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Author Topic:   Can you disprove this secular argument against evolution?
forexhr
Member (Idle past 90 days)
Posts: 86
Joined: 10-13-2015


Message 241 of 292 (805419)
04-18-2017 12:41 PM
Reply to: Message 240 by Tangle
04-18-2017 11:53 AM


Tangle writes:

Now you're really grasping at straws - that paper deals with e.coli bacteria not a sexually reproducing macro-organism.

That paper deals with non-random nature of mutations and not with differences between various life forms. You are the one grasping at straws.

Tangle writes:

You will also note that the moth's mutation placed a transposon in a place not associated with pigmentation - a properly random event.

Transposon was placed in an intron of the cortex gene. And guess what?

https://www.sciencenewsforstudents.org/...oth-went-dark-side

quote:
The teams have evidence that the cortex gene helps determine when certain wing scales grow. And in butterflies and moths, the timing of wing-scale development affects their colors, says Reed. “You see colors popping up almost like a paint-by-numbers.”

As we can see, besides being uneducated about evolution, biology, mathematics, logic and linguistic you've also shown yourself to be a lier.

Tangle writes:

It was an attempt to get you to deal with real world evolution and away from your fantasy numbers.

Transposons have nothing to do with neither randomness nor evolution. Barbara McClintock who was awarded with the Nobel Prize for her discovery of transposable elements said that transposable elements are controlling elements. Control and randomness are opposite concepts.

http://gos.sbc.edu/m/mcclintock.html

"... These proved to be transposable elements that could regulate gene expressions in precise ways. Because of this I called them " controlling elements ". Their origins and their actions were a focus of my research for many years thereafter. It is their origin that is important for this discussion, and it is extraordinary."

Edited by forexhr, : No reason given.


This message is a reply to:
 Message 240 by Tangle, posted 04-18-2017 11:53 AM Tangle has responded

Replies to this message:
 Message 242 by Tangle, posted 04-18-2017 1:06 PM forexhr has not yet responded
 Message 243 by Genomicus, posted 04-18-2017 1:30 PM forexhr has responded

    
Tangle
Member
Posts: 5102
From: UK
Joined: 10-07-2011
Member Rating: 2.2


(1)
Message 242 of 292 (805425)
04-18-2017 1:06 PM
Reply to: Message 241 by forexhr
04-18-2017 12:41 PM


forexhr writes:

That paper deals with non-random nature of mutations and not with differences between various life forms. You are the one grasping at straws.

So now you're behaving like a typical disingenuous creationist cherry picker. The paper actually tells you that.....

quote:
....it may not be practical to extrapolate very much from an asexually reproducing species such as E. coli to organisms that reproduce sexually.

And Stumpf warns that because bacteria live in such large populations, their evolution in aggregate may be more predictable than that of larger, more dispersed species.


Transposon was placed in an intron of the cortex gene.

It was a mutation in the cortex that changed the colour of the moth period. It's just too bad that you find it incovenient.

Transposons have nothing to do with neither randomness nor evolution.

And the mutation was random and affected the evolution of the moth. Weird huh?


Je suis Charlie. Je suis Ahmed. Je suis Juif. Je suis Parisien.

"Life, don't talk to me about life" - Marvin the Paranoid Android

"Science adjusts it's views based on what's observed.
Faith is the denial of observation so that Belief can be preserved."
- Tim Minchin, in his beat poem, Storm.


This message is a reply to:
 Message 241 by forexhr, posted 04-18-2017 12:41 PM forexhr has not yet responded

  
Genomicus
Member
Posts: 846
Joined: 02-15-2012


(3)
Message 243 of 292 (805435)
04-18-2017 1:30 PM
Reply to: Message 241 by forexhr
04-18-2017 12:41 PM


Transposons have nothing to do with neither randomness nor evolution. Barbara McClintock who was awarded with the Nobel Prize for her discovery of transposable elements said that transposable elements are controlling elements.

Read up on your molecular biology. Transposable elements can regulate nearby genes by virtue of methylation properties, etc., but transposons that "jump" into gene sequences are a form of mutation and are not regulating elements.

Control and randomness are opposite concepts.

There's often a happy medium between control and randomness in genomics, and they are both exploited by selection to "drive" the evolution of species.

As we can see, besides being uneducated about evolution, biology, mathematics, logic and linguistic you've also shown yourself to be a lier.

Why do you feel the need to insult people here?

Edited by Genomicus, : No reason given.


This message is a reply to:
 Message 241 by forexhr, posted 04-18-2017 12:41 PM forexhr has responded

Replies to this message:
 Message 245 by forexhr, posted 04-18-2017 3:43 PM Genomicus has responded

  
bluegenes
Member (Idle past 37 days)
Posts: 3119
From: U.K.
Joined: 01-24-2007


(1)
Message 244 of 292 (805448)
04-18-2017 3:08 PM
Reply to: Message 220 by forexhr
04-17-2017 6:34 AM


Re: The Texas sharpshooter rides again
forexhr writes:

Isn't it interesting how your entire response is focusing on issues that we both agree with.

Entire? If you agree with my post in its entirety, then you are disagreeing with your own O.P.

forexhr writes:

I agree that the Szostak sample wasn't tested for other functions and that it hit its target. I agree that as the polypeptide chain grows in size, the number of functional combinatorial possibilities increases exponentially. I agree that there are many functional amino acid sequences with respect to the vast combinatorial space of possibilities - I stated this explicitly few times already - this is from my last post: "Given the study referenced in the O.P., there are 10^56 "favorable outcomes" and 10^119 possible outcomes".

Right in everything except the numbers. In terms of the repressor function, there are probably far more "favourable outcomes". There could well be ~10^108 (Szostak). That's because the paper looks at function in a "family" of proteins derived from the one that's actually there, but not at the sequentially "unrelated" proteins that also might perform that specific function. The 10^57 would be identifiable as "family" by sequence similarity - they would all have at least 20 identical positions (there were 8 that they considered unchangeable in the sample of 33). That's one of your technical errors. I don't know why you made it, because you must know that there are "super-families" identifiable by function but not by sequence, and the paper doesn't actually claim that their 1 in 10^63 figure covers all proteins that could give a minimal selectable function in that context. As I said in my previous post, the first paper in your O.P. covers the highly degenerate "spellings" of the protein that's there, but not its "synonyms" and their multiple spellings.

forexhr writes:

So, you spent your entire post to repeat something that has already been said and that nobody disagrees with. But, you din't even consider to critically examine the logical consequences of the paper you talked about - if 10^11, out of 10^43 evolutionary resources must be spent just to extract one simple binding function, then how much resources must be spent to extract complex and structurally independent functionas like: conformational complementarity of enzyme and substrate, fertilisation, editing of the nascent precursor messenger RNA transcript, synchronization of the kicks of the hopping insect's legs via gear mechanism, blood pumping, visual perception,.... According to Wikipedia, whose editors savage anyone who criticizes the theory of evolution, "... Complex, image-forming eyes have evolved independently some 50 to 100 times."

Why not just skip to an entire complex organism, like Homo Sapiens. If you "critically examine the logical consequences" of the paper, the implications are that ~18*10^14 protein search resources would be required for our 18,000 proteins. I'm sure you won't make the mistake of multiplying that for all complex species, as they share many proteins. If our life system currently uses 1 billion proteins, then that would require 10^20 search resources.

forexhr writes:

On the other hand, you need 10^11 evolutionary resources to evolve something so simple as ATP binding protein.

Or any new functional protein in any context. Getting an added step in an already complex system with existing proteins is no more difficult than getting the first proteins in life from random assemblies. Probably easier.

forexhr writes:

But even that simple function is not useful biologically. In the real world, proteins that bind to ATP must also be able to release it to complete their function. That may substantially reduce functional sequences. Szostak and Co didn't test to see if their protein was able to perform that feat in vivo. Their experiment was done in vitro. That is a very large difference. Adding that extra requirement will substantially worsened their 1 in 10^11 ratio.

Really? By how much? Are you suggesting, say, ten times, so it would take 10^21 to get 1 billion proteins? Organisms do their protein searching "experiments" in vivo.

forexhr writes:

But this, of course, isn't something to critically think about. Instead, let us repeat something that nobody disagrees with to prove that those who think critically about the above issues are just stupid creationists.

I'm glad you agree with me so far. So, you can now see that there's no case "against evolution" in your O.P. to be "disproved". There's just a sharpshooter fallacy and technical mistakes.

Still, thanks to you for an O.P. that actually links to some interesting papers, and I think you might thank me for reading the papers and helping you through all this.


This message is a reply to:
 Message 220 by forexhr, posted 04-17-2017 6:34 AM forexhr has responded

Replies to this message:
 Message 247 by forexhr, posted 04-19-2017 4:11 AM bluegenes has responded

  
forexhr
Member (Idle past 90 days)
Posts: 86
Joined: 10-13-2015


Message 245 of 292 (805451)
04-18-2017 3:43 PM
Reply to: Message 243 by Genomicus
04-18-2017 1:30 PM


Genomicus writes:

Read up on your molecular biology. Transposable elements can regulate nearby genes by virtue of methylation properties, etc., but transposons that "jump" into gene sequences are a form of mutation and are not regulating elements.

Yes, landing inside a gene can affect its potential protein-coding capacity, but from that it does not follow that the "jump" in the genome of the peppered moth was not pre-programmed, especially if we take into account that it resulted in a phenotypic effect and is located in intronic region of the cortex gene.

Genomicus writes:

There's often a happy medium between control and randomness in genomics, and they are both exploited by selection to "drive" the evolution of species.

Control and randomness have nothing to do with evolution. Control is an instance of functional living systems, while randomness is the lack of predictability in events, which is the general characteristic of natural processes. Evolution on the other hand is concerned with the origin of higher life forms. Higher life forms are characterized by organs, organ systems, de novo molecular machines, metabolic pathways,... none of which can be produced by evolution due to lack of resources, as I already explained.

Genomicus writes:

Why do you feel the need to insult people here?

Not people, but only one intellectually dishonest individual.


This message is a reply to:
 Message 243 by Genomicus, posted 04-18-2017 1:30 PM Genomicus has responded

Replies to this message:
 Message 248 by Genomicus, posted 04-19-2017 6:11 AM forexhr has responded

    
bluegenes
Member (Idle past 37 days)
Posts: 3119
From: U.K.
Joined: 01-24-2007


(1)
Message 246 of 292 (805456)
04-18-2017 4:36 PM
Reply to: Message 221 by forexhr
04-17-2017 6:47 AM


Re: Lambda hits Target with spectacular speed.
Key Innovation in Lambda Phage

forexhr writes:

I don't know what the fuss is all about.

Really?

forexhr writes:

This paper has nothing to do with the issue at hand since it talks neither about evolution of new functional protein folds nor about the ratio of functional amino acid sequences versus the vast combinatorial space.

It didn't take much crossing of that vast space to find a new specific function, did it? You should understand by now from the second paper you linked to in the O.P., the Szostak paper and the one linked to above that potentially functional proteins cannot be very rare islands in a huge sea of non-functionality, as you want them to be.

forexhr writes:

It just talks about the pre-existing viral J protein that acquired the ability to bind a different protein on E. coli, called OmpF, once the LamB protein, to which it normally binds, was turned off. Since both, LamB and OmpF have similar three-dimensional structures, a few mutations in the viral gene fortuitously led to ability of J protein to bind to OmpF. Hence, one out of three functional pre-existing proteins gained the ability to bind a protein similar to one it normally binds, without any change in its native 3-dimensional structure.

It stayed exactly the same while gaining a new function?

forxhr writes:

And this binding ability proves what exactly? That you can produce circulatory system, all joints and bones in your body, or complex, image-forming eyes 100 times independently with 10^43 changes in the spatial positions of molecules?

It is really amazing how you evolution believers explain how everything could have happened: due to few mutations, the pre-existing protein can now stick to something it coud not before - therefore it is a fact that mutations produced all bio-structures that that we observe.

Why is it amazing? If our ancestors observed some rabbits being born from others, why would it be amazing if they inferred that all rabbits came into existence this way? And why would it be amazing if they were sceptical of an alternative suggestion by conjurers that they could produce new rabbits ex nihilo out of hats?


This message is a reply to:
 Message 221 by forexhr, posted 04-17-2017 6:47 AM forexhr has not yet responded

  
forexhr
Member (Idle past 90 days)
Posts: 86
Joined: 10-13-2015


Message 247 of 292 (805526)
04-19-2017 4:11 AM
Reply to: Message 244 by bluegenes
04-18-2017 3:08 PM


Re: The Texas sharpshooter rides again
bluegenes writes:

If you "critically examine the logical consequences" of the paper, the implications are that ~18*10^14 protein search resources would be required for our 18,000 proteins. I'm sure you won't make the mistake of multiplying that for all complex species, as they share many proteins. If our life system currently uses 1 billion proteins, then that would require 10^20 search resources.

I think I already addressed this nonsensical point of yours. Resources that are already spent on search for protein A, which is located in a specific location in the genome of a particular species, cannot be spent on search for protein B which is located in other location of the genome or in other species. Let me use an example for illustration.

Suppose that each of these two words: "CAT" and "DOG", represents a functional protein fold that needs to be found for adaptation purposes, while the text below represents the genomes of three individual organisms(A, B, C), that all have two duplicated gens, "wdc" and "aii", that are free to explore the above mentioned folds:

A) ..............wdc..................................aii
B) ..............wdc..................................aii
C) ..............wdc..................................aii

After the reproduction, we have these changes(mutations):

A) .....A........wdc...........P........U............Dii
B) .......H......wdc........T.......E................aFi
C) .....T........wdc..........P........Z..............aKi

As we can see, although we have spent 12 mutational resources, we have produced just 3 changes in the "aii" gene, while the "wdc" gene didn't get any change. Since the sequence space of "aii" gene is 17,576(26^3) we need on average 17,576 changes on its locus to produce the "DOG" fold. Once these resources are spent they cannot be spent on search for "CAT" fold on "wdc" loci, or search for any other functional fold. To find the "CAT" fold we need another 17,576 resources.

What you did in your nonsensical statement, is put together all the mutations in the history of life that occured in all species of organisms and in all genes, and than you used this number as a separate instance for every new search. This is like writing down every dollar you spent this year and then saying that these, already spent dollars, can now be used for new purchases. All other points in your response are based on misunderstanding of this concept.

Given the fact that you cannot comprehend something so simple(that you cannot spend something that has already been spent), it's no wonder that you bought the theory of evolution from the Darwinian evangelists.

Edited by forexhr, : No reason given.

Edited by forexhr, : No reason given.


This message is a reply to:
 Message 244 by bluegenes, posted 04-18-2017 3:08 PM bluegenes has responded

Replies to this message:
 Message 256 by bluegenes, posted 04-19-2017 10:15 AM forexhr has responded

    
Genomicus
Member
Posts: 846
Joined: 02-15-2012


Message 248 of 292 (805530)
04-19-2017 6:11 AM
Reply to: Message 245 by forexhr
04-18-2017 3:43 PM


Yes, landing inside a gene can affect its potential protein-coding capacity, but from that it does not follow that the "jump" in the genome of the peppered moth was not pre-programmed...

Pre-programmed by what? You can't just drop the word "pre-programmed" around and let that take care of your problems. What do you hypothesize pre-programmed this class II transposon to jump specifically into the intron sequence that it did?

Introns have a ton of sequences. The inverted repeats of transposable elements consist of very short nucleotide sequences, so there's a huge number of possible intronic sites that the transposon could be ligated to.

So where's your evidence that this insertion mutation was pre-programmed in a meaningful way?


This message is a reply to:
 Message 245 by forexhr, posted 04-18-2017 3:43 PM forexhr has responded

Replies to this message:
 Message 249 by forexhr, posted 04-19-2017 7:23 AM Genomicus has responded

  
forexhr
Member (Idle past 90 days)
Posts: 86
Joined: 10-13-2015


Message 249 of 292 (805532)
04-19-2017 7:23 AM
Reply to: Message 248 by Genomicus
04-19-2017 6:11 AM


I presented my evidences already. Given the fact that most mutations are neutral or harmful, while mutation in British peppered moths resulted in a phenotypic effect(non-neutreal) and it didn't negatively affect the protein-coding capacity of the cortex gene(non-harmful) that indicates that this mutation was pre-programmed in the genome. But nevertheless, whatever the cause is, this doesn't change the physical impossibility of evolution.

Edited by forexhr, : No reason given.

Edited by forexhr, : No reason given.


This message is a reply to:
 Message 248 by Genomicus, posted 04-19-2017 6:11 AM Genomicus has responded

Replies to this message:
 Message 250 by Genomicus, posted 04-19-2017 7:27 AM forexhr has responded

    
Genomicus
Member
Posts: 846
Joined: 02-15-2012


Message 250 of 292 (805533)
04-19-2017 7:27 AM
Reply to: Message 249 by forexhr
04-19-2017 7:23 AM


Given the fact that most mutations are neutral or harmful, while mutation in British peppered moths resulted in a phenotypic effect(non-neutreal) and it didn't negatively affect the protein-coding capacity of the cortex gene(non-harmful) that indicates that this mutation was pre-programmed in the genome.

Why does that indicate that this mutation was pre-programmed in the genome? Your logic doesn't add up. And what is the biochemical mechanism of this pre-programming? Describe it to me.

Edited by Genomicus, : No reason given.


This message is a reply to:
 Message 249 by forexhr, posted 04-19-2017 7:23 AM forexhr has responded

Replies to this message:
 Message 251 by forexhr, posted 04-19-2017 8:08 AM Genomicus has responded

  
forexhr
Member (Idle past 90 days)
Posts: 86
Joined: 10-13-2015


Message 251 of 292 (805537)
04-19-2017 8:08 AM
Reply to: Message 250 by Genomicus
04-19-2017 7:27 AM


I am not an expert in this area, but Barbara McClintock, who was, said that the occurrence of the movement and placement of transposable elements is non-random. I believe that these elements are used by cells to regulate specific coding regions of the genome in response to a certain environmental factor. How this happens, exactly, I don’t know.
This message is a reply to:
 Message 250 by Genomicus, posted 04-19-2017 7:27 AM Genomicus has responded

Replies to this message:
 Message 252 by Pressie, posted 04-19-2017 8:13 AM forexhr has responded
 Message 253 by Genomicus, posted 04-19-2017 8:15 AM forexhr has responded
 Message 258 by Taq, posted 04-19-2017 10:58 AM forexhr has responded

    
Pressie
Member
Posts: 1808
From: Pretoria, SA
Joined: 06-18-2010
Member Rating: 2.3


Message 252 of 292 (805540)
04-19-2017 8:13 AM
Reply to: Message 251 by forexhr
04-19-2017 8:08 AM


Ahm great, you came around here pretending to know everything.
Ah, great, you came around here pretending to know everything. Now you're backing off.
This message is a reply to:
 Message 251 by forexhr, posted 04-19-2017 8:08 AM forexhr has responded

Replies to this message:
 Message 254 by forexhr, posted 04-19-2017 9:21 AM Pressie has not yet responded

    
Genomicus
Member
Posts: 846
Joined: 02-15-2012


(3)
Message 253 of 292 (805542)
04-19-2017 8:15 AM
Reply to: Message 251 by forexhr
04-19-2017 8:08 AM


I am not an expert in this area...

It shows.

...but Barbara McClintock, who was, said that the occurrence of the movement and placement of transposable elements is non-random.

So what's her exact quote?

It's only non-random insofar as the inverted repeats in the transposon sequence restricts the reposition of that transposon to genomic locations with complementary sequences; but given that the inverted repeat regions of transposons consist of only a small number of nucleotides, there are many, many regions in the genome which would have complementary sequences.

I believe that these elements are used by cells to regulate specific coding regions of the genome in response to a certain environmental factor. How this happens, exactly, I don’t know.

Blargh. It gets frustrating when the people who claim to be refuting a theory held by the vast majority of molecular biologists don't take the time to, like, actually study molecular biology. We're not talking about how transposable elements regulate genes; we're talking about why you think that the act of a transposon jumping into another genomic region is a pre-programmed act. So describe to me the pre-programming mechanism that makes you think that the insertion in this moth's genome doesn't count as a beneficial mutation.

Edited by Genomicus, : No reason given.

Edited by Genomicus, : No reason given.


This message is a reply to:
 Message 251 by forexhr, posted 04-19-2017 8:08 AM forexhr has responded

Replies to this message:
 Message 255 by forexhr, posted 04-19-2017 9:29 AM Genomicus has responded

  
forexhr
Member (Idle past 90 days)
Posts: 86
Joined: 10-13-2015


Message 254 of 292 (805558)
04-19-2017 9:21 AM
Reply to: Message 252 by Pressie
04-19-2017 8:13 AM


Re: Ahm great, you came around here pretending to know everything.
Pressie writes:

Ah, great, you came around here pretending to know everything. Now you're backing off.


Providing arguments for statements is not "pretending to know everything" but appropriate form of discussing or debating. Is this statement of yours some kind of projection, or some kind of reflection of your personality?
This message is a reply to:
 Message 252 by Pressie, posted 04-19-2017 8:13 AM Pressie has not yet responded

    
forexhr
Member (Idle past 90 days)
Posts: 86
Joined: 10-13-2015


Message 255 of 292 (805562)
04-19-2017 9:29 AM
Reply to: Message 253 by Genomicus
04-19-2017 8:15 AM


Genomicus writes:

It shows.

So, you are an “expert” at every single level of biology?

Genomicus writes:

So what's her exact quote?

There is no quote, you need to read her papers.

Genomicus writes:

It's only non-random insofar as the inverted repeats in the transposon sequence restricts the reposition of that transposon to genomic locations with complementary sequences; but given that the inverted repeat regions of transposons consist of only a small number of nucleotides, there are many, many regions in the genome which would have complementary sequences.

This is non sequitur. We're talking about the causes of the jumps, and not about the characteristics of transposable elements.

Genomicus writes:

Blargh. It gets frustrating when the people who claim to be refuting a theory held by the vast majority of molecular biologists don't take the time to, like, actually study molecular biology.

WOW. What an ignorance. Using an authority as evidence against an argument belongs to the category of logical fallacies. Also, the ToE has nothing to do with biology, but it is a concept, a human mental construct about unseen past events that is contradicted by every instance of observation in biology.

Genomicus writes:

We're not talking about how transposable elements regulate genes; we're talking about why you think that the act of a transposon jumping into another genomic region is a pre-programmed act. So describe to me the pre-programming mechanism that makes you think that the insertion in this moth's genome doesn't count as a beneficial mutation.

I already said why I think so: "given the fact that most mutations are neutral or harmful, while mutation in British peppered moths resulted in a phenotypic effect(non-neutreal) and it didn't negatively affect the protein-coding capacity of the cortex gene(non-harmful) that indicates that this mutation was pre-programmed in the genome." Hence, simple probability.

There is no need for me to describe the exact pre-programming mechanism. Even the most important molecular mechanisms, like those responsible for sperm-egg binding and fusion are largely unknown to science, and yet you are expecting from me to describe the exact mechanisms for something that was largely ignored by geneticists for several decades after Barbara McClintock discovered transposons.


This message is a reply to:
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Replies to this message:
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