Creationists: Explain your understanding of microevolution and macroevolution

[tas8831]

Non-Coding DNA
But some might say that the US government is some kind of cult.

You're hilarious! You're really going to take that and conclude the genome is mostly functional DNA?? LOL!!! You're such a creationist.

This is Ewen Birney's blog. He pretends to interview himself, in a sneaky attempt to admit that they were wrong in their claims by not totally admitting it.
ENCODE: My own thoughts - Ewan's Blog: Bioinformatician at large

Q. Hmmm. Let’s move onto the science. I don’t buy that 80% of the genome is functional.

A. It’s clear that 80% of the genome has a specific biochemical activity – whatever that might be. This question hinges on the word “functional” so let’s try to tackle this first. Like many English language words, “functional” is a very useful but context-dependent word. Does a “functional element” in the genome mean something that changes a biochemical property of the cell (i.e, if the sequence was not here, the biochemistry would be different) or is it something that changes a phenotypically observable trait that affects the whole organism? At their limits (considering all the biochemical activities being a phenotype), these two definitions merge. Having spent a long time thinking about and discussing this, not a single definition of “functional” works for all conversations. We have to be precise about the context. Pragmatically, in ENCODE we define our criteria as “specific biochemical activity” – for example, an assay that identifies a series of bases. This is not the entire genome (so, for example, things like “having a phosphodiester bond” would not qualify). We then subset this into different classes of assay; in decreasing order of coverage these are: RNA, “broad” histone modifications, “narrow” histone modifications, DNaseI hypersensitive sites, Transcription Factor ChIP-seq peaks, DNaseI Footprints, Transcription Factor bound motifs, and finally Exons.

Q. So remind me which one do you think is “functional”?

A. Back to that word “functional”: There is no easy answer to this. In ENCODE we present this hierarchy of assays with cumulative coverage percentages, ending up with 80%. As I’ve pointed out in presentations, you shouldn’t be surprised by the 80% figure. After all, 60% of the genome with the new detailed manually reviewed (GenCode) annotation is either exonic or intronic, and a number of our assays (such as PolyA- RNA, and H3K36me3/H3K79me2) are expected to mark all active transcription. So seeing an additional 20% over this expected 60% is not so surprising.

However, on the other end of the scale – using very strict, classical definitions of “functional” like bound motifs and DNaseI footprints; places where we are very confident that there is a specific DNA-protein contact, such as a transcription factor binding site to the actual bases – we see a cumulative occupation of 8% of the genome. With the exons (which most people would always classify as “functional” by intuition) that number goes up to 9%. Given what most people thought earlier this decade, that the regulatory elements might account for perhaps a similar amount of bases as exons, this is surprisingly high for many people – certainly it was to me!

In addition, in this phase of ENCODE we did sample broadly but nowhere near completely in terms of cell types or transcription factors. We estimated how well we have sampled, and our most generous view of our sampling is that we’ve seen around 50% of the elements. There are lots of reasons to think we have sampled less than this (e.g., the inability to sample developmental cell types; classes of transcription factors which we have not seen). A conservative estimate of our expected coverage of exons + specific DNA-protein contacts gives us 18%, easily further justified (given our sampling) to 20%​

Wow - 20% is totally most of the genome!

 

[tas8831]

Did you even read your own links you dumb cluck?

Look at you, all religionist and such!
Yes, I did. You did the creationist shuffle - saw something you thought you could run with and ignored the refutation of your dopey, uninformed claim.
Not my fault you can't hang. You claimed tiny bits, remember? WHOLE GENOMES ARE NOT TINY BITS YOU CREATIONIST.

This paper is making my argument against junk DNA!

You're hilarious and predictable.
This paper rebuts the ENCODE claims, or we can just see what the numbers ENCODE folks came up with ACTUALLY indicated, straight from the director of the project:

This is Ewen Birney's blog. He pretends to interview himself, in a sneaky attempt to admit that they were wrong in their claims by not totally admitting it.
ENCODE: My own thoughts - Ewan's Blog: Bioinformatician at large

Q. Hmmm. Let’s move onto the science. I don’t buy that 80% of the genome is functional.

A. It’s clear that 80% of the genome has a specific biochemical activity – whatever that might be. This question hinges on the word “functional” so let’s try to tackle this first. Like many English language words, “functional” is a very useful but context-dependent word. Does a “functional element” in the genome mean something that changes a biochemical property of the cell (i.e, if the sequence was not here, the biochemistry would be different) or is it something that changes a phenotypically observable trait that affects the whole organism? At their limits (considering all the biochemical activities being a phenotype), these two definitions merge. Having spent a long time thinking about and discussing this, not a single definition of “functional” works for all conversations. We have to be precise about the context. Pragmatically, in ENCODE we define our criteria as “specific biochemical activity” – for example, an assay that identifies a series of bases. This is not the entire genome (so, for example, things like “having a phosphodiester bond” would not qualify). We then subset this into different classes of assay; in decreasing order of coverage these are: RNA, “broad” histone modifications, “narrow” histone modifications, DNaseI hypersensitive sites, Transcription Factor ChIP-seq peaks, DNaseI Footprints, Transcription Factor bound motifs, and finally Exons.

Q. So remind me which one do you think is “functional”?

A. Back to that word “functional”: There is no easy answer to this. In ENCODE we present this hierarchy of assays with cumulative coverage percentages, ending up with 80%. As I’ve pointed out in presentations, you shouldn’t be surprised by the 80% figure. After all, 60% of the genome with the new detailed manually reviewed (GenCode) annotation is either exonic or intronic, and a number of our assays (such as PolyA- RNA, and H3K36me3/H3K79me2) are expected to mark all active transcription. So seeing an additional 20% over this expected 60% is not so surprising.

However, on the other end of the scale – using very strict, classical definitions of “functional” like bound motifs and DNaseI footprints; places where we are very confident that there is a specific DNA-protein contact, such as a transcription factor binding site to the actual bases – we see a cumulative occupation of 8% of the genome. With the exons (which most people would always classify as “functional” by intuition) that number goes up to 9%. Given what most people thought earlier this decade, that the regulatory elements might account for perhaps a similar amount of bases as exons, this is surprisingly high for many people – certainly it was to me!

In addition, in this phase of ENCODE we did sample broadly but nowhere near completely in terms of cell types or transcription factors. We estimated how well we have sampled, and our most generous view of our sampling is that we’ve seen around 50% of the elements. There are lots of reasons to think we have sampled less than this (e.g., the inability to sample developmental cell types; classes of transcription factors which we have not seen). A conservative estimate of our expected coverage of exons + specific DNA-protein contacts gives us 18%, easily further justified (given our sampling) to 20%​

Wow - 20% is totally most of the genome!

Max Libbrecht also publicly stated that 'nobody' at ENCODE actually thinks the genome is 80+% functional.

But you're a creationist, so...

I accept your concession re: extent of genome comparisons and reject your claims of superior knowledge on any topic.

 

[tas8831]

Breeding of variants with specific alleles that already exist in the gene pool.

How do alleles arise?

I don't expect citations from macroevolutionists, I expect citations from those with a serious interest in dealing with the problem of drug resistance and failed cancer treatments.

Which would make sense because your papers are irrelevant to macroevolution. But... none of your target audience seems to find them worthy of consideration, either. You poor loser...

Do you think two centuries of mathematically incompetent stories about evolution is going to be washed away instantly?

Do I think your depiction of the situation is anything more than dopey megalomania?
You're predictable and tiresome.

I may not have very many citations for my paper (yet)

You never will. Nobody buys into such pap.

, but you don't have any papers at all.

Sure I do. I am not going to put my name out there because I have seen what righty creationist-types do when they get hold of someone's name.

Maybe I will dismiss your nonsense later, but I have better things to do right now.

ADDED IN EDIT:
Ooh! I just checked my stats and I got yet another citation today! How about you?.....

 

[Alan Kleinman]

You're hilarious! You're really going to take that and conclude the genome is mostly functional DNA?? LOL!!! You're such a creationist.

This is Ewen Birney's blog. He pretends to interview himself, in a sneaky attempt to admit that they were wrong in their claims by not totally admitting it.
ENCODE: My own thoughts - Ewan's Blog: Bioinformatician at large

Q. Hmmm. Let’s move onto the science. I don’t buy that 80% of the genome is functional.

A. It’s clear that 80% of the genome has a specific biochemical activity – whatever that might be. This question hinges on the word “functional” so let’s try to tackle this first. Like many English language words, “functional” is a very useful but context-dependent word. Does a “functional element” in the genome mean something that changes a biochemical property of the cell (i.e, if the sequence was not here, the biochemistry would be different) or is it something that changes a phenotypically observable trait that affects the whole organism? At their limits (considering all the biochemical activities being a phenotype), these two definitions merge. Having spent a long time thinking about and discussing this, not a single definition of “functional” works for all conversations. We have to be precise about the context. Pragmatically, in ENCODE we define our criteria as “specific biochemical activity” – for example, an assay that identifies a series of bases. This is not the entire genome (so, for example, things like “having a phosphodiester bond” would not qualify). We then subset this into different classes of assay; in decreasing order of coverage these are: RNA, “broad” histone modifications, “narrow” histone modifications, DNaseI hypersensitive sites, Transcription Factor ChIP-seq peaks, DNaseI Footprints, Transcription Factor bound motifs, and finally Exons.

Q. So remind me which one do you think is “functional”?

A. Back to that word “functional”: There is no easy answer to this. In ENCODE we present this hierarchy of assays with cumulative coverage percentages, ending up with 80%. As I’ve pointed out in presentations, you shouldn’t be surprised by the 80% figure. After all, 60% of the genome with the new detailed manually reviewed (GenCode) annotation is either exonic or intronic, and a number of our assays (such as PolyA- RNA, and H3K36me3/H3K79me2) are expected to mark all active transcription. So seeing an additional 20% over this expected 60% is not so surprising.

However, on the other end of the scale – using very strict, classical definitions of “functional” like bound motifs and DNaseI footprints; places where we are very confident that there is a specific DNA-protein contact, such as a transcription factor binding site to the actual bases – we see a cumulative occupation of 8% of the genome. With the exons (which most people would always classify as “functional” by intuition) that number goes up to 9%. Given what most people thought earlier this decade, that the regulatory elements might account for perhaps a similar amount of bases as exons, this is surprisingly high for many people – certainly it was to me!

In addition, in this phase of ENCODE we did sample broadly but nowhere near completely in terms of cell types or transcription factors. We estimated how well we have sampled, and our most generous view of our sampling is that we’ve seen around 50% of the elements. There are lots of reasons to think we have sampled less than this (e.g., the inability to sample developmental cell types; classes of transcription factors which we have not seen). A conservative estimate of our expected coverage of exons + specific DNA-protein contacts gives us 18%, easily further justified (given our sampling) to 20%​

Wow - 20% is totally most of the genome!

Why don't you read your own link?

However, the coding (coding for proteins, ribosomal RNAs, transfer RNAs, and other functional RNAs) portions of mammalian genomes can amount to as little as 1–3% of the whole genomic sequence, and it is debatable whether species phylogenies derived from a small, alignable subfraction of the whole genome are reliable. As for the noncoding sequence (the other 99%), much of its function is unknown, yet much of this portion is indeed transcribed.

 

[Ponderous Curmudgeon]

This paper is making my argument against junk DNA!

Now, if you want to see how macroevolutionists bungle the mathematics of phylogenetics, read this link:
How to build a phylogenetic tree

First, Tas's paper is pointing out that it seems to matter little what type of genome subset you use you still get similar trees. This would argue that even if it is junk, it follows the same patterns as the macroevolutionary path that leads to the same phylogeny of conserved DNA.
As to your link, what is wrong with it? your math does not preclude it without a definition of time which is not relevant to the method. Ie even if your math is correct it could still happen that way, so why is it wrong?

 

[Alan Kleinman]

How do alleles arise?

Now tas wants to discuss abiogenesis.

Which would make sense because your papers are irrelevant to macroevolution. But... none of your target audience seems to find them worthy of consideration, either. You poor loser...

tas is now going to present his mathematical model of macroevolution and present experimental evidence that substantiates that model. NOT!

Do I think your depiction of the situation is anything more than dopey megalomania?
You're predictable and tiresome.

Maybe I will dismiss your nonsense later, but I have better things to do right now.

Whatever it is that you do, it isn't the correct explanation of the evolution of drug resistance and why cancer treatments fail.

ADDED IN EDIT:
Ooh! I just checked my stats and I got yet another citation today!

Oh my! Why don't you give us a link to this paper so we see a bit of your wisdom?

 

[pitabread]

That is priceless coming from a creationist who doesn't know the difference between a species and dog breed.

Dunning-Kruger effect maybe?

 

[FrumiousBandersnatch]

You do know that reptiles don't have a loop of Henle and birds do? If you don't know what a loop of Henle is, look it up.

I'm familiar with anatomy; I graduated in human biology. Modern reptiles may not have anything long enough to constitute an LoH (although there is some ambiguity over this), but that doesn't mean the coelurosaurian dinosaurs didn't. The LoH in birds is short compared to mammals. Do you have any evidence that coelurosaurian dinosaurs didn't have LoH? Have any fossilised dinosaur kidneys been discovered?

 

[Hans Blaster]

I don't expect citations from macroevolutionists, I expect citations from those with a serious interest in dealing with the problem of drug resistance and failed cancer treatments.

Are macroevolutionists some sort of fantasy giant people?

This thread isn't about drug resistance or cancer treatments -- it's about how creationists understand the terms macro/micro evolution. Your understanding seems to fall within the standard definitions. Your other positions...

 

[Ponderous Curmudgeon]

Breeding of variants with specific alleles that already exist in the gene pool.

I don't expect citations from macroevolutionists, I expect citations from those with a serious interest in dealing with the problem of drug resistance and failed cancer treatments. Do you think two centuries of mathematically incompetent stories about evolution is going to be washed away instantly? The problem is trying to explain the physics and mathematics of evolution to those whose scientific training is limited to a couple of courses in dumbbell math and a survey course in physics. You macroevolutionists even bungled the very simple physics and mathematics of evolutionary competition. How pathetic can a college education in biology get?

I may not have very many citations for my paper (yet), but you don't have any papers at all. You macroevolutionists can't even explain the Kishony experiment and that mathematics is trivial. We all can see what a couple of courses of dumbbell math and a survey course in physics get you, the ability to write science-fiction.

Claiming the consensus is wrong is about as useful as standing on a street-corner expounding. Even if you are right, no-one takes it as anything more than petulance until you offer something useful to replace it. If you are waiting for someone else to have an epiphany it is less likely than your odds of macroevolution. Identifying a problem is the smallest part of a gain in knowledge, the work comes in in finding a better solution. Get to it.

 

[Frank Robert]

Are macroevolutionists some sort of fantasy giant people?

This thread isn't about drug resistance or cancer treatments -- it's about how creationists understand the terms macro/micro evolution. Your understanding seems to fall within the standard definitions. Your other positions...

Alan has to use what he has and if the only tool he has is a hammer...

 

[FrumiousBandersnatch]

Give us one experiment, just one, that you claim confirms macroevolution, and let's discuss that experiment.

Fossil tea-leaf readers construct phylogenetic trees to fit their theory. The only correct way to construct a phylogenetic tree is using genetics, actual genetic sequences. Do you have any idea how that is done? Macroevolutionists can't even do that correctly.

I'm not arguing whether evolution or occurs or not, I'm arguing the correct physics and mathematics of the evolutionary process. You will not present a single experimental example demonstrating that the model I"m presenting of microevolution is incorrect. And then your clique claims that macroevolution is simply the addition of a series of microevolutionary events. They obviously didn't cover introductory probability theory in the dumbbell math courses biologists take. If they did you would understand that you don't compute joint probabilities of random events by adding the individual probabilities of each of these events, you have to multiply those probabilities.

If the fossil record explains so much about evolution, take that understanding you get from reading the fossil record and explain the Kishony and Lenski biological evolutionary experiments. You can't because the fossil record is a (mis)interpretation of a phenomenon based on incorrect assumptions. You start with the belief that common descent is true and then look for fossils that justify that assumption.

You can search through 3 billion base sequences and find matches here and there. It's the differences in the genomes that you ignore and these differences are the way you determine whether replicators are related or not.

There are very specific scientific and mathematical reasons why I reject these claims. That's why I try to pin you down to what you think your best claim is so we can discuss that claim in detail so that you can understand why I reject the claim. That's the way I challenge your reasoning. I present a model of microevolution that even Frank can understand. Your clique argues back that it only models 2 evolutionary experiments, I argue, present an experimental example that contradicts this math, you don't do it.

So present what you think is the best argument you have for macroevolution and let's discuss it. This forum is as good as anywhere elese.

Frankly, I've given enough links and spent enough time on your wild goose chase. It's the experts in the field you need to persuade, and you won't do it here.

 

[Ponderous Curmudgeon]

tas8831 said: ↑
How do alleles arise?

Now tas wants to discuss abiogenesis.

What, you think that generation of alleles is abiogenesis? many weird emoticons.

 

[Alan Kleinman]

First, Tas's paper is pointing out that it seems to matter little what type of genome subset you use you still get similar trees. This would argue that even if it is junk, it follows the same patterns as the macroevolutionary path that leads to the same phylogeny of conserved DNA.

Read carefully what they wrote:

However, the coding (coding for proteins, ribosomal RNAs, transfer RNAs, and other functional RNAs) portions of mammalian genomes can amount to as little as 1–3% of the whole genomic sequence, and it is debatable whether species phylogenies derived from a small, alignable subfraction of the whole genome are reliable. As for the noncoding sequence (the other 99%), much of its function is unknown, yet much of this portion is indeed transcribed.

If the "junk" portions of the genome are conserved, they shouldn't have to cherry-pick small alignable subfractions of the genome to determine relatedness.

As to your link, what is wrong with it? your math does not preclude it without a definition of time which is not relevant to the method. Ie even if your math is correct it could still happen that way, so why is it wrong?

It has to do with what I bold-faced from the quote above from tas's link. When doing statistical analysis, the sampling process must be random. For example, let's say I want to see whether humans and chimpanzees are related. Based on this strategy, I would go to the human genome, find a gene (eg preproinsulin), look for the same gene in the chimpanzee genome, and use some model such as the Jukes-Cantor model to see how many generations needed to account for any genetic difference. Then, let's say I want to see how closely related humans are to bananas. I would search the human and banana genome, see if I could find an alignable subfraction, and crunch the numbers. There is no reason why you couldn't prove that we are more closely related to bananas than chimpanzees using this kind of sampling process.

The correct way to do this type of analysis would be to use the entire genome. But since the computational load would be massive, the subfractions of the genome have to be selected randomly. This is the major problem from that link on building phylogenetic trees. There is a smaller but significant problem when using DNA evolution models such as the Jukes-Cantor and derivative models when doing this type of calculation but that explanation is much more complex than the math I've already presented. It requires an understanding of how to do Markov process mathematics.

 

[Alan Kleinman]

I'm familiar with anatomy; I graduated in human biology. Modern reptiles may not have anything long enough to constitute an LoH (although there is some ambiguity over this), but that doesn't mean the coelurosaurian dinosaurs didn't. The LoH in birds is short compared to mammals. Do you have any evidence that coelurosaurian dinosaurs didn't have LoH? Have any fossilised dinosaur kidneys been discovered?

These authors don't seem to think there is any ambiguity:
Structure of avian loop of Henle as related to countercurrent multiplier system - PubMed

The ultrastructural detail of the avian loop of Henle was examined, and comparisons were made to the loop of Henle of mammalian kidneys. Birds are the only group of vertebrates other than mammals that have the capability of elaborating a urine more concentrated than the plasma.

 

[tas8831]

Why don't you read your own link?

LOL!

I guess you are unaware of spurious transcription and that kind of thing.
My gosh you are a Dunning-Kruger effect creationist Prom Queen, aren't you?

Again, I accept your concession re: 'tiny bits" of genomes used in phylogenetic analyses.

 

[Alan Kleinman]

Are macroevolutionists some sort of fantasy giant people?

No, they are little people with a giant fantasy.

This thread isn't about drug resistance or cancer treatments -- it's about how creationists understand the terms macro/micro evolution. Your understanding seems to fall within the standard definitions. Your other positions...

Hans, I understand you haven't done any study in this area and have no expertise on this subject but the evolution of drug resistance and the failure of cancer treatments are microevolutionary processes. And those processes are predicted by the math that I've presented.

 

[Alan Kleinman]

Frankly, I've given enough links and spent enough time on your wild goose chase. It's the experts in the field you need to persuade, and you won't do it here.

I understand, there are no experts here to debate with that understand the physics and mathematics of biological evolution. But at least Warden has learned how evolutionary competition is a first law of thermodynamics process.

If I were you, I wouldn't want to defend any of the so-called evidence of macroevolution. It's too easy to find the illogic in the claims.

 

[Alan Kleinman]

How do alleles arise?

Now tas wants to discuss abiogenesis.

What, you think that generation of alleles is abiogenesis? many weird emoticons.

The generation of new alleles from an already existing gene (allele of that gene) by mutations is microevolution, for alleles to arise where the gene never existed is abiogenesis.

 

[Hans Blaster]

ADDED IN EDIT:
Ooh! I just checked my stats and I got yet another citation today! How about you?.....

Me too! Up one from when I checked on the weekend.