As few as 19 000 human protein-coding genes?

_{Denyse O'Leary

July 7, 2014

Human evolution, Intelligent Design, News}

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Abstract: Determining the full complement of protein-coding genes is a key goal of genome annotation. The most powerful approach for confirming protein-coding potential is the detection of cellular protein expression through peptide mass spectrometry (MS) experiments. Here, we mapped peptides detected in seven large-scale proteomics studies to almost 60% of the protein-coding genes in the GENCODE annotation of the human genome. We found a strong relationship between detection in proteomics experiments and both gene family age and cross-species conservation. Most of the genes for which we detected peptides were highly conserved. We found peptides for >96% of genes that evolved before bilateria. At the opposite end of the scale, we identified almost no peptides for genes that have appeared since primates, for genes that did not have any protein-like features or for genes with poor cross-species conservation. These results motivated us to describe a set of 2001 potential non-coding genes based on features such as weak conservation, a lack of protein features, or ambiguous annotations from major databases, all of which correlated with low peptide detection across the seven experiments. We identified peptides for just 3% of these genes. We show that many of these genes behave more like non-coding genes than protein-coding genes and suggest that most are unlikely to code for proteins under normal circumstances. We believe that their inclusion in the human protein-coding gene catalogue should be revised as part of the ongoing human genome annotation effort. Open access

See also: The Science Fictions series at your fingertips (human evolution)

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Comments

It makes sense to me as a programmer that regulatory genes should outnumber protein coding genes by a very large margin.Mapou_{July 8, 2014
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There must be a lot of non-human in humans.Mung_{July 8, 2014
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Dr JDD, thank you for taking the time to do, IMHO, such a fair and balanced analysis of the study. I found your explanation easy to follow, i.e. not over my head, and I really appreciated that! :)bornagain77_{July 8, 2014
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As I have said before when discussions have arisen about such a peptide approach, we must remember that it relies on the sensitivity of your Mass Spec (MS) capabilities. As described even by the authors of this paper in the introduction:
However, while MS evidence can be used to verify protein-coding potential, the low coverage of proteomics experiments implies that the reverse is not true. Not detecting peptides does not prove that the corresponding gene is non-coding because it may be a consequence of the protein being expressed in few tissues, having very low abundance, or being degraded quickly.
I would also add myself, a point about sensitivity here as well. Some proteins may be expressed, but very transiently, in varying stresses and other conditions (there is a lot of good evidence for this) but also at very low levels. MS requires enough signal to be above the noise and to be able to distinguish that signal confidently as a real event, i.e. a peptide it can distinguish. If the signal is too low, it will be lost in the noise. Of course more recent machines and sensitivities have increased with improvements in the last few years, but the principle still remains. What the authors here are doing is taken already published work, setting criteria for inclusion of peptides in their analysis, and making their conclusions from that. This is a fair approach of course when taking all of the caveats that come with this type of work into account. Let us look firstly at the source for these peptides:
We collected peptides from seven separate MS sources. Two came from large-scale proteomics databases, PeptideAtlas (26) and NIST (http://peptide.nist.gov/). Another four, referred to as ‘Geiger’, ‘Muñoz’, ‘Nagaraj’ and ‘Neuhauser’ throughout the paper, were recently published large-scale MS experiments (20,22–24). For all six datasets, the starting point was the list of peptides provided by the authors or databases. We generated the final set of peptides (referred to as ‘CNIO’) in house from an X!Tandem (27) search against spectra from the GPM (28) and PeptideAtlas databases, following the protocol set out in Ezkurdia et al. (18) with a false discovery rate of 0.1%. These seven studies cover a wide range of search engines, tissues and cell types.
So they used a mixture of already described sources, and also used confidence levels to determine what to include. - Peptide Atlas – a public domain repository of MS peptide data - NIST – as per peptide atlas, linked in some way I think - 4 others from published datasets: Geiger was from 11 “common” cell lines (which are really poor representatives as they will be immortalised cells heavily cultured and not representative of the real scenario for sure – are they human??), Munoz was from embryonic and induced pluripotent stem cells alone, Nagaraj was from a single cancer cell line (very unrepresentative) and Neuhauser I cannot figure out what they did as it is not clear (see abstract here: http://www.ncbi.nlm.nih.gov/pubmed/23611042?dopt=Abstract with note to the final sentence
We apply our high performance platform to investigate incremental coverage of the human proteome by high resolution MS data originating from in-depth cell line and cancer tissue proteome measurements.
where again, I highlight cell line and cancer tissue – no mention of different developmentally stages different tissue normal primary cells). - Finally, their own approach appears to me to be a modified search algorithm of their own, applied to databases already described They make the statement:
These seven studies cover a wide range of search engines, tissues and cell types.
However to me, 2 of the papers just like at 1-2 types, a third looks at 11 cell lines (cell lines as said are highly unrepresentative of the real in vivo situation, are also 2-d models where we already know have differential gene expression than 3-d models as evidenced by anyone who works in cell biology in pharmaceuticals will currently know, etc). Now let’s look at what they state in the conclusion, related to the quoted point in the introduction:
Of course, the absence of peptides in proteomics analyses does not imply that a protein is not expressed. There are many reasons why peptides are not detected in proteomics experiments, for example, the proteins may be present in limited tissues or developmental stages, they may be expressed in very low quantities or, like the HOX genes, have a very short half-lives. Some may be only activated by certain stresses (25), and still other proteins will have features, such as multiple trans-membrane helices, that make them difficult to detect for technical reasons. However, the seven proteomics studies covered a wide range of cell types, making it less likely that one of the main reasons for not detecting a protein, i.e. that it is expressed in limited tissues or developmental stages. The PeptideAtlas database alone is a compendium of experiments carried out on 51 different tissue and cell types, and the PeptideAtlas database forms just a part of the CNIO study and the NIST database. Six of the seven studies were carried out on a range of tissues, and together these studies cover considerably more cell types than UniGene. Although the Human Proteome Project (25) has reported that early developmental stages are still under represented in proteomics experiments, the Muñoz analysis used in this paper (22) interrogated embryo and pluripotent stem cells and found relatively few previously undetected proteins. However, despite the variety of tissues interrogated in our analysis, it is to be expected that some proteins will remain undetected because they are tissue specific.
So they seem to dismiss the idea that it is tissue restriction, yet much of what these databases and papers they cite, have come from analysis of cultured cells that are immortalised. This is not representative at all. Cells that are in 2-d growth, immortalised, in DMEM or RPMI supplemented with fetal calf serum, antibiotics and l-glutamine have very different characteristics and look very different to real, normal primary cells. From what I can see, most of the data they have taken comes from cell lines that will have been treated in this way. Now this is not a criticism – the work is good and sound but the limitations must be taken and I find it odd that this is not commented on more. Also there is little discussion about some of the more pertinent points and limitations of MS and too much weight is given to the apparent “breadth” of these databases and publications they have used. What the paper seems to suggest to me, is that when you look at the common datasets that the most conserved proteins generate the most reliable data and are most commonly found. That is not a surprise. We also know that it is NOT simply tissue expression where differential gene expression occurs – it is also environmental stresses. This has recently been shown with many 100s-1000s of new genes identified in Drosophila due to various stresses, such as alcohol, temperature, etc, etc. This analysis is very much unlikely to be able to even start to address this question. Finally, we need to place this paper into the context of other recent findings, using NEW and more sensitive and more directed specific approaches, to overcome the limitations of these existing datasets used here. One big one came out very recently, and found some proteins that came from genetic regions predicted to have no genes present. That is a testament in itself to how more modern analyses (rather than older datasets) may be able to better address these questions about rarer more novel/specifically expressed proteins: http://www.ncbi.nlm.nih.gov/pubmed/24870542 Finally, I point you to another recent publication here: http://www.ncbi.nlm.nih.gov/pubmed/24960282 Note this in the abstract:
Chromosome-centric human proteome project (C-HPP) is a global initiative to comprehensively characterize proteins encoded by genes across all human chromosomes by teams focusing on individual chromosomes. Here, we report mass spectrometry-based identification and characterization of proteins encoded by genes on chromosome 12. Our study is based on proteomic profiling of 30 different histologically normal human tissues and cell types using high-resolution mass spectrometry. In our analysis, we identified 1,535 proteins encoded by 836 genes on human chromosome 12. This includes 89 genes that are designated as "missing proteins" by "neXtProt" as they did not have any prior evidence either by mass spectrometry or by antibody-based detection methods. We identified several variant peptides that reflected coding SNPs annotated in dbSNP database. We also confirmed the start sites of ?200 proteins by identifying protein N-terminal acetylated peptides. We also identified alternative start sites for 11 proteins that were not annotated in public databases until now. Most importantly, we identified 12 novel protein coding regions on chromosome 12 using our proteogenomics strategy. All of the 12 regions have been annotated as pseudogenes in public databases. This study demonstrates that there is scope for significantly improving annotation of protein coding genes in the human genome using mass-spectrometry-derived data. Individual efforts as part of C-HPP initiative should significantly contribute toward enriching human protein annotation. The data have been deposited to ProteomeXchange with identifier PXD000561.
Emphasis in bold is mine. Please note that >10% of the genes were designated “missing proteins”, that annotated pseudogenes had real protein products, and most relevant to this discussion, these 10% genes designated as missing proteins were not previously found by MS. So while this original study posted is interesting, it must be taken with all the caveats and other information we have at hand. I think the case for novel proteins is still pretty strong, and this does not defeat ORFans. If anything as others have said, it is all the more amazing we are SO different to organisms yet with relatively few proteins. Which leads onto a final point. Clearly, the regulation by non-proteinacious components of the cell is crucial to defining characteristics of an organism. Much of our genome is being found to, and is likely to encode for regulatory components such as regulatory RNA molecules or simply moieties itself. Evolutionists have always focused on the evolution of proteins through mutation in the DNA to give new amino acid changes and new protein functions. However it seems that this is not a shrinking problem for them as there is a whole other random mutation “space” for evolution to account for and that is the plethora of regulatory molecules that are quite different to the simple DNA-->RNA-->protein central dogma.Dr JDD_{July 8, 2014
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ORFans are lineage-specific genes that are annotated as being protein coding. This paper sugggests that many lineage-specific sequences annotated as being protein coding are in fact not making proteins. Since folks here have made a big deal about ORFans this seems like an interesting result, no?wd400_{July 8, 2014
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wd400: Then why did you bring up the whole issue of ORFan genes? Again, if we're dealing with annotated lineage-specific sequences that are 'not' protein-coding (i.e., are non-coding) then this is just what ID has been expecting to find for years.PaV_{July 8, 2014
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ORF stands for Open Reading Frame -- you can't have a non-coding ORF.wd400_{July 8, 2014
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wd400: I suppose you're trying to say that the lineage-specific sequences (ORFans) found in humans is "non-coding." But this is exactly as IDists would have predicted.PaV_{July 8, 2014
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bornagain77 re post 10: That is a pretty devastating takedown of evolution. Great source of information.phoodoo_{July 8, 2014
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PaV, They find no evidence for proteins being made from most of the lineage-specific sequences annotated as protein-coding -- I think the relvance is pretty self explanatory from there?wd400_{July 8, 2014
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So instead of 21,000 types of the billion trillion proteins that make up a human, we only have 19,000 types of the billion trillion proteins that make up a human? Well I guess that simplifies everything immensely. :) Now if a Darwinist would be so kind as to tell us how these 19,000 types of the billion trillion proteins actually self assemble themselves into a human from a fertilized egg I guess we can all call it a day and go home:
HOW BIOLOGISTS LOST SIGHT OF THE MEANING OF LIFE — AND ARE NOW STARING IT IN THE FACE - Stephen L. Talbott - May 2012 Excerpt: “If you think air traffic controllers have a tough job guiding planes into major airports or across a crowded continental airspace, consider the challenge facing a human cell trying to position its proteins”. A given cell, he notes, may make more than 10,000 different proteins, and typically contains more than a billion protein molecules at any one time. “Somehow a cell must get all its proteins to their correct destinations — and equally important, keep these molecules out of the wrong places”. And further: “It’s almost as if every mRNA [an intermediate between a gene and a corresponding protein] coming out of the nucleus knows where it’s going” (Travis 2011),,, Further, the billion protein molecules in a cell are virtually all capable of interacting with each other to one degree or another; they are subject to getting misfolded or “all balled up with one another”; they are critically modified through the attachment or detachment of molecular subunits, often in rapid order and with immediate implications for changing function; they can wind up inside large-capacity “transport vehicles” headed in any number of directions; they can be sidetracked by diverse processes of degradation and recycling... and so on without end. Yet the coherence of the whole is maintained. The question is indeed, then, “How does the organism meaningfully dispose of all its molecules, getting them to the right places and into the right interactions?” The same sort of question can be asked of cells, for example in the growing embryo, where literal streams of cells are flowing to their appointed places, differentiating themselves into different types as they go, and adjusting themselves to all sorts of unpredictable perturbations — even to the degree of responding appropriately when a lab technician excises a clump of them from one location in a young embryo and puts them in another, where they may proceed to adapt themselves in an entirely different and proper way to the new environment. It is hard to quibble with the immediate impression that form (which is more idea-like than thing-like) is primary, and the material particulars subsidiary. Two systems biologists, one from the Max Delbrück Center for Molecular Medicine in Germany and one from Harvard Medical School, frame one part of the problem this way: "The human body is formed by trillions of individual cells. These cells work together with remarkable precision, first forming an adult organism out of a single fertilized egg, and then keeping the organism alive and functional for decades. To achieve this precision, one would assume that each individual cell reacts in a reliable, reproducible way to a given input, faithfully executing the required task. However, a growing number of studies investigating cellular processes on the level of single cells revealed large heterogeneity even among genetically identical cells of the same cell type. (Loewer and Lahav 2011)",,, And then we hear that all this meaningful activity is, somehow, meaningless or a product of meaninglessness. This, I believe, is the real issue troubling the majority of the American populace when they are asked about their belief in evolution. They see one thing and then are told, more or less directly, that they are really seeing its denial. Yet no one has ever explained to them how you get meaning from meaninglessness — a difficult enough task once you realize that we cannot articulate any knowledge of the world at all except in the language of meaning.,,, http://www.netfuture.org/2012/May1012_184.html#2 Stephen Meyer - Functional Proteins And Information For Body Plans - video http://www.metacafe.com/watch/4050681 Dr. Stephen Meyer comments at the end of the preceding video,,, ‘Now one more problem as far as the generation of information. It turns out that you don’t only need information to build genes and proteins, it turns out to build Body-Plans you need higher levels of information; Higher order assembly instructions. DNA codes for the building of proteins, but proteins must be arranged into distinctive circuitry to form distinctive cell types. Cell types have to be arranged into tissues. Tissues have to be arranged into organs. Organs and tissues must be specifically arranged to generate whole new Body-Plans, distinctive arrangements of those body parts. We now know that DNA alone is not responsible for those higher orders of organization. DNA codes for proteins, but by itself it does not insure that proteins, cell types, tissues, organs, will all be arranged in the body. And what that means is that the Body-Plan morphogenesis, as it is called, depends upon information that is not encoded on DNA. Which means you can mutate DNA indefinitely. 80 million years, 100 million years, til the cows come home. It doesn’t matter, because in the best case you are just going to find a new protein some place out there in that vast combinatorial sequence space. You are not, by mutating DNA alone, going to generate higher order structures that are necessary to building a body plan. So what we can conclude from that is that the neo-Darwinian mechanism is grossly inadequate to explain the origin of information necessary to build new genes and proteins, and it is also grossly inadequate to explain the origination of novel biological form.’ Stephen Meyer - (excerpt taken from Meyer/Sternberg vs. Shermer/Prothero debate - 2009) Darwin's Doubt narrated by Paul Giem - The Origin of Body Plans - video http://www.youtube.com/watch?list=PLHDSWJBW3DNUaMy2xdaup5ROw3u0_mK8t&v=rLl6wrqd1e0&feature=player_detailpage#t=290
bornagain77_{July 8, 2014
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"The number of new genes that separate humans from mice [those genes that have evolved since the split from primates] may even be fewer than ten," study co-author David Juan said in the press release." http://www.the-scientist.com/?articles.view/articleNo/40441/title/Human-Gene-Set-Shrinks-Again/ Seems genes are not really that important in differentiating? Gosh, which book has more errors - Origin of Species or The Selfish Gene? Tough one.ppolish_{July 8, 2014
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@wd400 You're right. I had two papers open at the same time and the text I copied was from the wrong one. Sorry about that.JoeCoder_{July 8, 2014
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wd400: My initial perusal tells me that their results are perfectly conformable to ID expectations. I don't see the problem. What does this have to do with ORFan genes?PaV_{July 8, 2014
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of related interest to this claim,,, “We found peptides for >96% of genes that evolved before bilateria.” ,,,Is the fact that yeast and bacteria are both found to be very uncooperative to assumptions of common descent,,, Here Are Those Incongruent Trees From the Yeast Genome - Case Study - Cornelius Hunter - June 2013 Excerpt: We recently reported on a study of 1,070 genes and how they contradicted each other in a couple dozen yeast species. Specifically, evolutionists computed the evolutionary tree, using all 1,070 genes, showing how the different yeast species are related. This tree that uses all 1,070 genes is called the concatenation tree. They then repeated the computation 1,070 times, for each gene taken individually. Not only did none of the 1,070 trees match the concatenation tree, they also failed to show even a single match between themselves. In other words, out of the 1,071 trees, there were zero matches. Yet one of the fundamental predictions of evolution is that different features should generally agree. It was “a bit shocking” for evolutionists, as one explained: “We are trying to figure out the phylogenetic relationships of 1.8 million species and can’t even sort out 20 yeast.” In fact, as the figure above shows, the individual gene trees did not converge toward the concatenation tree. Evolutionary theory does not expect all the trees to be identical, but it does expect them to be consistently similar. They should mostly be identical or close to the concatenation tree, with a few at farther distances from the concatenation tree. Evolutionists have clearly and consistently claimed this consilience as an essential prediction. But instead, on a normalized scale from zero to one (where zero means the trees are identical), the gene trees were mostly around 0.4 from the concatenation tree with a huge gap in between. There were no trees anywhere close to the concatenation tree. This figure is a statistically significant, stark falsification of a highly acclaimed evolutionary prediction. http://darwins-god.blogspot.com/2013/06/here-are-those-incongruent-trees-from.html Widespread ORFan Genes Challenge Common Descent – Paul Nelson – video with references http://www.vimeo.com/17135166 Estimating the size of the bacterial pan-genome - Pascal Lapierre and J. Peter Gogarten - 2008 Excerpt: We have found greater than 139 000 rare (ORFan) gene families scattered throughout the bacterial genomes included in this study. The finding that the fitted exponential function approaches a plateau indicates an open pan-genome (i.e. the bacterial protein universe is of infinite size); a finding supported through extrapolation using a Kezdy-Swinbourne plot (Figure S3). This does not exclude the possibility that, with many more sampled genomes, the number of novel genes per additional genome might ultimately decline; however, our analyses and those presented in Ref. [11] do not provide any indication for such a decline and confirm earlier observations that many new protein families with few members remain to be discovered. http://www.paulyu.org/wp-content/uploads/2010/02/Estimating-the-size-of-the-bacterial-pan-genome.pdf At the 12:40 minute mark of the following 'The Dictionary of Life' video, Dr. Nelson describes the breaking point for Darwinian scenarios from the genetic evidence of Bacteria: The Dictionary of Life | Origins with Dr. Paul A. Nelson - video http://www.youtube.com/watch?feature=player_detailpage&v=zJaetK9gvCo#t=760s The essential genome of a bacterium - 2011 Figure (C): Venn diagram of overlap between Caulobacter and E. coli ORFs (outer circles) as well as their subsets of essential ORFs (inner circles). Less than 38% of essential Caulobacter ORFs are conserved and essential in E. coli. Only essential Caulobacter ORFs present in the STING database were considered, leading to a small disparity in the total number of essential Caulobacter ORFs. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3202797/pdf/msb201158.pdfbornagain77_{July 8, 2014
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as to this comment from the abstract:
"we identified almost no peptides for genes that have appeared since primates"
Although I find the preceding comment to be suspect, because of,,
An integrated encyclopedia of DNA elements in the human genome - Sept. 6, 2012 Excerpt: Analysis,,, yielded 57 confidently identified unique peptide sequences in intergenic regions relative to GENCODE annotation. Taken together with evidence of pervasive genome transcription, these data indicate that additional protein-coding genes remain to be found. http://www.nature.com/nature/journal/v489/n7414/full/nature11247.html etc..
Nonetheless, even it is true that 'almost no peptides for genes that have appeared since primates' this would make the claim that humans evolved from apes even more remarkable than it already is since the anatomical differences between chimps and humans are far greater than many people have realized,,,
In “Science,” 1975, M-C King and A.C. Wilson were the first to publish a paper estimating the degree of similarity between the human and the chimpanzee genome. But…in the second section of their paper King and Wilson honestly describe the deficiencies of such reasoning: “The molecular similarity between chimpanzees and humans is extraordinary because they differ far more than sibling species in anatomy and way of life. Although humans and chimpanzees are rather similar in the structure of the thorax and arms, they differ substantially not only in brain size but also in the anatomy of the pelvis, foot, and jaws, as well as in relative lengths of limbs and digits (38). Humans and chimpanzees also differ significantly in many other anatomical respects, to the extent that nearly every bone in the body of a chimpanzee is readily distinguishable in shape or size from its human counterpart (38). Associated with these anatomical differences there are, of course, major differences in posture (see cover picture), mode of locomotion, methods of procuring food, and means of communication. Because of these major differences in anatomy and way of life, biologists place the two species not just in separate genera but in separate families (39). So it appears that molecular and organismal methods of evaluating the chimpanzee human difference yield quite different conclusions (40).” King and Wilson went on to suggest that the morphological and behavioral between humans and apes,, must be due to variations in their genomic regulatory systems. David Berlinski - The Devil's Delusion - Page 162&163 Evolution at Two Levels in Humans and Chimpanzees Mary-Claire King; A. C. Wilson - 1975
And indeed it is in the genomic regulatory regions where the differences are found to be 'orders of magnitude' different between chimps and humans:
"Where (chimps and humans) really differ, and they differ by orders of magnitude, is in the genomic architecture outside the protein coding regions. They are vastly, vastly, different.,, The structural, the organization, the regulatory sequences, the hierarchy for how things are organized and used are vastly different between a chimpanzee and a human being in their genomes." Raymond Bohlin (per Richard Sternberg) - 9:29 minute mark of video http://www.metacafe.com/watch/8593991/ Evolution by Splicing – Comparing gene transcripts from different species reveals surprising splicing diversity. – Ruth Williams – December 20, 2012 Excerpt: A major question in vertebrate evolutionary biology is “how do physical and behavioral differences arise if we have a very similar set of genes to that of the mouse, chicken, or frog?”,,, A commonly discussed mechanism was variable levels of gene expression, but both Blencowe and Chris Burge,,, found that gene expression is relatively conserved among species. On the other hand, the papers show that most alternative splicing events differ widely between even closely related species. “The alternative splicing patterns are very different even between humans and chimpanzees,” said Blencowe.,,, http://www.the-scientist.com/?articles.view%2FarticleNo%2F33782%2Ftitle%2FEvolution-by-Splicing%2F
Yet, it is in these regulatory regions (dGRNS) where random mutations are least likely to be tolerated:
A Listener's Guide to the Meyer-Marshall Debate: Focus on the Origin of Information Question -Casey Luskin - December 4, 2013 Excerpt: "There is always an observable consequence if a dGRN (developmental gene regulatory network) subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal, and since the subcircuits are all interconnected, the whole network partakes of the quality that there is only one way for things to work. And indeed the embryos of each species develop in only one way." - Eric Davidson http://www.evolutionnews.org/2013/12/a_listeners_gui079811.html Darwin or Design? - Paul Nelson at Saddleback Church - Nov. 2012 - ontogenetic depth (excellent update) - video Text from one of the Saddleback slides: 1. Animal body plans are built in each generation by a stepwise process, from the fertilized egg to the many cells of the adult. The earliest stages in this process determine what follows. 2. Thus, to change -- that is, to evolve -- any body plan, mutations expressed early in development must occur, be viable, and be stably transmitted to offspring. 3. But such early-acting mutations of global effect are those least likely to be tolerated by the embryo. Losses of structures are the only exception to this otherwise universal generalization about animal development and evolution. Many species will tolerate phenotypic losses if their local (environmental) circumstances are favorable. Hence island or cave fauna often lose (for instance) wings or eyes. http://www.saddleback.com/mc/m/7ece8/
Thus where Darwinian theory most needs flexibility in order to be viable as a hypothesis, i.e. in developmental gene regulatory networks, is the place where it is found to be least flexible. Yet, it is in these gene regulatory networks where the greatest differences are found! Here are a few more notes on the dramatic anatomical differences between chimps and humans that need to be honestly addressed by Darwinists
The Red Ape - Cornelius Hunter - August 2009 Excerpt: "There remains, however, a paradoxical problem lurking within the wealth of DNA data: our morphology and physiology have very little, if anything, uniquely in common with chimpanzees to corroborate a unique common ancestor. Most of the characters we do share with chimpanzees also occur in other primates, and in sexual biology and reproduction we could hardly be more different. It would be an understatement to think of this as an evolutionary puzzle." http://darwins-god.blogspot.com/2009/08/red-ape.html
In fact so great are the anatomical differences between humans and chimps that a Darwinist actually proposed that a chimp and pig mated with each other and that is what ultimately gave rise to humans:
A chimp-pig hybrid origin for humans? - July 3, 2013 Excerpt: Dr. Eugene McCarthy,, has amassed an impressive body of evidence suggesting that human origins can be best explained by hybridization between pigs and chimpanzees. Extraordinary theories require extraordinary evidence and McCarthy does not disappoint. Rather than relying on genetic sequence comparisons, he instead offers extensive anatomical comparisons, each of which may be individually assailable, but startling when taken together.,,, The list of anatomical specializations we may have gained from porcine philandering is too long to detail here. Suffice it to say, similarities in the face, skin and organ microstructure alone is hard to explain away. A short list of differential features, for example, would include, multipyramidal kidney structure, presence of dermal melanocytes, melanoma, absence of a primate baculum (penis bone), surface lipid and carbohydrate composition of cell membranes, vocal cord structure, laryngeal sacs, diverticuli of the fetal stomach, intestinal "valves of Kerkring," heart chamber symmetry, skin and cranial vasculature and method of cooling, and tooth structure. Other features occasionally seen in humans, like bicornuate uteruses and supernumerary nipples, would also be difficult to incorporate into a purely primate tree. http://phys.org/news/2013-07-chimp-pig-hybrid-humans.html Human hybrids: a closer look at the theory and evidence - July 25, 2013 Excerpt: There was considerable fallout, both positive and negative, from our first story covering the radical pig-chimp hybrid theory put forth by Dr. Eugene McCarthy,,,By and large, those coming out against the theory had surprisingly little science to offer in their sometimes personal attacks against McCarthy. ,,,Under the alternative hypothesis (humans are not pig-chimp hybrids), the assumption is that humans and chimpanzees are equally distant from pigs. You would therefore expect chimp traits not seen in humans to be present in pigs at about the same rate as are human traits not found in chimps. However, when he searched the literature for traits that distinguish humans and chimps, and compiled a lengthy list of such traits, he found that it was always humans who were similar to pigs with respect to these traits. This finding is inconsistent with the possibility that humans are not pig-chimp hybrids, that is, it rejects that hypothesis.,,, http://phys.org/news/2013-07-human-hybrids-closer-theory-evidence.html
The obvious question for me is, of course, since Darwinists are having such a hard time proving that we did not come from pig-chimp hybrids, what makes Darwinists so sure that we evolved from apes or anything else in the first place? Any reasonable person would realize that if such a dubious theory such as the pig-chimp hybrid theory can cause such havoc to their empirical basis, for what was suppose to be such well established science, then perhaps the Darwinian story for human origins is not nearly as strong as Darwinists have dogmatically held it to be in the first place. Some might even hold that such 'flimsiness' would suggest that the original theory was rubbish as to being hard science.bornagain77_{July 8, 2014
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As to this comment from the abstract: "We found peptides for >96% of genes that evolved before bilateria." So there has been almost no 'evolution' of proteins since before the Cambrian? But from whence are all the differences arising if there are practically no new proteins since before the Cambrian? And why are they allowed to go all the way back to before bilateria to establish similarity? As Dr. Axe has said before, its not the similarities that need explaining but the differences: Indeed, instead of assuming evolution to be true in the first place and then forcing the evidence to fit, it would be nice if Darwinists would actually try to prove Darwinism to be feasible before assuming it to be true: Peacefulness, in a Grown Man, That is Not a Good Sign - Cornelius Hunter - August 2011 Excerpt: Evolution cannot even explain how a single protein first evolved, let alone the massive biological world that ensued. From biosonar to redwood trees, evolution is left with only just-so stories motivated by the dogma that evolution must be true. That dogma comes from metaphysics, http://darwins-god.blogspot.com/2011/08/peacefulness-in-grown-man-that-is-not.html Thou Shalt Not Put Evolutionary Theory to a Test - Douglas Axe - July 18, 2012 Excerpt: "For example, McBride criticizes me for not mentioning genetic drift in my discussion of human origins, apparently without realizing that the result of Durrett and Schmidt rules drift out. Each and every specific genetic change needed to produce humans from apes would have to have conferred a significant selective advantage in order for humans to have appeared in the available time (i.e. the mutations cannot be 'neutral'). Any aspect of the transition that requires two or more mutations to act in combination in order to increase fitness would take way too long (>100 million years). My challenge to McBride, and everyone else who believes the evolutionary story of human origins, is not to provide the list of mutations that did the trick, but rather a list of mutations that can do it. Otherwise they're in the position of insisting that something is a scientific fact without having the faintest idea how it even could be." Doug Axe PhD. http://www.evolutionnews.org/2012/07/thou_shalt_not062351.html Accounting for Variations - Dr. David Berlinski: - video http://www.youtube.com/watch?v=aW2GkDkimkEbornagain77_{July 8, 2014
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I think you are reading a different paper?wd400_{July 7, 2014
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@wd400 In the paper they say they only looked at genes that had similar sequence in other organisms:
To be a candidate de novo originated gene, in addition to having a potentially translatable open reading frame in the human genome, the gene must have been present, and disrupted (i.e., non-translatable), in both the chimpanzee and orangutan genomes, e.g., the chimpanzee and orangutan sequences must lack an ATG start codon or have frameshift-inducing indels or nucleotide differences that result in a premature stop codon.
These are the genes that many evolutionists cited as evidence of genes evolving from non-genes. Meanwhile ID proponents have been making a deal out of "true orphans", that lack any sequence identity at all in other organisms. So if anything this seems to be evidence against de novo proteins evolving? I'm not a biologist so please correct me if I've understood something incorrectly.JoeCoder_{July 7, 2014
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Well this should be interesting. Anyone who has made a big deal out ORFans wish to comment?wd400_{July 7, 2014
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