Uncommon Descent Serving The Intelligent Design Community

1,177 human orphan genes removed by evolutionists from databases

Share
Facebook
Twitter
LinkedIn
Flipboard
Print
Email

Here is a case of evolutionary bias causing misrecognition of orphan genes in humans. Orphan genes are presumed protein coding genes that exist in only one species and have such non-similarity to anything in any other species they are called orphans (a play on words of the ORF acroym for Open Reading Frame).

This came up in the Nelson-Velasco debate where Velasco said there are 0 orphan genes, and Nelson pointed out the reason some say they are zero is because of their biases.

Nelson has been vindicated as I pointed out in New Mechanism of Evouion — POOF

Here’s is the proof of this cover up Distinguishing protein-coding and noncoding genes in the human genome:

1. “The remaining 1,177 cases were declared to be orphans, because they lack orthology, paralogy, or homology to known genes and are not obvious artifacts… If the orphans represent valid human protein-coding genes, we would have to conclude that the vast majority of the orphans were born after the divergence from chimpanzee. Such a model would require a prodigious rate of gene birth in mammalian lineages and a ferocious rate of gene death erasing the huge number of genes born before the divergence from chimpanzee. We reject such a model as wholly implausible. We thus conclude that the vast majority of orphans are simply randomly occurring ORFs that do not represent protein-coding genes… We found… 12 reported cases of orphans with experimental evidence for an encoded protein”

The problem with these authors is in 2007 they didn’t invoke the POOF mechanism of evolution which other evolutionists happily embrace now in 2013:

However, with the advent of sequencing of full genomes, it became clear that approximately 20–40% of the identified genes could not be associated with a gene family that was known before. Such genes were originally called ‘orphan’ genes

Evolutionary Origin of Orphan Genes

20-40% of the genes discovered cannot be explained by common ancestry or common descent. So what mechanism is left to explain it? Special creation? But evolutionists can’t accept special creation, so they just pretend they’ve made a discovery of a new mechanism of evolution that can work just as well.

They haven’t given it a name yet, so let us call it POOF. What is POOF? POOF is the mechanism by which proteins can easily arise out random nucleotide sequences like a poem can emerge out of randomly tossed scrabble letters. I bold one of their euphemisms for the POOF mechanism in the following paragraph:

Orphan genes may have played key roles in generating lineage specific adaptations and could be a continuous source of evolutionary novelties. Their existence suggests that functional ribonucleic acids (RNAs) and proteins can relatively easily arise out of random nucleotide sequences, although these processes still need to be experimentally explored.

😯

The reasoning they use goes like this, “we have all these genes that can’t be explained by slight successive modifications, so they must have arisen spontaneously out of nowhere. Because evolution is fact, this implies evolution can just take random material and create functional systems in a flash. We’ve made a fabulous discovery about the miracles of evolution even though we can’t demonstrate it experimentally.”

HT JoeCoder
www.reddit.com/r/creation

Comments
tjguy @126,
Common genetic code is a predicted feature of purposefully engineered systems in the genomes of creatures that share the same environment and have similar requirements. It’s just like a computer programmer who uses common pieces of code in different software programs.
Excellent point. That we find in a genome both code-reuse and code specific to the given kind is precisely what intelligent design predicts. It is exactly what programmers do all day long: Reuse code where possible and add new code specific to whatever new features an application requires. What is more difficult is to write software that will run on various operating systems and hardware, and will cope with unexpected, undefined input and still function meaningfully. For the software of life, "functioning meaningfully" is surviving long enough to reproduce. This requires an adaptability being built into life's software that is way beyond human-written software. We already knew from experience with "artificial" selection, like dog breeding, that a given kind could have a wild variety of possible traits. Dog breeders had powerfully demonstrated this, and if evolution worked the way Darwin had proposed, breeders would have eventually bred dogs into something that couldn't be called a dog. That didn't happen.* So, what the canine genome contained was the information to construct a wild variety of canines, but nothing else; it appears to be information composed for a specific purpose: the creation of a particular kind. The adaptability to changing environments provided by the various versions of dogs that can be derived from that information indicates its composer's genius as well His intentions: The dog-kind was to last for a while. The fossil record is full of evidence that a given kind suddenly appears and lasts until the magnitude of the changes to the environment exceeds the adaptability of that kind. It's as though it was all preprogrammed. Maybe that's because it was. ;o) * Yes, I know the objection: "Dog breeders haven't been at it for millions of years." That objection fails miserably. What would take forever to happen mindlessly and accidentally, like the scattered jigsaw puzzle pieces of a 500 piece puzzle being correctly assembled accidentally, takes only a few hours for an intelligence to accomplish. If evolution worked the way Darwin proposed, dog breeders would have bred dogs into something else by now. We now know that didn't happen because the information required to build something else just isn't in the "dog-kind" genome. That information is as unlikely to be arrived at accidentally as it is for that jigsaw puzzle to get assembled accidentally, which is to say that it just isn't going to happen.harry
January 23, 2016
January
01
Jan
23
23
2016
08:05 AM
8
08
05
AM
PDT
BA77, I have put up the Dawkins video clip and some screen shots on the FOXP family: https://uncommondescent.com/atheism/ba77-and-a-vid-on-foxp-123-molecular-trees-vs-dawkins-claim-of-you-get-the-same-family-tree/ Let us see what this is, gross error by Dawkins or the grand daddy of all hoaxes and quote mines. KFkairosfocus
January 23, 2016
January
01
Jan
23
23
2016
04:56 AM
4
04
56
AM
PDT
http://www.icr.org/article/9145 Genetic Gap Widens Between Humans and Chimps by Jeffrey P. Tomkins, Ph.D. * Evidence for Creation › Evidence from Science › Evidence from the Life Sciences › All Life Systems Were Created by God › DNA Was Created as a Reservoir for the Information of Life Increasingly, orphan genes defy evolution and support the Genesis account of creation. These genes are unique sets of coding sequences specific to particular creatures. This is a big problem for evolutionary ideas to explain. In a recent research report, scientists describe a new set of 1,307 orphan genes that are completely different between humans and chimpanzees.1 Orphan genes, as the name implies, are found in no other type of creature and therefore have no evolutionary history. This finding is another key prediction of the creation model. Not only should creatures have similar code for similar functions, but they should also have unique code that makes them distinct from other creatures. In support of this creation prediction, scientists discovered that orphan genes are incredibly important for specific biological processes and traits that correspond with specialized adaptations. Several previous articles published on the ICR news site have described these types of genes discovered in zebrafish and honey bees.2,3 Many creatures with similar types of body plans and other shared biological traits, possess similar sets of core genes. Evolutionists claim that this is evidence of common ancestry. However, creationists propose a more obvious and efficient explanation: Common genetic code is a predicted feature of purposefully engineered systems in the genomes of creatures that share the same environment and have similar requirements. It's just like a computer programmer who uses common pieces of code in different software programs. In yet another recent research report, scientists describe 634 orphan genes in humans and 780 in chimpanzees.1 In other words, we now have a new set of 1,307 genes that are completely different between humans and chimpanzees. In fact, the chimp-specific genes are not found in any other supposed chimp ancestor—like macaque, an extant monkey. They are unique to the chimps just like the human orphan genes are unique to humans. Darwinian evolution did not predict this remarkable discovery. Essentially exposing evolution's weakness in explaining orphan genes, the researchers say, "For the past 20 years scientists have puzzled over a strange-yet-ubiquitous genomic phenomenon; in every genome there are sets of genes which are unique to that particular species i.e. lacking homologues [similar counterparts] in any other species."1 Another interesting fact about these newly discovered orphan genes is that they represent just a subset of the genes unique to chimp or human. The researchers only analyzed genes expressed in liver, heart, brain, and testes. Many other bodily tissues still need to be examined. In addition, the team only analyzed genes that were spliced, meaning complex genes that have coding and non-coding regions, with the coding regions being snipped out of the RNA transcript after they are copied from the DNA. Many other genes in the genome are not spliced and were not included in this study. Needless to say, the numerous gene differences that scientists discovered between humans and chimps cannot be accounted for by Darwin's theory of common ancestry. Not only do orphan genes and the amazing creature-specific traits they encode challenge evolution, they also help creationists understand the patterns of genome structure related to created kinds. While obvious differences between humans and chimps defy evolution on a grand scale, the presence of orphan genes underscores the uniqueness of humans created in God's image.tjguy
January 23, 2016
January
01
Jan
23
23
2016
03:05 AM
3
03
05
AM
PDT
BA: OK, thank you. I don't really understand your points, but that's fine.gpuccio
April 18, 2014
April
04
Apr
18
18
2014
10:44 AM
10
10
44
AM
PDT
Via the videos, I don't find your points empirically strong to the conclusion you would like to make. Via the sheer disconnect between information for form and information for sequences (Meyer) I don't find your beliefs to be scientifically relevant. Via the punctuated fossil record (Gould) I don't find your beliefs to be anything more than philosophical presuppositions. i.e. the case for common descent simply is not there empirically.bornagain77
April 18, 2014
April
04
Apr
18
18
2014
08:47 AM
8
08
47
AM
PDT
BA: Is it possible to have your personal answers and arguments? I don't like to discuss with videos.gpuccio
April 18, 2014
April
04
Apr
18
18
2014
08:26 AM
8
08
26
AM
PDT
as to: 1) Homologies between non coding sequences and new orphan genes (as discussed here). Orphan Genes (And the peer reviewed ‘non-answer’ from Darwinists) – lifepsy video http://www.youtube.com/watch?v=1Zz6vio_LhY and 2) Sequence differences in structurally and functionally similar homologous proteins in species, with differences usually increasing in more distant species. (FoxP2) Dawkins Best Evidence Refuted - video https://www.youtube.com/watch?v=IfFZ8lCn5uUbornagain77
April 18, 2014
April
04
Apr
18
18
2014
06:28 AM
6
06
28
AM
PDT
BA: Just to know, how do you explain the following two observations? 1) Homologies between non coding sequences and new orphan genes (as discussed here). 2) Sequence differences in structurally and functionally similar homologous proteins in species, with differences usually increasing in more distant species. With that, I have no personal agenda about CD. I have no reason to accept it and no reason to reject it, out of what I sincerely think because of the facts I know. I have absolutely no religious or philosophical position about common descent. Moreover, I don't think that at present we have a definite tree of life which is consistent or credible. I am aware that trees of life generate great inconsistencies according to how they are built. Maybe that means that no tree of life exists, and that CD needs to be reconsidered. Or maybe it means something about the validity, or lack of it, of the different methods used. Or maybe it means something else, that we still need to understand. Whatever it is, I am very interested in understanding it. I don't believe that CD should necessarily be universal, nor that it must be the only or even the main modality of evolution. I am fully open to any interpretation, provided that facts and good scientific reasoning be in favor of it. I thank you sincerely for your respect, and I want to ensure you that I appreciate very much your contributions here. You have given me many fundamental ideas and informations. And I believe we share the most fundamental ideas about design in biology. So, I fully respect your position. Please, do the same with mine.gpuccio
April 18, 2014
April
04
Apr
18
18
2014
06:20 AM
6
06
20
AM
PDT
gpuccio, though I usually greatly respect your opinion (and your work in general against Darwinists), your reason for supporting common descent lacks much to be desired empirically. If body forms are disregarded and sequences are allowed priority, as you hold, even though there is severe incongruousness in sequence data, and even though information of 'form' is not reducible to sequential information, then how is your view to be regarded with any more respect than the typical Darwinian views? i.e. regarded as empirically relevant and 'scientific'? You are basically stating your personal opinion as if it should have 'scientific' weight, and, as far as empirical evidence is concerned, there is not such weight to be had for your opinion. a few notes to that effect: Logged Out - Scientists Can't Find Darwin's "Tree of Life" Anywhere in Nature by Casey Luskin - Winter 2013 Excerpt: the (fossil) record shows that major groups of animals appeared abruptly, without direct evolutionary precursors. Because biogeography and fossils have failed to bolster common descent, many evolutionary scientists have turned to molecules—the nucleotide and amino acid sequences of genes and proteins—to establish a phylogenetic tree of life showing the evolutionary relationships between all living organisms.,,, Many papers have noted the prevalence of contradictory molecule-based phylogenetic trees. For instance: • A 1998 paper in Genome Research observed that "different proteins generate different phylogenetic tree[s]."6 • A 2009 paper in Trends in Ecology and Evolution acknowledged that "evolutionary trees from different genes often have conflicting branching patterns."7 • A 2013 paper in Trends in Genetics reported that "the more we learn about genomes the less tree-like we find their evolutionary history to be."8 Perhaps the most candid discussion of the problem came in a 2009 review article in New Scientist titled "Why Darwin Was Wrong about the Tree of Life."9 The author quoted researcher Eric Bapteste explaining that "the holy grail was to build a tree of life," but "today that project lies in tatters, torn to pieces by an onslaught of negative evidence." According to the article, "many biologists now argue that the tree concept is obsolete and needs to be discarded.",,, Syvanen succinctly summarized the problem: "We've just annihilated the tree of life. It's not a tree any more, it's a different topology entirely. What would Darwin have made of that?" ,,, "battles between molecules and morphology are being fought across the entire tree of life," leaving readers with a stark assessment: "Evolutionary trees constructed by studying biological molecules often don't resemble those drawn up from morphology."10,,, A 2012 paper noted that "phylogenetic conflict is common, and [is] frequently the norm rather than the exception," since "incongruence between phylogenies derived from morphological versus molecular analyses, and between trees based on different subsets of molecular sequences has become pervasive as datasets have expanded rapidly in both characters and species."12,,, http://www.salvomag.com/new/articles/salvo27/logged-out.php podcast - Molecular Data Wreak Havoc on (Darwin's) Tree of Life - Casey Luskin - March 2014 http://intelligentdesign.podomatic.com/entry/2014-03-14T16_17_31-07_00 Shark Proteins Contradict the Standard Phylogeny of Vertebrates - Casey Luskin - January 6, 2014 Excerpt: there's almost no dataset that can contradict (falsify) common descent. Every time you find that one trait predicts one phylogeny, and another trait predicts a conflicting phylogeny, you can effect a reconciliation by invoking at will more evolutionary steps of convergent loss or gain of traits, or invoking a host of other ad hoc explanations. In a worst case scenario, if genes were distributed in the most un-treelike manner imaginable, I suppose you could take all the known genes present in the most recent presumed common ancestor of that group, and then simply invoke losses (and gains) of genes to reconcile the observed distribution with a tree. - http://www.evolutionnews.org/2014/01/shark_proteins_080781.htmlbornagain77
April 18, 2014
April
04
Apr
18
18
2014
05:39 AM
5
05
39
AM
PDT
BTW sez fits because you definitely cannot support anything you post wrt biology and evolution. You are nothing but a deluded little punk first year biology student.Joe
April 18, 2014
April
04
Apr
18
18
2014
05:05 AM
5
05
05
AM
PDT
AVS you are definitely a cowardly projector. You trying to insult me is laughable. But I understand that is all you have.Joe
April 18, 2014
April
04
Apr
18
18
2014
05:03 AM
5
05
03
AM
PDT
"sez"? Joe, you're definitely a pre-pubescent with a single-digit IQ. No wonder you fit in here at UD.AVS
April 18, 2014
April
04
Apr
18
18
2014
05:00 AM
5
05
00
AM
PDT
AS for Allen's "engines of variation", it should be noted that no one has any methodology to determine that they are blind and undirected processes. On the contrary we know that regulation requires guidance. Something has to know what to regulate, when to regulate and how much to regulate. The same goes for transcription, editing, proof-reading and error-correction. Only evolutionary propaganda sez these are blind and undirected processes- just because we can observe them happening without any observed intervention! And that is beyond pathetic.Joe
April 18, 2014
April
04
Apr
18
18
2014
04:03 AM
4
04
03
AM
PDT
AVS:
Look, BA, evolutionary biology provides the most likely explanation for our existence as a species as far as science is concerned.
Yet evolutionary biology can't explain anything as unguided evolution cannot be modelled nor tested. It doesn't produce any predictions and is useless as a research heuristic.
Your buddies here can ignore science all they want
And yet AVS can't say what science we are ignoring- quite the lying coward this one is
Your “intelligent design” hypothesis is interesting, but leads to nowhere, as there is no evidence to back it up.
And yet we have provided the evidence to back it up and said where it leads. AVS- ignorant and proud of it.Joe
April 18, 2014
April
04
Apr
18
18
2014
03:57 AM
3
03
57
AM
PDT
AVS: Long time, no see! Please, stay. We really need you to lift our mood. :)gpuccio
April 18, 2014
April
04
Apr
18
18
2014
01:32 AM
1
01
32
AM
PDT
BA:
So body forms don’t matter in your argument for common descent? Only sequence homologies matter in your argument for common descent?
Yes. I hope that is clear now.
Shark and human proteins “stunningly similar”; shark closer to human than to zebrafish – December 9, 2013 Excerpt: “We were very surprised to find, that for many categories of proteins, sharks share more similarities with humans than zebrafish,” Stanhope said. “Although sharks and bony fishes are not closely related, they are nonetheless both fish … while mammals have very different anatomies and physiologies. https://uncommondescent.com.....zebrafish/ now THAT’S embarrassing!
Not at all! It's simply interesting. As I already said (but you seem not to consider what I write): "I am well aware that not all molecular observations are in favor of CD, and that some of them cast serious doubts on the idea of an universal CD. I am very interested in all the facts that will be discovered that can bring new light to the issue. But, for the moment, I remain of the idea that CD is the best explanation. And I state, again, that this implies nothing about the origin of new forms and body plans." Emphasis added. Well, that remains my position. And I have no reason to be embarrassed by it.gpuccio
April 18, 2014
April
04
Apr
18
18
2014
01:29 AM
1
01
29
AM
PDT
Thank you for the info Allen. Nice to hear from you. What textbook are you using to teach these topics?scordova
April 18, 2014
April
04
Apr
18
18
2014
12:36 AM
12
12
36
AM
PDT
Allen_MacNeill: Thank you for your very interesting contribution. Just a few comments. 1) I am absolutely convinced that non coding DNA, including long repetitive sequences, can have a lot of functions. Some of them we already understand, and many we will probably understand better in the future. If you look at my post #76, you will see that I wrote there: "Now, the simple point is that the non coding sequence in chimps (or any other precursor species) is not there from OOL. Whenever it originated, it originated by variation. And that variation is by definition “neutral”, because it does not affect any function. Or, even if the non coding region were functional at other levels (for example, regulatory), and the variation that modifies it be negative, positive or neutral) that will be completely unrelated to the future ORF, which at present is not an ORF, is not translated and therefore is not visible to NS. So, what we have is variation which is neutral, or anyway unrelated to the “ORF to come”, which builds in some way the correct sequence for the future functional protein, without any help from NS. Obviously, once the ORF is “completed”, and in some lucky way it becomes translated, then NS can help fixing it. But that mean nothing. The role of NS in a classical darwinist scenario is to build gradually the sequence, not just to use it when it is ready." (Emphasis added). So, my point is very simple: even if non coding sequences are functional, that function is obviously non related to their sequence as a potential symbolic sequence that codes for AAs. Therefore, even if NS acts on RV of the non coding sequence, it will act in a way that is completely random in relation to the "coding sequence to come". Therefore, the "evolution" of he future ORF remains completely random in this scenario. 2)You say:
As for the “engines of variation,” I would like to emphasize that the kind of variation I have written about is both genetic and phenotypic variation. Indeed, the majority of the mechanisms I listed in my “engines of variation” posts at The Evolution List are mechanisms that primarily affect gene expression, rather than gene sequence.
That's exactly what makes your list wholly ambiguous. I will try to be more clear. The "mechanisms that primarily affect gene expression" are a bulk of information that is transmitted, and indeed efficiently transmitted, if species continue to exists in time. Therefore, that information must be in the genome, or in some epigenetic configuration. Wherever it is, it is functional information, and it is part of the "genome" in a wide sense (the total information that is transmitted from being to being in reproduction). Therefore, that regulatory information is part of the "genotype" (in a wide sense), and is not a "phenotype". Any variation acquired by interaction with the environment will not be part of that wide "genotype" unless and until it is integrated in some way in what is transmitted. I have nothing against neo Lamarkism: it certainly is an important part of our new understanding of molecular mechanisms. But, again, if and when neo Lamarkian mechanisms are proved to exists, they will be adaptive mechanisms, which willl show high organization and functional information in the mechanisms itself. I have cited many times the mechanism of somatic antibody maturation as a very good example of the genetic engineering of existing genes in response to environmental information (the contact with specific epitopes). Even if that mechanism does not generate transmittable information (because it takes place in somatic cells), it is a good example of an adaptive mechanism. But it is extremely complex and functional, and is in itself a very good argument for design of the mechanism itself. That's why your list is ambiguous. It does not discriminate between the mechanisms which are only "variations of random variation" and those which, if proved, would be complex functional adaptation which incorporate environmental information into transmittable information. And it does not discriminate between true explanatory mechanisms and simple vague suggestions of possible results of unknown mechanisms. IOWs, it is not useful to just mention a lot of supposed "engines of variation" without detailing why they are engines, and what type of variation they can explain. 3) You say:
Simply knowing the number of coding sequences in the genome of a multicellular eukaryote (especially an animal), for example by knowing the number and location of promoter sequences, tells you almost nothing about how the coding sequences (i.e. “genes”) are expressed and regulated. There are hierarchical biochemical systems involving anti-sense RNAs, small polypeptides, proteins, and non-coding sequences in DNA that all interact to produce the components of the phenotype.
I agree. And so? Protein coding genes are the final effectors. Regulatory information is obviously the real thing. And so? Regulatory information is as much a part of the genotype (be it in the narrow sense, that is written in DNA configurations, or in the wider sense which includes epigenetically transmitted information) as protein coding genes. Where do you think that "anti-sense RNAs, small polypeptides, proteins, and non-coding sequences in DNA" are written and transmitted? They certainly "interact to produce the components of the phenotype", but they are transmitted information. In my arguments for a design inference for biological information, I stick to protein coding genes for a very simple reason: they are what we know better. We know the code, we know how they work, so it's easier to make a detailed and quantitative argument for them. But there is no doubt that regulatory information is a level of higher functional information, and it is a potentially much stronger evidence for design. 4)About your "kludgeware" argument. I will not debate whether the biological designer can really be compared to Microsoft designers :). One of the two could take offense! But I will make a very simple point: good or bad, designers they are all the same. However, I certainly agree with a very important point, which I have made myself many times. You say:
This “kludginess” of gene expression/regulation in eukaryotic cells is an apparently inescapable concomitant of both the complexity of the systems involved and the history of their implementation
That's perfectly true. The more a system is complex, the more it is "frail", the more it needs complex functional subsystems to allow its bare survival: complex error management systems, and so on. That is always true, however good or bad the implementation of the system is, and especially, as you correctly mention, if ad when the implementation of the system is sequential (which I absolutely believe, as you will have understood from my defending Common Descent here). This is, in itself, one of the most powerful arguments against any kind of darwinian evolution, based on the concepts survival and reproductive advantages, and ID theory, based on the concept of functions and the need to implement new, ever more complex, functions as the "driving engine" of designed evolution. The simple fact is: optimal survival and reproduction were already achieved at the beginning of OOL, with prokaryotes. Prokaryotes are still the most successful, and simplest, biological reproducing beings. All the complexity which has been added has made new beings, up to humans, more frail, less efficient in survival and reproduction, much more dependent on very complex repair and defense mechanisms. IOWs, much more strictly design dependent. 5) You say:
The assertion that the origin of such homologies is the result of the intervention of an intelligent designer, however, is not empirically verifiable or falsifiable, and so I won’t address it.
That is simply not true. ID is all about the empirical verification of the origin of functional information from an intelligent designer. All the arguments I have ever made here are exclusively about that. Empirical design inference. You may not agree that ID is in any way successful in its empirical purpose, but simply dismissing it by saying that "is not empirically verifiable or falsifiable, and so I won’t address it" is really pointless. Many times I have shown here that the fundamental statements of ID (about complex functional information in biological molecules, and the design inference from it) are completely ans simply falsifiable, and therefore perfectly scientific. 6) Finally, about "functional orphans". I find your final argument really strange. If I understand you well, you are simply suggesting that new functional orphan genes are simply the reactivation of inactivated older genes. But that would simply mean that their functional information is old. First of all, it would not explain in any way how that information was generated in the beginning. New orphan genes would simply be old genes which are recruited again. But, beyond the complete lack of explanatory power of such a scenario, it is however wholly implausible. In some of the papers we quoted here, extensive checks have been made to exclude that the new orphans were some kind of recently inactivated genes. And obviously, they have no homologies with any known protein coding genes in the whole known proteome. That's exactly why they are called "orphans". So, I am very happy that you state that:
Transforming a very long sequences of repeated tandem repeats into a coding sequence, complete with a promoter, terminator, and enhancing sequences would indeed be miraculous.
Because that's exactly what we observe, and probably will observe ever more as our knowledge and understanding increases.gpuccio
April 17, 2014
April
04
Apr
17
17
2014
10:10 PM
10
10
10
PM
PDT
How is that embarrassing? Obviously all life that is based on the same properties is going to have similar structures an functions. Care to elaborate on this, or are you just quote mining?AVS
April 17, 2014
April
04
Apr
17
17
2014
09:42 PM
9
09
42
PM
PDT
So body forms don't matter in your argument for common descent? Only sequence homologies matter in your argument for common descent? Shark and human proteins “stunningly similar”; shark closer to human than to zebrafish – December 9, 2013 Excerpt: “We were very surprised to find, that for many categories of proteins, sharks share more similarities with humans than zebrafish,” Stanhope said. “Although sharks and bony fishes are not closely related, they are nonetheless both fish … while mammals have very different anatomies and physiologies. https://uncommondescent.com/intelligent-design/shark-and-human-proteins-stunningly-similar-shark-closer-to-human-than-to-zebrafish/ now THAT'S embarrassing!bornagain77
April 17, 2014
April
04
Apr
17
17
2014
09:17 PM
9
09
17
PM
PDT
Don't bother. "Because science can't explain exactly how organisms develop, that means that science is wrong." Welcome to the world of UD.AVS
April 17, 2014
April
04
Apr
17
17
2014
09:15 PM
9
09
15
PM
PDT
BA:
gpuccio, if you have no viable connection between sequences and body form, the argument for common descent of body forms from sequence homologies (tenuous as the sequence comparisons are as you yourself admit) collapses.
This is becoming a little bit embarassing. I never made an "argument for common descent of body forms from sequence homologies". I just made an argument for common descent. I still don't understand where body forms are mentioned or implied in my argument. Please, explain, or just let it be.gpuccio
April 17, 2014
April
04
Apr
17
17
2014
09:08 PM
9
09
08
PM
PDT
Look, BA, evolutionary biology provides the most likely explanation for our existence as a species as far as science is concerned. Your buddies here can ignore science all they want, but the fact remains that evolution is the best that we can come up with based on reason. Your "intelligent design" hypothesis is interesting, but leads to nowhere, as there is no evidence to back it up. Enjoy convincing the scientific illiterate otherwise.AVS
April 17, 2014
April
04
Apr
17
17
2014
08:47 PM
8
08
47
PM
PDT
I hold that the reason why internal physiology and anatomy operate as if they were four-dimensional instead of three dimensional is because of exactly what Darwinian evolution has consistently failed to explain the origination of. i.e. functional information. ‘Higher dimensional’ information, which is bursting at the seams in life, simply cannot be reduced to any 3-dimensional energy-matter basis:
John Lennox – Is There Evidence of Something Beyond Nature? (Semiotic Information) – video http://www.youtube.com/watch?v=F6rd4HEdffw “One of the things I do in my classes, to get this idea across to students, is I hold up two computer disks. One is loaded with software, and the other one is blank. And I ask them, ‘what is the difference in mass between these two computer disks, as a result of the difference in the information content that they posses’? And of course the answer is, ‘Zero! None! There is no difference as a result of the information. And that’s because information is a mass-less quantity. Now, if information is not a material entity, then how can any materialistic explanation account for its origin? How can any material cause explain it’s origin? And this is the real and fundamental problem that the presence of information in biology has posed. It creates a fundamental challenge to the materialistic, evolutionary scenarios because information is a different kind of entity that matter and energy cannot produce. In the nineteenth century we thought that there were two fundamental entities in science; matter, and energy. At the beginning of the twenty first century, we now recognize that there’s a third fundamental entity; and its ‘information’. It’s not reducible to matter. It’s not reducible to energy. But it’s still a very important thing that is real; we buy it, we sell it, we send it down wires. Now, what do we make of the fact, that information is present at the very root of all biological function? In biology, we have matter, we have energy, but we also have this third, very important entity; information. I think the biology of the information age, poses a fundamental challenge to any materialistic approach to the origin of life.” -Dr. Stephen C. Meyer earned his Ph.D. in the History and Philosophy of science from Cambridge University for a dissertation on the history of origin-of-life biology and the methodology of the historical sciences. Information and entropy – top-down or bottom-up development in living systems? Excerpt: This paper highlights the distinctive and non-material nature of information and its relationship with matter, energy and natural forces. It is proposed in conclusion that it is the non-material information (transcendent to the matter and energy) that is actually itself constraining the local thermodynamics to be in ordered disequilibrium and with specified raised free energy levels necessary for the molecular and cellular machinery to operate. A.C. McINTOSH - Dr Andy C. McIntosh is the Professor of Thermodynamics Combustion Theory at the University of Leeds. (the highest teaching/research rank in U.K. university hierarchy) http://journals.witpress.com/paperinfo.asp?pid=420 Information and Thermodynamics in Living Systems - Andy C. McIntosh - May 2013 Excerpt: The third view then that we have proposed in this paper is the top down approach. In this paradigm, the information is non-material and constrains the local thermodynamics to be in a non-equilibrium state of raised free energy. It is the information which is the active ingredient, and the matter and energy are passive to the laws of thermodynamics within the system. As a consequence of this approach, we have developed in this paper some suggested principles of information exchange which have some parallels with the laws of thermodynamics which undergird this approach.,,, http://www.worldscientific.com/doi/pdf/10.1142/9789814508728_0008 Quantum entanglement between the electron clouds of nucleic acids in DNA - Elisabeth Rieper, Janet Anders and Vlatko Vedral - February 2011 http://arxiv.org/PS_cache/arxiv/pdf/1006/1006.4053v2.pdf
Moreover, matter and energy are now both shown to reduce to ‘quantum information/entanglement’. In fact an entire human can now, theoretically, be reduced to quantum information and teleported to another location in the universe:
Quantum Teleportation Of A Human? – video https://vimeo.com/75163272
Thus not only is Information not reducible to a 3-Dimensional energy-matter basis, as is presupposed in Darwinism, but in actuality energy and matter both reduce to a information basis as is presupposed in Christian Theism: Why the Quantum? It from Bit? A Participatory Universe? Excerpt: In conclusion, it may very well be said that information is the irreducible kernel from which everything else flows. Thence the question why nature appears quantized is simply a consequence of the fact that information itself is quantized by necessity. It might even be fair to observe that the concept that information is fundamental is very old knowledge of humanity, witness for example the beginning of gospel according to John: “In the beginning was the Word.” Anton Zeilinger – a leading expert in quantum teleportation: Verse and Music: John 1:1-4 In the beginning was the Word, and the Word was with God, and the Word was God. He was in the beginning with God. All things were made through Him, and without Him nothing was made that was made. In Him was life, and the life was the light of men. Redeemed – Big Daddy Weave http://myktis.com/songs/redeemed/bornagain77
April 17, 2014
April
04
Apr
17
17
2014
08:40 PM
8
08
40
PM
PDT
As well, Natural Selection is grossly inadequate to do the work required of it because of what is termed ‘the princess and the pea’ paradox. The devastating ‘princess and the pea’ paradox is clearly elucidated by Dr. John Sanford, at the 8:14 minute mark, of this following video,,,
Genetic Entropy – Dr. John Sanford – Evolution vs. Reality – video http://vimeo.com/35088933
Dr. Sanford points out, in the preceding video, that Natural Selection acts at the coarse level of the entire organism (phenotype) and yet the vast majority of mutations have effects that are only ‘slightly detrimental’, and have no noticeable effect on phenotypes, and are thus far below the power of Natural Selection to remove from genomes before they spread throughout the population.
“Selection Threshold Severely Constrains Capture of Beneficial Mutations” - John Sanford - September 6, 2013 Excerpt of concluding comments: Our findings raise a very interesting theoretical problem — in a large genome, how do the millions of low-impact (yet functional) nucleotides arise? It is universally agreed that selection works very well for high-impact mutations. However, unless some new and as yet undiscovered process is operating in nature, there should be selection breakdown for the great majority of mutations that have small impact on fitness.,,, We show that selection breakdown is not just a simple function of population size, but is seriously impacted by other factors, especially selection interference. We are convinced that our formulation and methodology (i.e., genetic accounting) provide the most biologically-realistic analysis of selection breakdown to date. http://www.worldscientific.com/doi/pdf/10.1142/9789814508728_0011
Here are a few more notes on this insurmountable ‘princess and the pea’ problem for natural selection:
Evolution vs. Genetic Entropy - Andy McIntosh - video https://vimeo.com/91162565 The GS Principle (The Genetic Selection Principle) – Abel – 2009 Excerpt: The GS Principle, sometimes called “The 2nd Law of Biology,” states that selection must occur at the molecular/genetic level, not just at the fittest phenotypic/organismic level, to produce and explain life.,,, Natural selection cannot operate at the genetic level. http://www.bioscience.org/2009/v14/af/3426/fulltext.htm
Moreover, as if that were not devastating enough as to undermining any credibility Natural Selection might have had as to having the causal adequacy to explain the highly integrated levels of overlapping functional information found in organisms, dimensionally speaking, Natural Selection is now known to not even be on the right playing field in the first place:
The predominance of quarter-power (4-D) scaling in biology Excerpt: Many fundamental characteristics of organisms scale with body size as power laws of the form: Y = Yo M^b, where Y is some characteristic such as metabolic rate, stride length or life span, Yo is a normalization constant, M is body mass and b is the allometric scaling exponent. A longstanding puzzle in biology is why the exponent b is usually some simple multiple of 1/4 (4-Dimensional scaling) rather than a multiple of 1/3, as would be expected from Euclidean (3-Dimensional) scaling. http://www.nceas.ucsb.edu/~drewa/pubs/savage_v_2004_f18_257.pdf “Although living things occupy a three-dimensional space, their internal physiology and anatomy operate as if they were four-dimensional. Quarter-power scaling laws are perhaps as universal and as uniquely biological as the biochemical pathways of metabolism, the structure and function of the genetic code and the process of natural selection.,,, The conclusion here is inescapable, that the driving force for these invariant scaling laws cannot have been natural selection.” Jerry Fodor and Massimo Piatelli-Palmarini, What Darwin Got Wrong (London: Profile Books, 2010), p. 78-79
Here is, what a Darwinist termed, a ‘horrendously complex’ metabolic pathway (which operates as if it were ’4-Dimensional):
ExPASy - Biochemical Pathways - interactive schematic http://web.expasy.org/cgi-bin/pathways/show_thumbnails.pl
And remember, Darwinian evolution has yet to explain a single gene of those ‘horrendously complex’ metabolic pathways.
"Charles Darwin said (paraphrase), 'If anyone could find anything that could not be had through a number of slight, successive, modifications, my theory would absolutely break down.' Well that condition has been met time and time again. Basically every gene, every protein fold. There is nothing of significance that we can show that can be had in a gradualist way. It's a mirage. None of it happens that way. - Doug Axe PhD. - Nothing In Molecular Biology Is Gradual - video http://www.metacafe.com/watch/5347797/
The reason why a ‘higher dimensional’ 4-Dimensional structure, such as a ‘horrendously complex metabolic pathway, would be, for all intents and purposes, completely invisible to a 3-Dimensional process, such as Natural Selection, is best illustrated by ‘flatland’:
Flatland – 3D to 4D shift – Dr. Quantum – video http://www.youtube.com/watch?v=BWyTxCsIXE4
bornagain77
April 17, 2014
April
04
Apr
17
17
2014
08:38 PM
8
08
38
PM
PDT
Another primary reason why Darwinian evolution is more realistically thought of as a pseudo-science rather than a proper physical science is that Darwinian evolution does not have a demonstrated empirical basis to support its claims (in fact empirical evidence also consistently shows us that Darwinian evolution is astronomically unlikely),,
“The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain – Michael Behe – December 2010 Excerpt: In its most recent issue The Quarterly Review of Biology has published a review by myself of laboratory evolution experiments of microbes going back four decades.,,, The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function. Of course we had already known that the great majority of mutations that have a visible effect on an organism are deleterious. Now, surprisingly, it seems that even the great majority of helpful mutations degrade the genome to a greater or lesser extent.,,, I dub it “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain. http://behe.uncommondescent.com/2010/12/the-first-rule-of-adaptive-evolution/ Where’s the substantiating evidence for neo-Darwinism? https://docs.google.com/document/d/1q-PBeQELzT4pkgxB2ZOxGxwv6ynOixfzqzsFlCJ9jrw/edit Waiting Longer for Two Mutations – Michael J. Behe Excerpt: Citing malaria literature sources (White 2004) I had noted that the de novo appearance of chloroquine resistance in Plasmodium falciparum was an event of probability of 1 in 10^20. I then wrote that ‘for humans to achieve a mutation like this by chance, we would have to wait 100 million times 10 million years’ (1 quadrillion years)(Behe 2007) (because that is the extrapolated time that it would take to produce 10^20 humans). Durrett and Schmidt (2008, p. 1507) retort that my number ‘is 5 million times larger than the calculation we have just given’ using their model (which nonetheless “using their model” gives a prohibitively long waiting time of 216 million years). Their criticism compares apples to oranges. My figure of 10^20 is an empirical statistic from the literature; it is not, as their calculation is, a theoretical estimate from a population genetics model. http://www.discovery.org/a/9461 Don’t Mess With ID (Overview of Behe’s ‘Edge of Evolution’ and Durrett and Schmidt’s paper at the 20:00 minute mark) – Paul Giem – video http://www.youtube.com/watch?v=5JeYJ29-I7o
Another reason why Darwinian evolution is more realistically thought of as a pseudo-science rather than a proper physical science is that the two foundational pillars of Darwinian evolution, Random Mutation/Variation and Natural Selection, are both now shown to be severely compromised as to having the causal adequacy that Darwinists have presupposed for them. For instance, although Darwinian evolution appeals to unguided ‘random mutations/variations’ to DNA as the main creative source for all evolutionary novelty, there are now known to be extensive layers of error correction in the cell to protect against any unguided “random” changes happening to DNA in the first place:
The Evolutionary Dynamics of Digital and Nucleotide Codes: A Mutation Protection Perspective – February 2011 Excerpt: “Unbounded random change of nucleotide codes through the accumulation of irreparable, advantageous, code-expanding, inheritable mutations at the level of individual nucleotides, as proposed by evolutionary theory, requires the mutation protection at the level of the individual nucleotides and at the higher levels of the code to be switched off or at least to dysfunction. Dysfunctioning mutation protection, however, is the origin of cancer and hereditary diseases, which reduce the capacity to live and to reproduce. Our mutation protection perspective of the evolutionary dynamics of digital and nucleotide codes thus reveals the presence of a paradox in evolutionary theory between the necessity and the disadvantage of dysfunctioning mutation protection. This mutation protection paradox, which is closely related with the paradox between evolvability and mutational robustness, needs further investigation.” http://www.arn.org/blogs/index.php/literature/2011/04/26/dna_repair_mechanisms_reveal_a_contradic
Moreover, for the vast majority of times that changes do happen to DNA, they are now known to be ‘directed changes’ by sophisticated molecular machines, not unguided ‘random changes’ from a cosmic ray, chemical imbalance, or some such entropy driven event as that:
How life changes itself: the Read-Write (RW) genome. – 2013 Excerpt: Research dating back to the 1930s has shown that genetic change is the result of cell-mediated processes, not simply accidents or damage to the DNA. This cell-active view of genome change applies to all scales of DNA sequence variation, from point mutations to large-scale genome rearrangements and whole genome duplications (WGDs). This conceptual change to active cell inscriptions controlling RW genome functions has profound implications for all areas of the life sciences. http://www.ncbi.nlm.nih.gov/pubmed/23876611 Shapiro on Random Mutation: “What I ask others interested in evolution to give up is the notion of random accidental mutation.” http://www.huffingtonpost.com/james-a-shapiro/jerry-coyne-fails-to-unde_b_1411144.html
What should be needless to say, having ‘cell-mediated processes’ direct changes to DNA is in direct contradiction to the ‘undirected randomness’ which is held to be foundational to neo-Darwinian thought. Moreover, Natural Selection, that other great pillar upon which Darwinian evolution rests, has also been undermined as having the causal adequacy that neo-Darwinists have attributed to it. First off, to the extent that Natural Selection does do anything, Natural Selection is found to be a eliminative force not a generative force:
"Natural selection does not act on anything, nor does it select (for or against), force, maximize, create, modify, shape, operate, drive, favor, maintain, push, or adjust. Natural selection does nothing…. Having natural selection select is nifty because it excuses the necessity of talking about the actual causation of natural selection. Such talk was excusable for Charles Darwin, but inexcusable for evolutionists now. Creationists have discovered our empty “natural selection” language, and the “actions” of natural selection make huge, vulnerable targets." The Origin of Theoretical Population Genetics, 2001 (pp. 199-200) William Provine - Professor of Evolutionary Biology - Cornell University "...but Natural Selection reduces genetic information and we know this from all the Genetic Population studies that we have..." Maciej Marian Giertych - Population Geneticist - member of the European Parliament - EXPELLED - Natural Selection And Genetic Mutations - video https://www.youtube.com/watch?v=6z5-15wk1Zk "A Dutch zoologist, J.J. Duyvene de Wit, clearly demonstrated that the process of speciation (such as the appearance of many varieties of dogs and cats) is inevitably bound up with genetic depletion as a result of natural selection. When this scientifically established fact is applied to the question of whether man could have evolved from ape-like animals,'.. the transformist concept of progressive evolution is pierced in its very vitals.' The reason for this, J.J. Duyvene de Wit went on to explain, is that the whole process of evolution from animal to man " ' . . would have to run against the gradient of genetic depletion. That is to say, . . man )should possess] a smaller gene-potential than his animal ancestors! [I] Here, the impressive absurdity becomes clear in which the transformist doctrine [the theory of evolution] entangles itself when, in flat contradiction to the factual scientific evidence, it dogmatically asserts that man has evolved from the animal kingdom!" —Op. cit., pp. 129-130. [Italics his; quotations from *J.J. Duyvene de Wit, A New Critique of the Transformist Principle in Evolutionary Biology (1965), p. 56,57.] http://www.godrules.net/evolutioncruncher/2evlch15.htm "We found an enormous amount of diversity within and between the African populations, and we found much less diversity in non-African populations," Tishkoff told attendees today (Jan. 22) at the annual meeting of the American Association for the Advancement of Science in Anaheim. "Only a small subset of the diversity in Africa is found in Europe and the Middle East, and an even narrower set is found in American Indians." Tishkoff; Andrew Clark, Penn State; Kenneth Kidd, Yale University; Giovanni Destro-Bisol, University "La Sapienza," Rome, and Himla Soodyall and Trefor Jenkins, WITS University, South Africa, looked at three locations on DNA samples from 13 to 18 populations in Africa and 30 to 45 populations in the remainder of the world.-
bornagain77
April 17, 2014
April
04
Apr
17
17
2014
08:29 PM
8
08
29
PM
PDT
Mr MacNeill you claim:
And may I say that gpuccio is entirely correct about the idea that homologies (combined with shared derived sequences) are indeed very strong evidence for common descent.
Unfortunately for you and your Darwinian thought police buddies, you do not get to decide what constitutes strong empirical evidence and what does not. Especially for the tea leaf reading enterprise of Darwinian evolution. The FACT the there is no empirical correlation between sequences and body plan morphogenesis, as well as the FACT that sequences, especially regulatory, are 'all over the place', pretty much makes the argument for correlation to collapse. 'Just so stories' do not help your pseudo-scientific Darwinian fantasies. Darwinism is a Pseudo-Science - Part II
“nobody to date has yet found a demarcation criterion according to which Darwin(ism) can be described as scientific” - Imre Lakatos (November 9, 1922 – February 2, 1974) a philosopher of mathematics and science, quote was as stated in 1973 LSE Scientific Method Lecture
What the vast majority of Darwinists fail to realize (or ever honestly admit to) is that Darwinian evolution is not even a 'real' physical science in any proper sense but that Darwinian evolution is more realistically thought of as a pseudo-science. Even Jerry Coyne himself, the self-appointed Grand Inquisitor of Darwinian evolution, admits that Darwinian evolution lacks the rigor of a proper physical science:
“In science’s pecking order, evolutionary biology lurks somewhere near the bottom, far closer to phrenology than to physics. For evolutionary biology is a historical science, laden with history’s inevitable imponderables. We evolutionary biologists cannot generate a Cretaceous Park to observe exactly what killed the dinosaurs; and, unlike “harder” scientists, we usually cannot resolve issues with a simple experiment, such as adding tube A to tube B and noting the color of the mixture.” - Jerry A. Coyne – Of Vice and Men, The New Republic April 3, 2000 p.27 - professor of Darwinian evolution at the University of Chicago
The main reason why Darwinian evolution is more properly thought of as a pseudo-science instead of a proper science is because Darwinian evolution has no rigid mathematical basis, like other overarching physical theories of science do. A rigid mathematical basis in order to potentially falsify it (in fact math, in so far as math can be applied to Darwinian claims, constantly shows us the Darwinian evolution is astronomically unlikely),,
“On the other hand, I disagree that Darwin’s theory is as `solid as any explanation in science.; Disagree? I regard the claim as preposterous. Quantum electrodynamics is accurate to thirteen or so decimal places; so, too, general relativity. A leaf trembling in the wrong way would suffice to shatter either theory. What can Darwinian theory offer in comparison?” (Berlinski, D., “A Scientific Scandal?: David Berlinski & Critics,” Commentary, July 8, 2003) Oxford University Seeks Mathemagician — May 5th, 2011 by Douglas Axe Excerpt: “Grand theories in physics are usually expressed in mathematics. Newton’s mechanics and Einstein’s theory of special relativity are essentially equations. Words are needed only to interpret the terms. Darwin’s theory of evolution by natural selection has obstinately remained in words since 1859.”… http://biologicinstitute.org/2011/05/05/oxford-university-seeks-mathemagician/ Active Information in Metabiology – Winston Ewert, William A. Dembski, Robert J. Marks II – 2013 Except page 9: Chaitin states [3], “For many years I have thought that it is a mathematical scandal that we do not have proof that Darwinian evolution works.” In fact, mathematics has consistently demonstrated that undirected Darwinian evolution does not work. http://bio-complexity.org/ojs/index.php/main/article/view/BIO-C.2013.4/BIO-C.2013.4 HISTORY OF EVOLUTIONARY THEORY – WISTAR DESTROYS EVOLUTION Excerpt: A number of mathematicians, familiar with the biological problems, spoke at that 1966 Wistar Institute,, For example, Murray Eden showed that it would be impossible for even a single ordered pair of genes to be produced by DNA mutations in the bacteria, E. coli,—with 5 billion years in which to produce it! His estimate was based on 5 trillion tons of the bacteria covering the planet to a depth of nearly an inch during that 5 billion years. He then explained that the genes of E. coli contain over a trillion (10^12) bits of data. That is the number 10 followed by 12 zeros. *Eden then showed the mathematical impossibility of protein forming by chance. http://www.pathlights.com/ce_encyclopedia/Encyclopedia/20hist12.htm Darwin's Doubt - Chapter 12 - Complex Adaptations and the Neo-Darwinian Math - Dr. Paul Giem - video http://www.youtube.com/watch?v=ZFY7oKc34qs&list=SPHDSWJBW3DNUaMy2xdaup5ROw3u0_mK8t&index=7 See also Mendel's Accountant and Haldane's Ratchet: John Sanford and company
bornagain77
April 17, 2014
April
04
Apr
17
17
2014
08:24 PM
8
08
24
PM
PDT
BTW, my thanks to Jerry for alerting me to this thread and the questions directed to me.Allen_MacNeill
April 17, 2014
April
04
Apr
17
17
2014
08:06 PM
8
08
06
PM
PDT
Long repetitive sequences (LINEs and SINEs) clearly do not have a coding function, as they lack promoter sequences (which are absolutely necessary for a sequence to be transcribed and subsequently translated). However, they may have other biological functions. For example, the coding sequences in eukaryotic DNA are not entirely randomly located. Rather, they are located in parts of the genome that allow them to be associated with the histone proteins in nucleosomes. This is because modification of DNA binding to histones is an important mechanism of gene regulation in eukaryotes. Therefore, the "spacer" non-coding DNA such as LINEs and SINEs could still influence the expression of genes located at significant distances away by modifying their binding to histones in nucleosomes. As for the "engines of variation," I would like to emphasize that the kind of variation I have written about is both genetic and phenotypic variation. Indeed, the majority of the mechanisms I listed in my "engines of variation" posts at The Evolution List are mechanisms that primarily affect gene expression, rather than gene sequence. Regulation of gene expression in eukaryotes is both complex and massive (I know, I'm teaching a course in it right now). Simply knowing the number of coding sequences in the genome of a multicellular eukaryote (especially an animal), for example by knowing the number and location of promoter sequences, tells you almost nothing about how the coding sequences (i.e. "genes") are expressed and regulated. There are hierarchical biochemical systems involving anti-sense RNAs, small polypeptides, proteins, and non-coding sequences in DNA that all interact to produce the components of the phenotype. Increasingly fine-grained analyses of these systems has revealed that many of them are "kludges;" that is, they work, but not well and not always consistently. This "kludginess" of gene expression/regulation in eukaryotic cells is an apparently inescapable concomitant of both the complexity of the systems involved and the history of their implementation Think about how kludgy a huge OS like Windows has become; it's essentially a small core of original integrated code, massively modified by an almost uncountable patchwork of "bug fixes" and "extensions." The surprising thing about such systems is not that they don't work well (they don't), but rather that they work at all. It is becoming clear that the "software" of a typical eukaryotic cell is really mostly "kludgeware." It generally works "just good enough" to not self-destruct. And, as it is replicated and modified (and especially as "foreign" sequences are introduced into it or removed from it by retrotranspositions, transposons, retroviral insertions, polymerase "skip-copying" and other "noise" events), it stumbles along in much the way that "Mendel's Accountant" and the nearly-neutral theories predict that it should. This is one of the main reason that germ cells are set aside very early in embryonic development in eukaryotes. The less often the genome is replicated, the fewer mistakes it accumulates. This is part of what is wrong with "Mendel's Accountant:" it doesn't take into account the particular kinds of cells that actually constitute the ongoing phylogenetic lines it purports to describe. THe MA model assumes that all cells change randomly at approximately constant rates, yet germ cells don't change at anything like the same rates as most cells, primarily because they don't undergo mitotic divisions at anything like the rates of most other cells. And may I say that gpuccio is entirely correct about the idea that homologies (combined with shared derived sequences) are indeed very strong evidence for common descent. This is especially the case for non-coding sequences that have little or no effect on phenotypes. There are a multitude of examples of homologous sequences that either have no effect on phenotypes or have surprisingly different effects in different organisms as a result of modified gene expression in diverging phylogenetic lines. The assertion that the origin of such homologies is the result of the intervention of an intelligent designer, however, is not empirically verifiable or falsifiable, and so I won't address it. As for how functional orphans can arise from non-coding sequences, one first has to specify what kind of non-coding sequences one is referring to. If one means LINEs and SINEs, then I agree completely. Transforming a very long sequences of repeated tandem repeats into a coding sequence, complete with a promoter, terminator, and enhancing sequences would indeed be miraculous. However, a significant fraction of the non-coding sequences in eukaryotes consist of sequences that were once viable coding sequences. These either were corrupted and thereby inactivated by mis-replication of their promoters/enhancers or (more commonly) were inserted into the genome as the result of retrotransposition, reverse transcription, transposon insertion, and similar processes, in which coding sequences with functional promoters, terminators, and enhancers are inserted or removed from the genome. In a great many cases, such sequences are quickly identified and inactivated by "surveillance/editing" mechanisms, which identify and inactivate the "rogue" sequences by inactivating their promoters and/or enhancers. However, this means that "dead" former coding sequences are scattered throughout the genome and can be reactivated by inserting new, active promoters/enhancers that can reactivate part or all of the "dead" sequences. This has actually been accomplished in the laboratory, where a "dead" retroviral sequence estimated at being inactive for millions of generations was "resurrected" by providing it with an active promoter sequence. The "fossil" sequence then acted like a functional virus, infecting host cells and generally acting like "its old (now extinct) self." So, can reactivation of non-coding sequences produce new, functional gene sequences? Yes, if the non-coding sequences were once active coding sequences that had been inactivated by modification of their promoters/enhancers.Allen_MacNeill
April 17, 2014
April
04
Apr
17
17
2014
07:55 PM
7
07
55
PM
PDT
gpuccio, if you have no viable connection between sequences and body form, the argument for common descent of body forms from sequence homologies (tenuous as the sequence comparisons are as you yourself admit) collapses.bornagain77
April 17, 2014
April
04
Apr
17
17
2014
04:08 PM
4
04
08
PM
PDT
1 2 3 5

Leave a Reply