Gene Function in Complex Evolution

[PB666]

So the recent discussion in the Paleo thread brings to light a difference in opinion based on perspective. And the question that comes to mind sometimes is why would someone with a molecular anthrpology background have such a difference in interpretation versus someone with a cultural anthropology or archaeology background.

In general they are trying to solve to very different problems which overlap in some area of physical anthropology. In molecular anthropology its generally not by choice, the discipline needs anchors and it needs aDNA and both require some sort of fossils or well preserve ancient bone.

Why do we care, why should we care. To know when a gene evolved you tend to follow the development of internal markers in that gene, SNPs (called snips) over time. The question is the time, to do that you have to have some guess about the rate, and the rates per nucleotide are in the 10^-19/sec range. You are not going to be able to estimate the long term rate of evolution looking at cells in a laboratory, you could try but you will find most mutations that are produced in real time rapidly disappear from the population (there are disease studies that look at that, but these are generally not common diseases). So alternatively we need to have surrogate. And the surrogates are the rate of evolution between two species, say a chimp and a human. So that period covers k*3.15x 10¹³ seconds were k is a measure in millions years. So that we have got a horrendously low mutation rate to a point where we can expect a mutation across 10,000 base pairs. Some areas evolve faster or slower. So basically now if you know when say species 1 and 2 branched then you can expect mutations in the vicinity of your gene which you can clock (or not depending on the rate of recombination).

What is the interest here, is it academic or is there some more nefarious reason for making archaeologists life difficult by throwing in facts that are difficult for them to understand. For example a forensic anthropologist might be looking for a specific allele that maps potential suspects to a given area of origin, a medical geneticist may want to link all members of a large family backward in time to the origin of that disease for example to find an notify all potential carriers. There could be a variety of reasons medically for have useful sets of markers based on ancestral origins that allow us to link people together by genes. But there are even deeper and more abstract reasons for wanting to know the evolutionary history of a population in a medical context.

So let me state what complex Evolution is, to do that we need a simple evolution model. In this simple model a proto-species moves into an area, it adapts through both evolution and adaptive behaviors (some of which are learned) over time the rate at which many genes, for example non-synonymous sites in mtDNA, slow down and this allows the population to expand, over time if the species remains in that habitat it can undergo formal speciation and will lose the ability to intermix with descendants along other branches, this could take 100ky or 100my, we don't care.

So a more complex model of evolution is actually the reality for most species. Kimura identified this in the 1950s or so replacing our idea of genetic drift with variable selection. Variable selection applies not only to static circumstances but a wide variety of circumstances where the selection coefficient on genes is difficult to determine. This can also break into heterozygous selection, cyclical selection,  .It is because of Kimura that we care about effective individuals (N_e) and population constrictions and all that technobabble. . . . . . In the more complex model of evolution then selection changes as time progresses and in reference to the coordinate system (as individuals or groups move around). Secondarily we do not assume that an isolate speciates, it can with regard to another subspecies, but the assumption is that under various condition that under some condition distal isolates can mix. Then they are free to go about the evolution of crossed genes (either positive or negative). It is only after the fact, for example, we want to ask the question why two genetically defined groups did not mate and one went extinct (usually the case in hominids), what was their limiting incompatibility. From about 1980 (really 1995) to 2008 this appeared not to be the case in humans, even though there were some slight indicators to the alternative. Some of these indicators were immune function genes.

There is a whole class of diseases in our society that are low penetrance. And many of you would think that the penetrance is due to other genes and that is true, but there are examples of disease where penetrance can be linked to environment. For example type II diabetes is linked to environment and maybe some genes. But type II diabetes is not the only form of diabetes.

Rheumatoid arthritis is common to just about every population on earth, and there are known environmental causes (smoking, dental problems). But for many of you it might come as a surprise that it has a genetic risk (other than being female), in fact relatively high so that an individual who carries a particular gene alternatives has 5 fold more risk than someone who does not.  But even more surprising is there is a city in Africa in which people sometimes carry the genes, but there is no rheumatoid arthritis, not a single case has been recorded in the indigenous population. Another example, the end of WWII and the cold war split a community in half the genetic makeup is insignificantly different, on one side of the border the people are at risk X for juvenile onset diabetes, on the other side the risk is 0.1X. In general, RA being the exception, inflammatory disease risk is increasing, and increasing quite rapidly for some diseases. The disease risk is evolving over time. There is a big expensive study going on in Europe right now called DAISY that is trying to parse out what those obviously environmental risk are, and to largely no avail. The epidemiology is not easy, it gets easier if you can factor groups into genetically defined risk categories.

These are extreme examples, but scattered about our genome are genes that give benefit under environment X and are negatively selective under environment Y.
Before I move on we need to first ask the question why should we care about this. . . .We know smoking is bad, and we should brush teeth,  too much sugar is bad.  What I seek to inform here is that moving, just the act of moving from one place to another is sufficient enough to vary selection in unpredictable ways. That is to say making a change of living circumstances from one location or a dramtaic change of culture in the same location in which there is no obvious risks differences still creates risk. Our genes are in a dynamic equilibrium of risk and benefit creation, if they even move a little bit in any direction from the lowest risk/highest benefit state then diseases can appear.

So what is space travel, if it not anything its traveling and it is exposing humans to risk and we tend to look at short term risk, but what about long term risk. . . .for example if you knew a given population of humans was particularly resistant to ionizing radiation, you might want to encourage them to travel in space. What about genes that lower risk for certain issues that arise in space (bone reduction, muscle reduction, blood pressure, eye problems, etc). But then we have to talk about settling, what about the risk of breathing 'Moon' dusts, or the infection/inflammation risk increased by exposure to atopic irritants. The you have situations like psoriasis, another genetically linked disease, also inflammatory, whereby the most cost effective treatment is exposure to sunlight at dawn or dusk in a humid environment. Natural synthesis of vitamin D close to the skin appears to lower risk in psoriasis and diabetes, and so in space its difficult to completely remove risk in a completely sheltered environment.
 

Spoiler

The most extreme example of bizarre regional evolution is hiding in plain site. A particular haplotype I will call 1-7-8-3-2-5 (each number is a component the variant at a given locus) it appears in part to have originated in W. Africa and N.W. Africa and somewhere, maybe 20 kya its components merged and became just one of many haplotypes in Iberia. The path into Africa is somewhat muddled but all the components are present in NW africa and along the N. West African coast so that sufficient enough to call its path of origin. There are other haplotypes that reached Europe in ancient times by the same path, so that is a plausible origin scenario. And 20 kya this haplotype would not look impressive to anyone, it would just be a stretch of DNA. Today it one of the longest runs of homozygosity identified in the human genome at its greatest length is ~9 million nucleotides in length. Of course, typically it is not that long, people who bear 1 component of the haplotype bear 85% of the core of 6 genes and 5 percent bear the entire 9.3 mNT segment, and given random recombination rates this is a statistical impossibility. A novelty or so we might think. As humans expanded into Europe from the Iberian refuge after the LGM this haplotype appears to have some very strange advantage, its not clear what the advantage was, some speculate that it was advantageous in the handling of shellfish, as in the bones of ancient western Europeans there is a high content of marine-derived carbon. And there are numerous shellfish caches to suggest to support this. Unlike haplotype frequency in most human populations, at time the haplotype frequency (or major portions thereof) may have approached 50%. But today 1-7-8-3-2-5 is regarded as a health risk, it is the principle risk factor for autoimmune gluten sensitivity, a secondary cause of juvenile diabetes, and a very long list of immune dysfunction diseases. The primary risk created by the haplotype is environment mediate as must have been the primary benefits at one time. This is an example of complex evolution. It is complex on many levels. First in the context of selection coefficients for chromosome 6p21 the apparent gene frequency is much higher than it should be. Second that rate of recombination does not fit well with rates of recombination at 6p21 or anywhere else in the human genome. Finally,  evolution of humans based on geographic changes of culture and genes has shifted the selection of the gene. We can see here that when preparing space food, you probably want to ovoid items that can create risk in your Astronauts, and when it comes to food, one size does not fit all.

The above is an example of how bad the analysis of evolution can be. In fact when we consider the evolution of the 6p21 region many evolution researchers just walk away.

But it does tell us one thing, we need to get the phylogenetic analysis correct, or some of these evolution studies wont make sense, or give us the wrong sense. The parameters that govern evolution of traits is subject to change arbitrarily and not in a particularly obvious ways. In the above example, no-one knows why recombination slowed down and why it specifically slowed down in one part of the chromosome in one part of Europe, There is another haplotype 3-7-7-15-1.2-6.2 that is similarly long, this particular long haplotype has a variant that carries among other things, the hereditary hemochromotosis gene. If you have never heard of the disease, its pretty much Western European in origin. Oddly these two genes appear to be the principle 6p21 representative  in a long history of coevolution (pre-Neolithic) in Western, NW and N Europe. There is some belief that 7-7-15 might be derived from Neanderthals, its not clear, but the 15 component is the major genetic risk factor in MS.

As we can imagine humans coming into to contact and mixing cultures and genes, now we have to imagine different archaic populations intermixing and sometimes exchanging culture and evolving new habits.
Sometimes those admixtures had beneficial traits and sometimes they were negatively selective.

So one might think that as humans moved around and entered new environments that the cognitive traits were most important, immune genes will not knap out a stone tool or half the end of a stick. But as a matter of fact, the most important genes that allow humans to be successful as they travel and that adapt as people move are the immune genes and the population size in Africa allowed humans to carry out of Africa more of those advantageous genes. This creates a different perspective on what we should be looking at and looking for. Its not as romantic as the archaeology, but it gives a better sense as to the risk that humans are exposing themselves to. And since archaics carried regionally adaptive genes we can ask questions about what human drew from these hominids during there evolution, potentially enhancing there ability to travel further, higher, colder.

So that here are some papers that deal with Neanderthal and Denisovan genes more common in humans and what traits they effect.

Again, I have to repeat I have no connection with these studies other than I used to publish on related materials in the field. And I have published on a collection of about 50 genes, 3 of the genes that I have published on fortuitously appear in the list (Obviously immune function genes).

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5751057/pdf/evx216.pdf
   The CCR3 is an immune gene and is involved in T-helper cell Immune cell interaction. (two of three SNPs are intragenic)
   The ORF5 multigene locus carrying multiple olfactory receptor 5 , rs12788102, is also associated with Malarial resistance. 
   The RNH1 locus, a gene involved in weight control. (Neandertals were robust relative to human and so this is not unexpected).

In East Asians these genes are more common (from Neanderthals but not Denisovans).
  The POU2F3 gene is involved in taste reception and may also be involved in the response to helminth infection. The gene interacts with IL25 a th-2 type T-cell factor. (East Asian and South Asia)
  The BCN2 is involved in keratinocyte maturation and influences skin pigmentation. (European)
  The OAS1 played an antiviral role against Dengue virus  (Eurasians)
  The LARS (Native American admixtures) involved in growth and liver function.
  The FAP/IFIH1 involved in protection against RNA type viruses.(Peru)
  The CHD2 (Peru) developmentally important. Epilepsy
  The TLR1-6 genes involved in immune function, part of the innate immune response and protection from gut pathogens.  (Eurasians)
  The ZFHX3 (Peru) possibly prevents prostate cancer.
---Gene possibly derived from Denisovans
  The LIPA (Asian and Amr) cholesterol metabolism
  The MUSTN1 ( S. Asian) gene is involved in collagen metabolism.

This stuff is not romantic at all, there are no fancy cognition genes or genes that make one taller or more handsome or a divot in your chin. There's nothing here really that makes you look more like a Neanderthal (despite half century belief amount anthropologist that it did). If we look at the list above, about half of the genes that were selective in some population after admixture are immune function genes, 3 of the loci are commonly associated with inflammatory diseases in humans. However in addition to the positive benefits of admixture I also have to point out that there were negative benefits. One of the papers I reviewed during the last week essentially shows that the more likely a Neanderthal marker was close to a gene, the more rapidly that the marker is eliminated from the population. I will try to find the reference.

So that there are some remaining questions, there are a handful of immune genes in Asia that appear not to be of OoA origin, but are not defined by the current Neanderthal sequences or Denisovan. The are tightly pocketed enough is Asian that a scenario of local introgression might have occurred. In addition it is unlikely that a Denisovan in Siberia would carry the same immune genes as an individual living in Indonesia or points in between. So more aDNA sampling is desired in both the Neanderthal and Denisovan gene clusters. While most of the late introgression of 'archaics' into Africa are localized, these are still very important, particularly when introgressed genes are positively selective within holoAfrican context.

I will add to this some of my experiences with PA over the years and some of the critiques in the way the science was done that slowed things down, some of the things that made advances.

 

 

 

  

 

 

[Green Baron]

Great care must be taken when working with ancient DNA. The first take on the neandertal genome by Pääbo et al. braught to light that neandertal and anatomically modern humans did not interbreed. At a time when the contrary was long clear to archaeology. It took them two years to change their mind, based on the same set of samples.

The Denisovian (i say neandertals just for provocation) are based on a single site and 4 fragments, a finger fragment and 3 teeth. It is not completely silly to wait for the analysis to crumble as new data comes in.

Don't get me wrong, i have no problem with ancient DNA, but it is not as safe as it may sound. By far not. It can add a mosaic part to the greater picture that comes together from physical, chemical, geographical, archaeological, sedimentary, palynological, climatological, anatomical and typological data gained from all sources at hand.

 

Given and signed by the friendly

Green  Baron :-)

Edited January 30, 2018 by Green Baron

[PB666]

4 hours ago, Green Baron said:

Great care must be taken when working with ancient DNA. The first take on the neandertal genome by Pääbo et al. braught to light that neandertal and anatomically modern humans did not interbreed. At a time when the contrary was long clear to archaeology. It took them two years to change their mind, based on the same set of samples.

The Denisovian (i say neandertals just for provocation) are based on a single site and 4 fragments, a finger fragment and 3 teeth. It is not completely silly to wait for the analysis to crumble as new data comes in.

Don't get me wrong, i have no problem with ancient DNA, but it is not as safe as it may sound. By far not. It can add a mosaic part to the greater picture that comes together from physical, chemical, geographical, archaeological, sedimentary, palynological, climatological, anatomical and typological data gained from all sources at hand.

 

Given and signed by the friendly

Green  Baron :-)

Oh I'm glad you brought the topic up. That's not actually the chronology. In 1997 krings et al published the HVR1 regions (partially truncated). I was there then, I had analyzed the sequence practically before the paper copy was published ( I was at the time doing mtDNA analysis on human HVR1 and actually I have a completely alligned list now of 50 or so mammalian mtDNA, it clocks the mdts between two sequences). It was a spectacular accomplishment, but as with any spectacular accomplishment there were flaws. Paabo later talks about he avoided the problem of cytosine deamination while others were not so lucky. This is not true actually, when I examined the sequence I found an excess of T-T in the sequence which were at unexpected sites, these were likely flaws. And in the later mt genome sequence these were removed ( I have all the mtDNA genomes of Neanderthal laid out in MS Excel if you want them, lol).

https://www.ncbi.nlm.nih.gov/pubmed/9230299
https://www.ncbi.nlm.nih.gov/pubmed/10318927

Following this Paabo published I thing 8 years later the genomic sequence. I have the revised this on my computer. there are numerous errors in the sequence and there are not near enough passes.

https://www.ncbi.nlm.nih.gov/pubmed/17108958
https://www.ncbi.nlm.nih.gov/pubmed/17110569

After this study the claimed that there was the presence of modern human genome in Neandertals. So some researchers, I believe at UC SB or Stanford poured over the sequences and found a stastical improbability that all the human sequences in Neandertal were in fact longer than the short peices of N DNA and they concluded that the Neanderthal DNA had been contaminated. A maximum likelihood study was done and it was found that the likelihood that humans had interbreed with Neandertals was next to zero. 

https://www.ncbi.nlm.nih.gov/pubmed/17937503
https://www.ncbi.nlm.nih.gov/pubmed/18304371

The group later verified this. More mitochondiral genomes were published and it found something rather odd, the TMRCA of Neandertals was about 50-75,000 years before they went extinct which the population size was really small, even before humans arrived. 

https://www.ncbi.nlm.nih.gov/pubmed/20336068
https://www.ncbi.nlm.nih.gov/pubmed/19608918

     
By about 2009 we see the skies basically open and we start see useful information coming along

https://www.ncbi.nlm.nih.gov/pubmed/21179161
https://www.ncbi.nlm.nih.gov/pubmed/22936568
And more refined analysis and better error detection regimes more completed African genomes allowed the elucidation of elements in the Eurasian genomes.

Finally we obtained an answer that was suitble for most.

It was a beautiful period in molecular anthropology, no illuminating data was gathered so quickly in such a short period of time.

Anecdotally, the period involved begins with alot of molecular studies making conclusions, many very poor conclusions, many fragmented studies (the X-chromosomal studies were broken into a dozen or so papers each with their own conclusion) and papers with no or really bad statistics. We had mtDNA papers that were all over the place from 50 kya constriction exit to TMRCA in the 400,000 year time frame. Once the genome standard had been set, these poor statistical papers began to fade into the background, and finally Africa began to become a focus of deep study (where study should have begun with).

At the end of this 15 year period the bar had been raised, not a little, but by magnitudes, now it was expected that comparisons studies would be far more involved and have much better statistics.

We have to remember that prior to 1997 we had many physical anthropologist claiming that >75% of human evolution occurred locally, there models claimed genes only flowed slowly from Africa over  100,000s of years, that most of the evolution in Eurasia of the last 200,000 years was regional. On the other side we had people like Stringer claiming weird things like humans left Africa 40,000 ago and that language (the name Klien rings a bell) saying that language appeared 40,000 years ago. There was no middle ground, you were either in one camp (clique) or the other. It was a nasty time. When the Neandertal genomes were complete these voices started to act with reason.

The battle peaked in Australia in 1999 between two researchers, the elder Bowler had originally dated LM3 to around 30 kya, his colleague Thorne redated with a variety of techniques to 62.5 kya (40 to 80 kya) and basically argued . . .look . . .LM3 could not be possibly solely OoA human. https://www.ncbi.nlm.nih.gov/pubmed/16468208 https://www.ncbi.nlm.nih.gov/pubmed/?term=Thorne+LM3 https://www.ncbi.nlm.nih.gov/pubmed/10799262  https://www.ncbi.nlm.nih.gov/pubmed/10799263  https://www.ncbi.nlm.nih.gov/pubmed/11209053  https://www.ncbi.nlm.nih.gov/pubmed/12594511   https://www.ncbi.nlm.nih.gov/pubmed/14580590 https://www.ncbi.nlm.nih.gov/pubmed/27274055     There was a flurry of papers and arguments in the Journals between supporters and detractors of each group. You take it for granted now that we are talking about exit times from Africa in the 60 to 80 ky period, the first mitochondrial genome was radical proposing exit times of 52.5 kya +/- 29 ky. While eventually the MREH crowd would lose the arguments magnitude, as with the argument surrounding Homo floresiensis (Flores hobbit; another battle that played out in the Journals) that effort regarding LM3 really pushed at the door of these incredibly late dates for human occupation in Asia and Oceania.

You like to look at things like someone forced Paabo to accept regional contribution, that was not problem. The MPI crowd had their problem; MCRE receptor debacle is one example where they made liberal assumptions about the dating, later proven to be wrong. People representing molecular studies were complaining about the blind usage of outdated calibration. But the bigger story was the demise of MREH its extreme form, along with some of the crazy bigoted ideas that went along with it.  I think from the point of view of what happened was the MREH crowd was, based on the anthropology that they had, were way to overzealous in their interpretation of regional variation, as a consequence a fair amount of backlash was created. Any objective outside viewer, could, applying just scientific principles would have realized they were way out on a limb. The writing was on the wall, and those with proper foresight would have been backing of into the 'maybe 10%' contribution range. Stringer took them on in his way. They needed absolute and convincing proof, because so much see-rap was being flung around. I was the same way about the Neandertal genome and Denisovan, we are in no hurry, lets let the critics have their say and then see where things fall. Things have settled and this stuff is now part of the record.

Some of us learned a lesson in all of this, wait for the dust to settle and then see who is right, the first volley in any fight cannot predict the outcome of a war (See above) I watched a few unveil. 

 

Edited January 31, 2018 by PB666

[Green Baron]

You said:

With regard to the he said/she said stuff . . . . . .what I will be able to demonstrate is the original wrong notions that were brought into the argument did not disappear, but in fact many of these notions persisted until it was shown that these notions were wrong. And what you will see is that only the subset that were proved wrong fade, but other wrong notions continue to persist even until recently. Archaeology did not release its biases easily, some of the changes were well fought over.

My reply:

You may do so, but do not put words in peoples mouth that they have not said. You have a patronizing tone that diminishes the work of others, and that is not ok imo. You repeatedly quote falsely and put forward false claims, only to evade if you were told not to do so. If they all were as wrong as possible, we are still standing on their shoulders and are relying on and greatly benefit from their work.

 

You said:

You don't quite get the point, you don't have the Marx brothers come in and do archaeology for 100 years and then say geeze now we are going to do the serious stuff.  What you have to say in the paper is to start this is how the samples were manhandled (not bury that fact deep in the text) and these are the things we could and could not do. Critics need details, what was the nature of the preservative placed on the calvaria? Was any means taken to characterized the chert and other material in which the bone fragments were recovered (how disturbed were they after deposition). And of the things we could do this is how we avoided all the created risk. The null hypothesis is that the dating is indeterminate, in all circumstances its up to the authors to prove that in the mess that they have adequately cleaned the sample, the critics responsibility is to point this out if they haven't.

I reply:

This is a common place you lay out. Everyone is aware. All restrictions, uncertainties etc. are described and openly available for everyone to read. The big picture comes from carrying information together and is valid until it changes because of new discoveries.

 

You said:

I should also point out that at a certain point in the purification, because the dating is so close to the limit of Carbon-14, that each step needs to be conducted from CO2 (from ancient carbonates that are acid treated to release gas)) purging of buffers and then degassing CO2 purified such that the CO2 itself is tested for ¹⁴C and found to contain none. (IOW all gasses used need to be completely free of radioactivity, N-15, C-14 . . . .) I  will deal with this problem later, it is not possible in all cases to get high count on the AMS dating.

My reply:

C-14 dating can go back to 50ky with reasonable confidence, in rare cases can be extended to 60/70ky. I am sure you can find a Wikipedia article on this. Limits, find circumstances, preparation etc. are described. The new dates were taken on recently found parts from the Feldhofer skeleton and confirm the old ones.

Edit: if it was a single date then you were absolutely right with warning about the significance. As such, the new dating on freshly found bones adds to to former incomplete picture, giving more certainty to the formerly unsafe dating. Hope that settles the matter ;-)

 

You said:

Another point here I will make later, even if the researchers are extremely careful, a cave is not dead, over the life of a cave, animals will come and go, bats, cave arthropods, etc.  In detail it needs to be certain with testing as excavation proceeds that the indicators of recent activity (mtDNA and other markers) have not accumulated in the soil. But in the case of Feldhofer I we are beyond that because the context was lost, so one has to assume for the sake of research that the sample was contaminated and then take the appropriate measures to remove that contamination.

My reply:

The clays were found 1997, i have been at the site. I myself doubt the DNA analysis because of i have a respect for ancient dna. But the dating does not rely on DNA. Variables that could play a role, like modern contaminations, cave sediments, relocation, etc. were accounted for. I don't say this is a final word because such a thing does not exist, but i doubt your right to generally put the work down.

 

You said:

As I said we have other reasons to believe that Feldhofer I was not greatly older than 40k because of the issues regarding the mtDNA persistence, and given the post disruption exposure to the elements we are lucky to have any DNA left in that sample, so it is reasonably to imply that the dates are close, but this really is 'in the ballpark' analysis. But getting the correct result may just be a matter of luck and the next time you may not be so lucky with the same technique. I will deal with this later with Oase 1.

My reply:

Correct, it is not greatly older than 40k. The dates and ranges are published. It is not a matter of luck as it was replicated through modern finds. Everything is nice so far :-)

 

At the end:

Besides all arguing and counting of molecules, it would be nice if you wouldn't repeatedly cite falsely but acknowledge the work that has been done so far. If you limit yourself to genetics, no problem for me, but don't put it as the only solution.

Edited February 2, 2018 by Green Baron
Edit

[Diche Bach]

@PB666 You know, most high-impact pubs require a SHORT abstract. Can you condense the point into say 150 or 200 words?

[Green Baron]

He doesn't even have a point or an argument chain were to hang up a critique. He is mostly destructive, negating and denying and evading and - which is not ok imo - falsely attributing words to people. This is all somewhat strange.

A few days ago i have introduced myself to him via pm and asked who he is, but have not received an answer.

Edit: but other things @PB666 writes are conclusive and even nice. I from time to time like posts from him :-)

Edited February 2, 2018 by Green Baron

[PB666]

7 hours ago, Green Baron said:

C-14 dating can go back to 50ky with reasonable confidence, in rare cases can be extended to 60/70ky. I am sure you can find a Wikipedia article on this. Limits, find circumstances, preparation etc. are described. The new dates were taken on recently found parts from the Feldhofer skeleton and confirm the old ones.

No it cannot, with modern technology like AMS it can. Statistically the results of the Felhofer dating has a problem which I can state as this. Great  statististics confidence is the inverse crossproduct of all independent sources of variation. But what the paper publish is the intrinsic source of variation. It makes no effort to describe extrinsic source of variation. For the physics folks here dP*dx= h/2pi is variation in that is intrinsic to nature, but poor experimental set up, faulty devices are extrinsic to the nature. The assumption you make in producing a +/- range as the published in the paper is that you have eliminated all extrinsic sources . . .but this is not true. Neither did they set up an experiment to test the possibility of extrensic variation or provided a result. For example, falling down the face of a rise and being crushed by various forces is a source of extrinsic variation. This is a huge problem in archeaology, although they have sought to improve the techniques over the last few decades, anyone who understands both the chemistry and the statistics can see the problem rapidly. 

Getting a dating before 40 kya requires you to get alot of things (as in everything) right, not just the instrument needs to be modern, but the samples need to be treated to remove the potential of all extraneous sources of ¹⁴C.

7 hours ago, Green Baron said:

ou may do so, but do not put words in peoples mouth that they have not said. You have a patronizing tone that diminishes the work of others, and that is not ok imo. You repeatedly quote falsely and put forward false claims, only to evade if you were told not to do so. If they all were as wrong as possible, we are still standing on their shoulders and are relying on and greatly benefit from their work.

As I stated who actually defended the sites context. Who stepped up and said this site is important, lets seek out and find all like kind items. If Furlochs work was great it would be done, otherwise, it makes little difference what he said.

7 hours ago, Green Baron said:

The clays were found 1997, i have been at the site. I myself doubt the DNA analysis because of i have a respect for ancient dna. But the dating does not rely on DNA. Variables that could play a role, like modern contaminations, cave sediments, relocation, etc. were accounted for. I don't say this is a final word because such a thing does not exist, but i doubt your right to generally put the work down.

Its not to cast doubt on their work, its a point that the system is flawed and tends to produce flawed results whenever all points along the path are not treated rigorously. Of course Felhofer I is of a higher class than Piltdown. But in fact it was the highest point in two generations of work, which does not sa much about those two generations. 

Everyone doubted the A mtDNA work, including myself, the first thing I did was look for cytosine deamination and I found it. I really could not see how they could get DNA from a sample treated as badly as that sample had been treated. But when the Vidijna cave sequences came in and we could see how close these were together, one has to accept it as a point. I doubt everything that MPI produces, because they have a track record of small errors, but in general those errors are corrected in a couple of years. In archaeology errors might not be corrected in decades. Thats not intended to be an insult its just a recognition that it lacks an objective basis for critique. Within weeks of the original Neandertal genome you had people including myself scouring the sequence looking for flaws, and within months the flaws were found and reported and MPI had to respond and modify their work in response.

 

[Green Baron]

4 minutes ago, PB666 said:

No it cannot, with modern technology like AMS it can.

Now, what ?

4 minutes ago, PB666 said:

Of course Felhofer I is of a higher class than Piltdown.

Is this a defamation ? Are you saying that people over a course of 170 years repeatedly produced and still produce frauds ? Do you have a conception of how a modern academic excavation and its post-processing goes along ? Do you think Schmitz produced bone fragments that fit the the finds from 1856 ? This is ridiculous.

 

[PB666]

1 minute ago, Green Baron said:

Now, what ?

Is this a defamation ? Are you saying that people over a course of 170 years repeatedly produced and still produce frauds ? Do you have a conception of how a modern academic excavation and its post-processing goes along ? Do you think Schmitz produced bone fragments that fit the the finds from 1856 ? This is ridiculous.

If you want to read that into it that's your choice.  For 41 years PA could not distinguish a fraud from fact and for 41 years PDM was part of the mileau of other finds. The fraud was there, in plain site to see, and still it could not be seen.

As per AMS, garbage in garbage out. The technique is great, its not a put down. But the sample preparation is what makes a great machine produce great results.

As I pointed out to you, if you invite a critique of paleontology, be prepared to be stung.

Let me lay it out to you.
First you take just the bone and do radiocarbon dating.
Next you extract the collagen then you do radiocarbon dating.
Then you carefully purify the collagen, then you do radiocarbon dating.
You might even have an antibody that is specific to human collagen, you can use that to further purify it and then acid release the antibody.

If the date increases with each purification you perform, then you had an extrinsic source of variation. Just as dust is extrinsic to glass^. This is not trivial either, collagen is just an acid soluble protein, bacteria also produce acid soluble proteins and any good biochemist knows that extractions contain impurities, proteins not of interest. That was the point of a Ph.D. is basically you can purify someting away from everything else and characterize it.

 

[Vanamonde]

This thread is not going any better than the one it split off from. Why don't we all just move on.