You're not going to get a different answer, because that is the answer your question. Insisting I haven't answered entails that you either didn't understand it, or that you're obfuscating to avoid admitting it. My answer isn't going to change, so have fun with that.

And I think you don't understand how evolution works because your explanations like "they could splice out", are based on hidden implicit assumptions that evolution has intelligence and foresight. Try to put yourself in evolution shoes and not in intelligent designer shoes when you try to explain how a particular evolutionary result was achieved.

In the beginning, there were protein coding genes only, without noncoding sections. Then, some protein coding genes were interrupted by introns - insertions that lead to non-functional proteins. From the evolution perspective there is no causal relationship between random DNA(intron) insertion in protein coding gene and splicing machinery or self splicing ability emergence. Organisms with intronic alteration of essential genes would be eliminated from the population by natural selection and intronic alteration of junk DNA would cause junk to stay junk. And that's all. Insertion won't trigger alarm signal about a problem and force organisms to rapidly evolve enzymes, splicing factors and ribonucleoprotein structures to assist in splicing signaling, insertion recognition, complex series of RNA–RNA rearrangements, precise looping process, splicing RNA back together, etc.

How is it that you repeatedly fail to understand non-existence of this causality, implicitly invoked in every explanation you provide? If you create a garden design plan that won't trigger some mysterious causal chains resulting in the natural gardening process according to the plan you've made. Cause and effect structure of the natural world is not determined by the existence of human needs represented in plans. Likewise, DNA insertion alteration resulting from a copying error during DNA replication won't trigger some mysterious causal chains resulting in a highly regulated cellular machinery. Mutation–selection dynamics is not determined by the cell's need to produce functional proteins but by the random and environmental events.

Btw, yesterday you asked me what was designer trying to achieve by cluttering the genomes of multicellular eukaryotes with massive amounts of nonfunctional introns.

Here you will find some reasons of why your non-functionality premise is false:

http://onlinelibrary.wiley.com/doi/10.1 ... 400138/pdf

-introns enhances genes transcription

-the presence of introns offers the potential for regulatory functions such as alternative splicing to create functionally different proteins from a single gene.

-the proper function of the vertebrate segmentation clock depend on delays introduced by the presence of
introns

-introns and splicing activity influence promoter-proximal chromatin profiles, Pol II occupancy, and overall transcriptional output

-some introns harbor non-coding RNAs such as miRNAs or snoRNAs, whose processing from introns can speed up or slow down the rate of expression of the host gene

-short first exons were shown to have more defined peaks of activating histone marks closer to the transcription start site , enhancing transcription accuracy and output

-genes with long first exons are less well-expressed and display reduced accuracy at the transcription start site

-an RNA polymerase II-mediated cross-talk between chromatin structure and exon-intron architecture, implying that exon selection may be modulated by chromatin structure.

MarioNovak wrote:@Rumraket
Thank you for showing me complexity related group of constructions or answers, but that's not what I asked. I asked you to demonstrate how to build a construction that matches exactly with the constructions drawings you never saw or how to answer the question you never saw?

Oh so something that has nothing to do with evolution.

MarioNovak wrote:

Rumraket wrote:

MarioNovak wrote:@Rumraket
Thank you for showing me complexity related group of constructions or answers, but that's not what I asked. I asked you to demonstrate how to build a construction that matches exactly with the constructions drawings you never saw or how to answer the question you never saw?

I'm afraid you don't actually understand my answer. We can explain the general concepts if we bother to understand the basic underlying mechanisms.

If we understand, for example, how molecules bind to each other, we can use this knowledge to explain how a piece of RNA can find a sequence and cut itself out.

You're not going to get a different answer, because that is the answer your question. Insisting I haven't answered entails that you either didn't understand it, or that you're obfuscating to avoid admitting it. My answer isn't going to change, so have fun with that.

And I think you don't understand how evolution works because your explanations like "they could splice out", are based on hidden implicit assumptions that evolution has intelligence and foresight.

No it isn't.

Try to put yourself in evolution shoes and not in intelligent designer shoes when you try to explain how a particular evolutionary result was achieved.

I did.

Do I really have to cut this out in small cubes and spoon-feed you the explanation? Okay, well then here goes.

The foundational assumption in explaining how intron excision originates is that originally there are no introns. Right? To explain how they originates, and later evolves the ability to cut themselves out, requires that there are none to begin with. So that's where we start. No introns.

Next step, what ARE introns really? Well they are basically large insertions in protein-coding regions. A kind of mutation you can call them. Basically, to begin with they are selfish genetic elements that become duplicated and randomly inserted in the genome during DNA replication (mitosis or binary fission).

Okay, so obviously not all cells in existence just so happen to produce introns in all their genes to begin with, right? I mean, that would be absurdly unlikely. So only a few cells out of a large population, suffer the kind of mutation that produce these selfish "proto-introns" we can call them. You with me?

Now, obviously, if one of these cells get one of these introns inserted into a critical gene, so it breaks the resulting protein, this cell will die and not leave any offspring. Right? So introns that kill cells cannot, by definition, become fixed in the population. There are in effect selection against them. Not "foresight" selection, but simply as a consequence of the fact that IF an intron happens in a critical gene, the cell dies because it can't make copies of itself. So lethal introns just can't proliferate.

But in another cell in this population, an intron doesn't happen in a critical gene. It happens in a gene that only makes the cell less fit. But it doesn't kill it. Now obviously, if this cell subsequently still manages to produce offspring(which it does, because the intron is deleterious, not lethal), there will emerge a subpopulation of cells with deleterious but non-lethal introns. You with me so far?

These descendant cells which are less fit, in turn have offspring of their own, which would obviously be much better off if they subsequently suffer mutations (when they reproduce) that make it possible for the intron to be removed again. But the subpopulation of cells with deleterious introns persist for a while, cells make copies of themselves and recieve mutations in their genomes. Those that carry lethal mutations (introns that happen in critical gene regions) simply die and leave no offpsring, while those that suffer mutations with little to no effect still manage to survive and reproduce. Still no "foresight", still only as a matter of chance mutations with the right effects being retain if and when they arise. See?

So anyway, mutations accumulate in the deleterious but non-lethal introns over generations until a mutant arises that has catalytic activity. It doesn't even have to be 100% effective at removing itself to begin with, the intron in the non-critical gene might suffer a mutation that gives it a very low catalytic activity, which is phosphodiester bond hydrolysis at a specific location on itself. Any amount of activity above zero here is better than none. So these cells in turn, which suffer these mutations, will be more fit again, than their immediate ancestors.

So now we have cells with introns that can cut themselves out again, at least some of the time. On average, while they are not MUCH better, they ARE better, so they produce more offspring than their ancestors (we say they are more fit). As a consequence of this, introns that can cut themselves out in effect proliferate in the population (we say the frequency of the allele increases). Even further, cells which carry introns that suffer mutations which make them even better at cutting themselves out(because they are better at finding the target binding site, or because they have higher catalytic efficiency) will ALSO be retained, because the cells which are carriers of these introns in turn do even better, they are more fit.

We have now in effect evolved cells with introns that can cut themselves out, from a state where there was no such introns to begin with. At no point in this chain of events was there any foresight, or selection for a future result.

Subsequent generations of cells with self-splicing introns provide the substrate for further intron evolution. They secondarily take on useful functions for the cells (because if they suffer mutations that make them do useful cellular functions that increase cell fitness, the cell is more fit and therefore the allele comes to dominate the population) etc. etc.

Rinse and repeat.

I have to say, it is silly I have to sit here and spell these things out in this much detail. You should be intelligent enough to figure out these things for yourself if you bothered.

What's next, I have to tell you how mutations in RNA sequence and structures produces catalytic folds at the atomic level?

It's the Michael Behe dover-defense retort when dusins of books and over 58 peer reviewed publications on the evolution of the immune system was presented to his face: Yeah but it's not in a sufficient, step-by-step, mutation-by-mutation level of detail.

One can always fall back on that. If he HAD been presented with that, he could just have said he wanted a complete spatial world-history of every quark and lepton involved at the sub-angstrom level. Where does it end? Do you demand the same level of detail when you get the weather forecast on TV ? "I demand to know where every drop of rain lands otherwise you can't tell me how rain works".

RR, I salute you. I just want you to know, that whether your herculean efforts make any difference to MN, and I have no doubt that you're under no illusion there, I appreciate them greatly.

I'm something of a genetics beginner (though even I had managed to Google that paper on spliceosomal introns myself before your post), and I find your Genetics 101 lectures enormously informative, for which I thank you.

Thank you I appreciate that

More on the evolution of jeans:-

MarioNovak wrote:Btw, yesterday you asked me what was designer trying to achieve by cluttering the genomes of multicellular eukaryotes with massive amounts of nonfunctional introns.

And the vitamin C pseudogene, you didn't answer that one.

MarioNovak wrote:Here you will find some reasons of why your non-functionality premise is false:

It's not a premise, it's an empirically elucidated fact. Notice how I didn't say ALL introns are nonfunctional, so my question is obviously about those that are.

MarioNovak wrote:http://onlinelibrary.wiley.com/doi/10.1002/bies.201400138/pdf

- Some introns enhances genes transcription

- the presence of some introns offers the potential for regulatory functions such as alternative splicing to create functionally different proteins from a single gene.

- the proper function of the vertebrate segmentation clock depend on delays introduced by the presence of
some introns

- Some introns and splicing activity influence promoter-proximal chromatin profiles, Pol II occupancy, and overall transcriptional output

- Some introns harbor non-coding RNAs such as miRNAs or snoRNAs, whose processing from introns can speed up or slow down the rate of expression of the host gene

- Some short first exons were shown to have more defined peaks of activating histone marks closer to the transcription start site, enhancing transcription accuracy and output

- Some genes with long first exons are less well-expressed and display reduced accuracy at the transcription start site

- an RNA polymerase II-mediated cross-talk between chromatin structure and exon-intron architecture, implying that exon selection may some times be modulated by chromatin structure.

FIFY.

The fact that some introns have secondarily acquired functions due to accumulation of mutations, and the propensity of the cell to adapt to their presence(since it couldn't get rid of them as fast as they proliferated, because they are at bottom selfish genetic elements(ala transposons) that can excise and insert themselves) doesn't mean they need to be there in the first place, nor does it mean they all are functional. They aren't.

You know scientists have actually found a rare eukaryote WITH NO INTRONS, which show signs of having subsequently lost it's spliceosome? Time for some inconvenient truthes for you to ponder:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2148396/
Nucleomorph genome of Hemiselmis andersenii reveals complete intron loss and compaction as a driver of protein structure and function

If introns is a strict necessity for organismal function, explain this organism!

Even more importantly, we know of species from which all the introns can be removed and the cell continues to function, though at a signficantly reduced fitness levels(because as expected, since the cells don't have a way to get rid of them easily, once they are there, some are bound to evolve secondary functions upon which the cell then starts relying).

In other words, it is an empirical fact that there is no clear boundary that makes it absolutely critical for cellular life to evolve or retain introns for function, they have emerged as selfish genetic elements that excise and insert themselves in protein coding regions and secondarily acquired functions for their host cells through chance mutations during the history of life.

Incidentally, loving the way this poster is using research arising from evolutionary theory to attempt to debunk evolutionary theory. One of the clearest commissions of the stolen concept fallacy I've seen in yonks.

Rumraket wrote:I did.

Do I really have to cut this out in small cubes and spoon-feed you the explanation? Okay, well then here goes.

The foundational assumption in explaining how intron excision originates is that originally there are no introns. Right? To explain how they originates, and later evolves the ability to cut themselves out, requires that there are none to begin with. So that's where we start. No introns.

Next step, what ARE introns really? Well they are basically large insertions in protein-coding regions. A kind of mutation you can call them. Basically, to begin with they are selfish genetic elements that become duplicated and randomly inserted in the genome during DNA replication (mitosis or binary fission).

Okay, so obviously not all cells in existence just so happen to produce introns in all their genes to begin with, right? I mean, that would be absurdly unlikely. So only a few cells out of a large population, suffer the kind of mutation that produce these selfish "proto-introns" we can call them. You with me?

Now, obviously, if one of these cells get one of these introns inserted into a critical gene, so it breaks the resulting protein, this cell will die and not leave any offspring. Right? So introns that kill cells cannot, by definition, become fixed in the population. There are in effect selection against them. Not "foresight" selection, but simply as a consequence of the fact that IF an intron happens in a critical gene, the cell dies because it can't make copies of itself. So lethal introns just can't proliferate.

But in another cell in this population, an intron doesn't happen in a critical gene. It happens in a gene that only makes the cell less fit. But it doesn't kill it. Now obviously, if this cell subsequently still manages to produce offspring(which it does, because the intron is deleterious, not lethal), there will emerge a subpopulation of cells with deleterious but non-lethal introns. You with me so far?

These descendant cells which are less fit, in turn have offspring of their own, which would obviously be much better off if they subsequently suffer mutations (when they reproduce) that make it possible for the intron to be removed again. But the subpopulation of cells with deleterious introns persist for a while, cells make copies of themselves and recieve mutations in their genomes. Those that carry lethal mutations (introns that happen in critical gene regions) simply die and leave no offpsring, while those that suffer mutations with little to no effect still manage to survive and reproduce. Still no "foresight", still only as a matter of chance mutations with the right effects being retain if and when they arise. See?

So anyway, mutations accumulate in the deleterious but non-lethal introns over generations until a mutant arises that has catalytic activity. It doesn't even have to be 100% effective at removing itself to begin with, the intron in the non-critical gene might suffer a mutation that gives it a very low catalytic activity, which is phosphodiester bond hydrolysis at a specific location on itself. Any amount of activity above zero here is better than none. So these cells in turn, which suffer these mutations, will be more fit again, than their immediate ancestors.

So now we have cells with introns that can cut themselves out again, at least some of the time. On average, while they are not MUCH better, they ARE better, so they produce more offspring than their ancestors (we say they are more fit). As a consequence of this, introns that can cut themselves out in effect proliferate in the population (we say the frequency of the allele increases). Even further, cells which carry introns that suffer mutations which make them even better at cutting themselves out(because they are better at finding the target binding site, or because they have higher catalytic efficiency) will ALSO be retained, because the cells which are carriers of these introns in turn do even better, they are more fit.

We have now in effect evolved cells with introns that can cut themselves out, from a state where there was no such introns to begin with. At no point in this chain of events was there any foresight, or selection for a future result.

Subsequent generations of cells with self-splicing introns provide the substrate for further intron evolution. They secondarily take on useful functions for the cells (because if they suffer mutations that make them do useful cellular functions that increase cell fitness, the cell is more fit and therefore the allele comes to dominate the population) etc. etc.

Rinse and repeat.

This is not detailed scientific explanation, but redundand retoric, tautology - an argument constructed in such a way, generally by repeating the same concept or assertion using different phrasing or terminology, that the proposition as stated is logically irrefutable, while obscuring the lack of evidence or valid reasoning supporting the stated conclusion. In short, you are repeating the same story over and over again, nothing more, nothing less.

In the first 15 lines of text you are saying what I summed up in one single sentence - "organisms with intronic alteration of essential genes would be eliminated from the population by natural selection".

This is really tragicomical if we consider this sentence of yours : "it is silly I have to sit here and spell these things out in this much detail...... You should be intelligent enough..."

Why are you saying this in this much detail if I agree that intronic alteration of essential genes would be eliminated from the population? You try to cover up your tautology and lack of valid reasoning by using ad hominem attack and shifting focus on me, on my intelligence?

The rest of the text is standard just so story - an unverifiable and unfalsifiable narrative explanation for a cell's self splicing ability. How self splicing ability arose? Mutations accumulate over generations until a mutant arises that has catalytic ability. This is the core of your argument - mutations accumulate... until a mutant arises that has... (name any biological function).. arises.

How catalytic enzyme arose? Mutations accumulate over generations until a mutant arises that has catalytic enzyme.

How spliceosome arose? Mutations accumulate over generations until a mutant arises that has spliceosome.

How complex RNA splicing process arose? Mutations accumulate over generations until a mutant arises that has complex RNA splicing machinery.

How X arose? Mutations accumulate over generations until a mutant arises that has X.

How Windows 8 arose? Copying errors accumulate in Windows 7 over generations until Windows 8 arises.

So basically in this extensive post you are repeating the same old evolutionary hypothesis which proposes that you can create new functions, new genes, new semiotic relations and closures, new meaningful text... by accumulating copying errors.
And despite the two largest evolutionary experiments that totally disproved this proposition and despite your inability to explain theoretically how evolutionary processes produce tripartite functionality in digital organisms, you are suggesting this is so obvious that only a lack of intelligence can lead to the opposite conclusion? Or, as you put it: "You should be intelligent enough to figure out these things for yourself ..."

Dude, this is sophistry at its best.

MN, you are tragically, comically and tediously wrong.

Why has been pointed out, in detail, at your insistence.

Now you insist on less detail.

Pointing and laughing at your contortions is the only valid response at this point.

Probably too much detail there, sorry bout that.

Fenrir wrote:MN, you are tragically, comically and tediously wrong.

Why has been pointed out, in detail, at your insistence.

Now you insist on less detail.

No, he actually wants even more. He wants to know which mutations and how they work. He wants to be told in detail how an RNA based genetic polymer can suffer mutations(and which specific mutations) to give it catalytic activity. And then he wants to know how, specifically, this particular splicing activity works.

As I expected, he's gone to the Michael Behe defense: If pressed, just demand more detail. No amount you supply will ever be enough. Supposing I bothered digging up references on the elucidation of the crystal structures and mechanisms of binding and catalysis of self-splicing RNA, he'd just demand even more. How did that atom get into that position? Why did those electrons alter their orbital structures? It would never be enough.

Pointing and laughing at your contortions is the only valid response at this point.

Yep.

Indeed.

Perhaps MN could explain nylonase to me then. Under whatever paradigm they claim likely. In detail.

MarioNovak wrote:This is the core of your argument - mutations accumulate... until a mutant arises that has... (name any biological function).. arises.

Yes, because that's how evolution works. The accumulation of mutations in populations of cells are randomly sampling the phenotypical space of the requisite biopolymers. Those that affect fitness in a positive way are retained.

Tell me what other form an evolutionary explanation can even take? Mutations accumulate but nothing ever happens? That's what you want to hear, because that's what you believe. But it would simply not be true.

Biological function is ubiquitous in RNA and protein sequence space. I'm sorry, but this is just a fact. It is also the quintessential point that MUST be denied by all IDcreationists. All their arguments against evolution ultimately reduce to insisting that the opposite is true, that biological function is so rare and hard to find in sequence space, that mutations would forever be hopelessly unable find anything of value through simple accumulations, so they will always and invariably destroy and degrade functional biopolymers. And in so far as a biopolymer is nonfunctional, mutations will never resurrect it to a state of functionality.
This imagination is the result of decades of creationist and ID propaganda, a vision you've got from reading bullshit like this -
A list of various creationists and ID proponents making up these lies to construct this picture(that evolution is basically impossible, because any kind of change through mutations eventually always destroys these marvelously finely-tuned organisms and molecules):

Diogenes wrote:CREATIONISTS and Intelligent Design proponents themselves have stated clearly that every and all mutations are CATASTROPHIC. Remember that? "Catastrophic."

Every human baby born has somewhere between 100 to 200 more mutations than its parents (depending on how you count)-- and twice that number relative to its grandparents-- and thrice that relative to its great-grandparents-- etc.

Young Earth Creationist Kent Hovind: “A change of only three [DNA] nucleotides is fatal to an animal. There is no possibility of [genetic] change.” (Ken Hovind, Source: http://media.drdino.com/sem/audio/mp3/books2.mp3 @ 82:10, March 2003, cited at http://kent-hovind.com/quotes/sciencei.htm)

Got that? Kent Hovind says only three mutations will kill an animal.

If creationism is correct, every baby has 100 to 200 new CATASTROPHES its parents didn't have-- and twice that number of CATASTROPHES relative to its grandparents-- and thrice that relative to its great-grandparents-- etc. Enough to kill every baby on Earth a hundred times over.

Pro-ID Philosopher William Dembski: “[T]here is now mounting evidence of biological systems for which any slight modification does not merely destroy the system’s existing function but also destroys the possibility of any function of the system whatsoever.” [Dembski, The Design Revolution, p. 113]

Pro-ID lawyer Phillip Johnson: “Biologists affiliated with the Intelligent Design movement nail down the distinction by showing that DNA mutations…make birth defects” ["Berkeley's Radical: An Interview with Phillip E. Johnson", November 2000.]

Pro-ID lawyer Edward Sisson: “[T]he theory of unintelligent evolution, which depends entirely on the supposed occurrence in history of trillions of DNA mutations that beneficially affect body shape, has not identified any such mutations” -- [Edward Sisson, “Darwin or Lose”, Touchstone, v. 17, issue 6, July/Aug. 2004]

Uncommon Descent: “As far as I know, the current consensus of population geneticists is that mutations do indeed have disastrously bad fitness.” [Eric Holloway. Uncommon Descent. August 28, 2011.]

Young Earth Creationist Henry Morris: “Inheritable and novel changes (mutations) which take place in organisms today have always been observed to be harmful.” [Henry Morris, The Remarkable Birth of Planet Earth, p.vii]

Young Earth Creationist Duane Gish: “the mutations we see occurring spontaneously in nature or that can be induced in the laboratory always prove to be harmful.” [Gish, Evolution? The Fossils Say No, p. 47]

Duane Gish: “all mutations are bad” [Gish, Dinosaurs by Design (1992), p.83]

Duane Gish: “Remember, all the changes were just mistakes, they were genetic errors, mutations, almost everything which is bad… they're all bad” [Keith Saladin-Duan Gish Debate II, 1988]

Creationist Don Boys: “Not only are mutations always harmful, but they produce changes in present characters, never producing new characters. Mutations are the catalyst for defects, deformity, disease, and death; yet evolutionists scream that they are the explanation for all the varieties we see… [T]he results of all mutations: disorder, defects, disease, deformity, and death.” -- ["Almost a Thousand Major Scientists Dissent from Darwin!", Don Boys. Canada Free Press. May 2, 2010.]

Muslim Creationist Harun Yahya: “[N]ot one single useful mutation has ever been observed… The slightest alteration in [genetic] information only leads to harm.”

The Muslim creationist sex-cult of Harun Yahya says all mutations cause only harm: “Mutations… like all accidents, they cause harm and destruction. The changes effected by mutations can only be like those experienced by people at Hiroshima, Nagasaki, Chernobyl … freaks of nature… because all efficient(?) observable mutations cause only harm to living things.”

There we have it. Plenty of creationist top dogs and professional ID proponents of the Discovery mIsinfotute go out of their ways to tell us that introducing mutations to extant functional DNA and proteins will invariably always lead to loss of function and dead sequences. Mutation just cannot create anything new that works(but again, newness is never defined). This is a deliberate lie they work hard to maintain, it is found in some form or another in ALL the creationist and ID books.

But that view is false, it is a deliberately constructed lie invented by religious fundamentalists. The reality is, again, that biological function is ubiquitous in RNA and protein sequence space.(And yes, I can prove that with plenty of references).
When you insist on denying this concrete empirical reality, all you're really accomplishing is a convincing demonstration that your position is not based on reason or evidence, but a prior commitment to deny inconvenient facts.

You are in effect espousing the classic and fundamental creationist methodology: If reality and doctrine differ, reality is wrong and doctrine is right!

Hry could I get some help. Been trying to look up a paper for a few days. It was about the coding region of a protein important in yeast metabolism being removed and the yeast evolving a new different protein that did the job.