Comment on Southern Adventist University opens Origins Exhibit by pauluc.
Sean
I am in 2 minds as to whether I should just stop thread or give it one more chance. As always I do it because I am concerned that readers here might give credence to your constructions which you insist are scientific rather than the faith positions which I think they are.
1] Regarding polygenic traits you say;
“So, why did you act like you didn’t know what I was talking about when I was describing the vast phenotypic potential of a breeding pair?”
I was just hoping that what you had written was not really what you thought. I have questioned your position that a breeding pair has vast phenotypic potential which I think is unsustainable scientifically but is quite acceptable as a faith position based on a particular reading of the text.
I have given you references to real studies with data that indicate that 2 animals is unquestionably a non-viable populations in any conservation breeding program which is the best we have in terms of replicating the ark scenario.
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Further I have suggested that doing the math does not allow one to even conceive of vast phenotypic potential on the basis of allelic variation in a population of 2.
You continue digging the hole by deprecating the role of new mutations and insisting that there is front loaded potential by a mechanism you cannot define in accepted genetic terms.
“How is that? Vast phenotypic potential is not based on the evolution of anything novel within the gene pool at all. Sure, novel mutations do happen all the time, but they aren’t needed or required for marked phenotypic diversity to occur via pre-existing genetic information.”
Regarding phenotypic selection and polygenic traits you say
“I’ve read and re-read this particular comment several times, but I’m still not sure what you’re try to say here? Perhaps you could explain it further?”
Having raised the issue of polygenic nature of phenotypic traits as an explanation of the vast potential I thought you would be familiar with some of the more foundational concepts in genetics. From your responses I once again seem to be in error. What is the conventional view.
The current concept of a gene is of a sequence of DNA in the genome that codes for a protein and has associated regulatory elements and non-coding RNA. See for example the review by Gingeras http://www.ncbi.nlm.nih.gov/pubmed/17567989
The organism at the level of the organelle cellular, organ, or organism is sustained by biochemical pathways and structures that rely on these genes.
Depending on levels of redundancy loss of a gene may affect the function and result in a particular change in the organism which is recognized by observation grossly biochemically or microscopically. This is often called a trait as in sickle cell trait or phenotype where there is a particular shape of the red cells. Usually this there are multiple characteristics associated with this trait. For Sickle cell disease this is rapid clearance of the red cells from the blood and anaemia. Trouble with red cells in the circulation leading to blocked blood vessels and resistance to malaria infection of the red cells.
Mendelian traits are those that map to a single gene locus and result in a phenotypic change. Sickle cell is one that maps to a gene coding for part of the haemoglobin molecule.
Now production of red cells containing haemoglobin red cells is dependent on very many genes. From the genes such as eythropoietin that regulate amount of haemoglobin and red cells that are produced in erythroblasts and progeny cells in the bone marrow to the genes controlling the the proteins and carbohydated structure of the red cell membrane all are related to the red cell physiology and physical characteristics or phenotype.
Now say a population of people move to the Himalayas or the Andes. They need more red cells. The response will be that those in the population that have the best ability to produce red cells will have better ability to carry oxygen in the presence of low oxygen tension and will have better fitness. This trait of high altitude fitness is unlikely to be a mendelian train but will be a polygenic trait. The initial measure of ability to carry oxygen will have something like a Gaussian distribution. If there is within the population multiple genes with some polymorphism or variability in function even through within that one gene it has minimal overall effect the selection will be on multiple such genes so that the fittest population with the high oxygen carrying phenotype will have a genotype that is has been selected for the phenotype. It is a not a selection of genes one at a time but a simultaneous selection. Allele frequency at multiple loci will be changes within a very short time. Now if one of the people in the population has a new mutation that has better function it will be quickly fixed in the population and carried along with a cluster of more or less useful genes. In other words selection integrated across a large number of genes. To argue about potential sequence space and absolute probabilities is a nonsense.
This concept I would have thought was familiar to you as even Sanford in his book “Genetic entropy” does accept there is phenotypic rather than genotypic selection (see chapter 4 and his cute Princess and the nucleotide paradox).
Current attempts to map diseases using genome wide arrays usually show that a disease process is polygenic. I will not go into the complexity of the reason for this in terms of founders and alternate genetic pathways to get to favourable phenotype.
What Sean is arguing is that things like size and coat colour in Dogs that are clearly polygenic the cis interactions between mjultiple variable genes can compensate for a lack of polymorphism at any genetic locus imposed by a population size of 2.
If we assume that dog size depends on products of pathways involving 5 genes [in fact this is vastly overestimating it as IGF-1 seems to be the predominant determinant]
Then in a population of 2 there are maximum of 4 alleles at 20 loci. The possible genotypes assuming absolutely no genetic linkage are then 4^50 = 1024 compared to 20^5 = 3.2 million for a population of 20 with the same level of genetic heterogeneity and allelic variation.
A population of 2 with complete heterogeneity over 5 loci is not what is seen in extant populations but allowing Seans assumption in any lottery I would take my chance with 3 millions rather than 1000 tickets.
“Actually, there are >1600 known allelic forms of HLA-B.
http://bioinformatics.oxfordjournals.org/content/early/2011/02/07/bioinformatics.btr061.full.pdf”
Thanks Sean, of course you know this is based on 4 digit typing which is the genotypic alleles and not the alleles that are serologically defined and correspond to protein sequence changes. As you know 4 digit typing is important in transplantation not because of the amino acid changes or an possible change in fitness or antigen binding by the alpha chain coded by that locus but because of the haplotype effect in that defining genetype predicts distant alleles and sequence variation in that haplotype.
You then go on to totally confuse the difference between mutation, allelic forms, phenotypes and polygenic traits not least of all because of your private nomenclature and concepts.
“Yes, that is obvious. These forms were produced by subsequent mutations in the offspring of the original parents.
Of course, I was never talking about mutant allelic forms like this – which I would have thought was originally obvious and which I have repeatedly pointed out to you in this thread. I was and am talking about variability of phenotypic trait expression. Note, in this line, that MHC functionality is also polygenic.”
What on earth are you talking about? you seem to be totally confusing a polygenic family and a polygenic trait. The MHC is not a phenotype or a function it is a region of 2 megabase or more contains a family of genes, likely of common origin, in tight linkage dysequilibrium and in which the different loci can be ascribed particular functions.
HLA-B codes for the alpha chain of class I molecules. This encodes the CDR region of the molecule that is the site that can bind to specific 9-11 amino acid peptides that have a structurally complementary sequence to the class I alpha chain. The high levels of polymorphism at this locus determined the phenotype or what will bind to that molecule and be recognized by a CD8 or cytotoxic T cells. This is the phenotype that is subject to selection; the allele that can recognize a particular pathogen structure.
Presence of the allele HLA*B57 has a clear survival advantage in HIV infection by recruiting particularly effective CD8 T cells that recognize that class I molecule. The HLA*B5701 haplotype as well as 5702 and 5703 and the related 5801 all have ability to create effective HIV specific CTL that determines the good responder phenotype not because of the associated changes outside the peptide binding groove or nucleotide variation elsewhere in the gene that defines the 4 digit specificity.
Geneticist do not see any qualitative difference between allelic variation and mutation except in frequency within a population. There is absolutely no reason to conceptualize some distinction between changes in nucleotide sequence because of some imagined ancestory.
It is up to you to provide a model and evidence if you wish to do so.
“Again, the production of sequence differences between alleles happens all the time – more and more commonly as populations increase in size. However, the majority of these mutational differences are near neutral with respect to function with the vast majority of these only affecting the degree of functionality and the vast majority being detrimental or degenerative in nature to one degree or another. Qualitatively novel functionality, while relatively rare, is not realized beyond very very low levels of functional complexity.”
“I’m not sure how many times I have to repeat this concept before you will stop mischaracterizing my position and start dealing with what I’m really talking about?”
“It doesn’t require intelligent design or a Divine miracle to rapidly produce mutated alleles for a particular site in a large population where the functional effects are either quantitative or at very low levels of qualitatively novel functionality. I’m really not sure why you’re even arguing this point? I don’t see how it is at all relevant to what I’ve been saying?”
I look forward to reading you PLOS one or PLOS genetics paper on the recognition and importance of mutations with “very very low levels of functional complexity”.
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pauluc Also Commented
Southern Adventist University opens Origins Exhibit
@AzGranpa:
I think you should read the critique about the assumptions implicit in the simulations looking for the common ancestor before using this to support your model of YEC.
http://www.nature.com/nature/journal/v431/n7008/full/431518a.html#f1
Southern Adventist University opens Origins Exhibit
@Sean Pitman:
“Do you really not see the exponential nature of the problem? There is really no point in further discussion if you will not discuss this particular question.”
I may well be dense in not understanding your view of the primacy of mathematical modelling.
We have had this discussion before apropos of the paper by ferrada on novel function in proteins.
As I see it your modelling and statistics is largely based on the premise that functional sequence/s must derive denovo and that the probability of this is infinitely small is akin to questions surrounding abiogenesis. I do not have any knowledge of that and do not think it is a question worth asking. To me it must at this time be relegated to the realm of non-science as there is no obvious mechanism for testing it. A conclusion perhaps reinforced by the lack of any significant literature on this, a finding that you have articulated on this thread and attributed to the lack of insight by scientists.
In terms of the reality of speciation and the associated functional change in existing sequences your statistical inferences premised as they are on assumptions about denovo production are not really helpful, at least in the mind of practising scientists.
The reality is that we agree that speciation has occurred largely due to new mutational changes in your case you say accumulating within 4000 years.
Now that is a question that can be addressed and will be addressed with rapid genomic sequencing and analysis. My predication is that there will be at the genomic level no essential qualitative difference in the process of genetic change for speciation/genetic diversity between subspecies like Neandertal and Denisova and between primates.
If you disagree the onus is on you to provide the evidence within this or other mammalian groups to show that there is some qualitative barrier at the level of a “kind”. If you think there is a 1000fsaar limit then show where that would apply in primate phylogeny.
Southern Adventist University opens Origins Exhibit
Sean
1] I’m afraid I am going to once again have to pass on your suggestion for wasting more time than I have in responding to your mantra about probability and complexity. Like accountants statistic is my servant not my master.
I disagree with your bottom up approach of looking at data from some preconceived theoretical reality. You model sequence space as being the arbiter of reality and your basis for accepting it is an immovable faith position not an attempt to model real observations. I approach the reality of speciation in a top down fashion the same way as Darwin did; we have evidence for speciation (which you do seem to accept) but how did this happen at the genome and molecular and is there evidence of limitations?
2] Your fixation on the front loading of genetic information ina a breeding pair seems impervious to logical or mathematical argument and you do not seem to be able to accept what any population geneticist would immediately see. 2 individuals is a gene puddle not a gene pool and arguments about evolution by allelic selection is completely unrealistic.
3] I do not think you have actually read the references I have suggested as relevant to discussions on mechanisms of speciation. If you have, you seem to have read them as an apologist not as a scientist and see only what you want to see instead of reading the publication for what is the message of that publication.
4] When I ask for an example of instances of 1000fsaar limitation in the human vs chimp comparisons I was, as a scientist, thinking perhaps you would give me a relevant response with some specificity including minimally a gene ID or base sequence ID so I can actually check what you are talking about.
Recent Comments by pauluc
Avondale College Arguing in Favor of Darwinian Evolution?
Bob Helm: With that said, I find your views to be spiritually dangerous and often scientifically weak. I detect a lot of smoke in your posts, but very little light. I hope you will continue to ponder these issues and try to have an open mind.
You are most welcome to your opinion and I know you would like nothing better than that anyone who takes Christianity and the Bible seriously but not literally to just go away. It is much better not to know of any possible problems with one current views. It very hard to get to the science when we cannot even agree on what is science. What passes as science on this site is so completely dismissive of its methodological basis and history and is entrained in a specific supernatural world view that allows arbitrary acceptance of any observation as miraculous. I think Roger’s paper may well be relevant to Adventist that believe that Christianity has and must respond to a careful study of physical reality by reconsidering its interpretations of the word of the Lord, but as Sean has indicated you are exception to that characterization. I still do not really understand why you should be interested at all in any science. It seems a bit messy to worry about facts. It really seems an unnecessary bother to argue whether the precambrian/cambrian boundary or the upper cenzoic (is that really what you meant?) as the evidence of a divine intervention.
Dont worry I do have an open mind which is why I still peruse this site to see how more knowledgable fundamentalist Adventists think. I wont worry you further.
Avondale College Arguing in Favor of Darwinian Evolution?
Sean Pitman: So, you do see the need for a police force and a military to maintain civil society, but somehow Christians should not provide what is an otherwise necessary part of that civil society? I’m with Abraham Lincoln on this one when he noted the inconsistency of such a position – like Orthodox Jews paying others to turn their lights on for them on Sabbath
On that logic you should not have any issue with working on Sabbath in any profession serving 24/7. Be that computer support, utilities firefighters. Those giving up those jobs because of inability to have sabbath observance were all deluded. They as Christians should be prepared to “provide what is otherwise a necessary part of civil society”
You cant have it both ways. You cant because of a moral postion claim that Adventists should have exception from working on Sabbath and at the same time deny me the right to consider immoral some occupations that may be very utilitarian in a world full of selfishness and the human acts of evil that comes from that.
Lets for a moment step back from lala land. Where are we and where did we come from on this thread?
1] You posted a rehash of all your usual arguments in response to an article about the more mainstream Adventist positions that may impact the way Adventism reacts to conventional science. All very straight forward.
2] The contention was that Adventism has accepted process for the orgin and evolution of the inanimate world. The birth and death of galaxys and stars and planets in black holes supernova and impacts of spiralling planets. This is where it gets really strange.
3] You contend that Adventism has always accepted the conclusions of that process but then expand on your view of the process which involves a little bit of order and natural law but large amounts of magic. God waited a few billions years until the interstellar material generated by the big band condensed into planets onto which God created life mature and complete. This included Heaven the place of his throne-room which he populated with physical being angels which it is implied have both mass and composition and metabolism.
4] When it was suggested that the same processes and natural law resulted in life on this planet this was claimed inconceivable and would never be done by any process involving life and death. Instead the life we see now is in reality designed to live for ever and has be chemically changed because it is deprived of a particular form of nutrient from a tree that existed on the Earth some 6000 years ago.
5] The inconguity of practicing medicine by the principles of process of natural law and the technology resulting from both the processes of the innanimate and the animate world rather than accepting the much more important process of divine intervention seems to be completely obsure.
6] When someone says that the process of life and death that gave us the physical substance of our universe is also the basis of the creation of life here he must be animal hating sadistic psychopath who cannot belieive in a God of love and grace and is lying when he says that non-violence characterizes the children of the heavenly father for one must always recognize that peace and freedom are only obtained over the bodies of 1/3 of the angels of heaven and the eternal physical and violent struggle against those who would practice violence.
I really cannot understand you Sean. Your ways are way beyond me. I am just sorry that Bob seems to be drawn into your twighlight zone.
Grace
Avondale College Arguing in Favor of Darwinian Evolution?
@Sean Pitman: sorry but your curious amalgam of magic and biology is not really comprehensible to me as a biologist or as a Christian . it. is neither logical or biologically feasible
Avondale College Arguing in Favor of Darwinian Evolution?
Sean Pitman: However, according to the Bible and Ellen White, before the Fall God specifically directed nature so that all sentient life was protected in a manner that there was no suffering or death. By eating from the “Tree of Life” God provided constant renewal and regeneration that worked against what would otherwise be inevitable entropic changes, decay, and death. It was by deliberately stepping away from the true Source of eternal life that mankind stepped away from God and into the full workings of mindless natural law alone – which does in fact inevitably lead to suffering and death.
And this interpretation is precisely why you need a theodicy. Where is the justice in killing all for the sake of the sins of one woman+man? It makes no sense logically. If they were conditionally immortal because of eating of the tree of life then did all the animals in all the world congregate around this tree like beasts around a water hole on the serengeti. how exactly do you as you are wont to do translate the account into a literal reality. And which beast had to come and eat. Or was it symbolic? Oh now that’s a thought.
Avondale College Arguing in Favor of Darwinian Evolution?
Sean Pitman: Come on now. Even I can imagine limitations to reproduction or the turnover of sentient carbon-based life. Surely you can at least imagine something similar? I know God can since such a world is described in the Bible and in the writings of Ellen White. Think about it…
Of course I have. This is not simply about reproduction. That is trivial. This is about metabolic process. Show me a carbon based life form that does not grow or metabolize anything and I will show you an organism in stasis as a spore “living” millions of year in amber. That is; effectively dead.
Real life cannot exist without metabolic process in a carbon based world and God has sanctified all this by a process of making good out of evil from the death of one comes life for others. Just as in the biological world so in the spiritual. By his death we have life. Just as God sanctified the practice of sacrifice of appeasement practiced by most cultures for thousands of years before and showed that in the Judeo-Christian tradition these same acts of sacrifice were emblematic of a monotheistic God that would become incarnate and bring life from death. So also he took the preceding accounts of creation derived as they were of the mesopotamian valley and recast it as an account of the monotheistic God who is above all but comes and dwells among us to become one of us. Participating in our life and death but showing us the importance of the transcendent life of the spirit that supercedes carbon based life and its inherent death. It is no fairy tale of 6 impossible things before breakfast. It is not pie in the sky by and by. It is rooted in a real world and it is about the transcendence of love and grace that is acted out in a real physical world by the incarnate God and us as we follow as His disciples.
That is the message I get from the images and visions of the Canon and EG White. But of course I read it for the message that it conveys not as a scientific text. That is where we fundamentally differ.
