Uncommon Descent Serving The Intelligent Design Community

Human evolution: Skull 1470, it turns out, has a multiple personality disorder

Share
Facebook
Twitter
LinkedIn
Flipboard
Print
Email

With respect to the skull in this story, “Two possible new homo species unearthed from time of homo erectus?”, it has been kicking around a lot and we were reminded this afternoon of what Jonathan Wells had to say about it in Icons of Evolution (2000), by a reader who says, “Yes, indeed. Skull 1470 has long been notorious for its ability to assume different shapes depending on how it is reconstructed.”

One famous fossil skull, discovered in 1972 in northern Kenya, changed its appearance dramatically depending on how the upper jaw was connected to the rest of the cranium. Roger Lewin recounts an occasion when paleoanthropologists Alan Walker, Michael Day, and Richard Leakey were studying the two sections of ³skull 1470.² According to Lewin, Walker said: ³You could hold the [upper jaw] forward, and give it a long face, or you could tuck it in, making the face short…. How you held it really depended on your preconceptions. It was very interesting watching what people did with it.² Lewin reports that Leakey recalled the incident, too: ³Yes. If you held it one way, it looked like one thing; if you held it another, it looked like something else.² [1]

Just recently, National Geographic magazine commissioned four artists to reconstruct a female figure from casts of seven fossil bones thought to be from the same species as skull 1470. One artist drew a creature whose forehead is missing and whose jaws look vaguely like those of a beaked dinosaur. Another artist drew a rather good-looking modern African-American woman with unusually long arms. A third drew a somewhat scrawny female with arms like a gorilla and a face like a Hollywood werewolf. And a fourth drew a figure covered with body hair and climbing a tree, with beady eyes that
glare out from under a heavy, gorilla-like brow. [2]

NOTES

[1] On the variable appearance of skull 1470, see Roger Lewin, Bones of ontention, Second Edition (Chicago: The University of Chicago Press, 1997), p 160; see also Ian Tattersall, The Fossil Trail: How We Know What We Think We Know About Human Evolution (New York: Oxford University Press, 1995), p.133.

[2] The drawings of Homo habilis by four different artists are in “Behind the Scenes,” National Geographic 197 (March, 2000): 140. The drawings are actually on an unnumbered page, buried among the advertisements at the end of the issue; the page number cited here was obtained by extrapolating from the last numbered page.

The thing is, why are they so desperate? Why does it matter so much? Is it just the summer and the need for hot weather stories or something?

Comments
it feel better to have scientific discussion now. bornagain77, please continue for enlightenmet discussion of issue. my ink pen for notes is ready. sergiosergiomendes
August 12, 2012
August
08
Aug
12
12
2012
09:25 PM
9
09
25
PM
PDT
That being said I think it should be obvious that a new study needs to be done without the inherent bias as this one had. Maybe a less biased one has been done and I just could not find it in my brief search. Given the over 1400 ORFan sequences (6% of total) I have a feeling that the results will not be at all what Darwinists would have presupposed beforehand.bornagain77
August 12, 2012
August
08
Aug
12
12
2012
01:36 PM
1
01
36
PM
PDT
The comparison is not fair in my view.bornagain77
August 12, 2012
August
08
Aug
12
12
2012
01:29 PM
1
01
29
PM
PDT
We're on the same side here, and I already have most of the sources you link among the notes I use for my own arguments. But the 80-20% still seems to me like saying the dead sea scrolls and masoretic text are only 20% similar, because 80% of the chapters have at least one letter different, and that's a biased result because it doesn't even include the many apocryphal works found among the dead sea scrolls.JoeCoder
August 12, 2012
August
08
Aug
12
12
2012
12:39 PM
12
12
39
PM
PDT
JoeCoder, I hate to belabor this paper, but if you will also notice in the pdf on page 216 of paragraphs 2.1 & 2.2 that the sample set of proteins was severely biased towards the Darwinian presupposition so as to give the most favorable alignment they could get for proteins. This sentence in 2.2 is particularly telling as to the bias they introduced into the analysis:
Multigene families such as major histocompatibility complex (MHC), immunoglobulin, olofactory receptor, and KIR receptor gene families were excluded from analysis because of difficulties in detecting orthologous (i.e. evolutionary) relationships. Mitochondrial proteins were also excluded from the analysis.
As well the percent difference in protein domain-domain interactions (DDIs) is completely unaddressed as well (which is something, from a 'regulatory point of view' of ID, we should reasonably expect a fairly large difference in.) Thus Joe Coder, this study is, given all it biases towards getting a Darwinian conclusion for similar proteins, surprisingly friendly to ID in that, despite the bias, the differences were far larger than can be explained by Darwinian processes.bornagain77
August 12, 2012
August
08
Aug
12
12
2012
06:31 AM
6
06
31
AM
PDT
But you are right JoeCoder, that the paper, by itself, without the other evidence, is not nearly as strong as the ORFan argument.bornagain77
August 12, 2012
August
08
Aug
12
12
2012
04:05 AM
4
04
05
AM
PDT
JoeCoder you state:
I think this is a nearly meaningless benchmark and isn’t a good argument to use.
Well actually I think, even though this study certainly is lacking for the many questions it leaves unanswered, the study is still far stronger to use for a ID perspective than one might be inclined to think at first since, as I noted previously, even two coordinated mutations are shown to be extremely problematic for Darwinists to show the origination of:
More from Ann Gauger on why humans didn’t happen the way Darwin said – July 2012 Excerpt: You don’t have to take my word for it. In 2007, Durrett and Schmidt estimated in the journal Genetics that for a single mutation to occur in a nucleotide-binding site and be fixed in a primate lineage would require a waiting time of six million years. The same authors later estimated it would take 216 million years for the binding site to acquire two mutations, if the first mutation was neutral in its effect. Facing Facts But six million years is the entire time allotted for the transition from our last common ancestor with chimps to us according to the standard evolutionary timescale. Two hundred and sixteen million years takes us back to the Triassic, when the very first mammals appeared. One or two mutations simply aren’t sufficient to produce the necessary changes— sixteen anatomical features—in the time available. At most, a new binding site might affect the regulation of one or two genes. https://uncommondescent.com/intelligent-design/more-from-ann-gauger-on-why-humans-didnt-happen-the-way-darwin-said/
Further notes:
Response from Ralph Seelke to David Hillis Regarding Testimony on Bacterial Evolution Before Texas State Board of Education, January 21, 2009 Excerpt: He has done excellent work showing the capabilities of evolution when it can take one step at a time. I have used a different approach to show the difficulties that evolution encounters when it must take two steps at a time. So while similar, our work has important differences, and Dr. Bull’s research has not contradicted or refuted my own. http://www.discovery.org/a/9951 Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness - Ann K. Gauger, Stephanie Ebnet, Pamela F. Fahey, and Ralph Seelke – 2010 Excerpt: When all of these possibilities are left open by the experimental design, the populations consistently take paths that reduce expression of trpAE49V,D60N, making the path to new (restored) function virtually inaccessible. This demonstrates that the cost of expressing genes that provide weak new functions is a significant constraint on the emergence of new functions. In particular, populations with multiple adaptive paths open to them may be much less likely to take an adaptive path to high fitness if that path requires over-expression. http://bio-complexity.org/ojs/index.php/main/article/view/BIO-C.2010.2/BIO-C.2010.2 Testing Evolution in the Lab With Biologic Institute's Ann Gauger - audio http://www.idthefuture.com/2010/05/testing_evolution_in_the_lab_w.html
The limits found on Darwinian processes is simply far more severe than anyone had at first imagined: here are a few more assorted notes along that line
Epistasis between Beneficial Mutations - July 2011 Excerpt: We found that epistatic interactions between beneficial mutations were all antagonistic—the effects of the double mutations were less than the sums of the effects of their component single mutations. We found a number of cases of decompensatory interactions, an extreme form of antagonistic epistasis in which the second mutation is actually deleterious in the presence of the first. In the vast majority of cases, recombination uniting two beneficial mutations into the same genome would not be favored by selection, as the recombinant could not outcompete its constituent single mutations. https://uncommondescent.com/epigenetics/darwins-beneficial-mutations-do-not-benefit-each-other/ Mutations : when benefits level off - June 2011 - (Lenski's e-coli after 50,000 generations) Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually. http://www2.cnrs.fr/en/1867.htm?theme1=7 Extreme functional sensitivity to conservative amino acid changes on enzyme exteriors - Doug Axe Excerpt: Contrary to the prevalent view, then, enzyme function places severe constraints on residue identities at positions showing evolutionary variability, and at exterior non-active-site positions, in particular. http://nsmserver2.fullerton.edu/departments/chemistry/evolution_creation/web/AxeProteinEvolution.pdf Nature Paper,, Finds Darwinian Processes Lacking - Michael Behe - Oct. 2009 Excerpt: Now, thanks to the work of Bridgham et al (2009), even such apparently minor switches in structure and function (of a protein to its supposed ancestral form) are shown to be quite problematic. It seems Darwinian processes can’t manage to do even as much as I had thought. (which was 1 in 10^40 for just 2 binding sites) http://www.evolutionnews.org/2009/10/nature_paper_finally_reaches_t.html The Ribosome: Perfectionist Protein-maker Trashes Errors Excerpt: The enzyme machine that translates a cell's DNA code into the proteins of life is nothing if not an editorial perfectionist...the ribosome exerts far tighter quality control than anyone ever suspected over its precious protein products... To their further surprise, the ribosome lets go of error-laden proteins 10,000 times faster than it would normally release error-free proteins, a rate of destruction that Green says is "shocking" and reveals just how much of a stickler the ribosome is about high-fidelity protein synthesis. http://www.sciencedaily.com/releases/2009/01/090107134529.htm Proteins with cruise control provide new perspective: "A mathematical analysis of the experiments showed that the proteins themselves acted to correct any imbalance imposed on them through artificial mutations and restored the chain to working order."
As well, the 'errors/mutations' that are found to 'naturally' occur in protein sequences are found to be 'designed errors':
Cells Defend Themselves from Viruses, Bacteria With Armor of Protein Errors - Nov. 2009 Excerpt: These "regulated errors" comprise a novel non-genetic mechanism by which cells can rapidly make important proteins more resistant to attack when stressed,
bornagain77
August 12, 2012
August
08
Aug
12
12
2012
04:01 AM
4
04
01
AM
PDT
From the study: > Only 25 (20%) of these proteins showed the identical amino acid sequence between humans and chimpanzees. In other words, the proportion of different proteins was 80%, in contrast to the 1–2% difference at the nucleotide level. So yes, even one aa different in a string hundreds long will qualify the whole protein for being different, even though most of such substitutions will have no affect on protein structure, and nearly zero will change function. I think this is a nearly meaningless benchmark and isn't a good argument to use. Your argument about new proteins in humans is much better, especially compared to the observed evolution HIV and malaria in the last several decades, which have produced far less with a million times more mutation and selection events.JoeCoder
August 11, 2012
August
08
Aug
11
11
2012
07:08 PM
7
07
08
PM
PDT
correction: Of note, many times when I have shown this study to Darwinists it seems as if it is almost a knee jerk reaction on their part to state that many of the differences found between the proteins of chimps and humansbornagain77
August 11, 2012
August
08
Aug
11
11
2012
01:38 PM
1
01
38
PM
PDT
Well Joe Coder, here is the pdf of the article:
Eighty percent of proteins are different between humans and chimpanzees. - 2005 https://homes.bio.psu.edu/people/faculty/nei/Lab/2005-glazko-etal.pdf
where in the second paragraph of the introduction they tell us how they conducted their research. Please note that they assumed 'non-coding DNA to be 'non-functional', i.e. junk. As well, on page 217 and 218 they show, and discuss, the 100%, 99%, 98% and less than 98% distribution of differences, as well as they briefly discuss some limited aspects of their study that need to be further studied and extended. Of note, many times when I have shown this study to Darwinists it seems as if it is almost a knee jerk reaction on their part to state that many of the differences in the proteins in chimps and apes are only a few amino acids, yet, as Dr. Gauger has pointed out in the citation I listed previously, a 'few' amino acids difference is certainly no small problem to just brush aside as if it did not matter,,, not to mention the fact that there are now found to be over 1400 hundred novel ORFan genes in humans which simply can't be brushed aside with a handwave as Darwinists seem all too willing to do with most evidence:
From Jerry Coyne, More Table-Pounding, Hand-Waving – May 2012 Excerpt: “More than 6 percent of genes found in humans simply aren’t found in any form in chimpanzees. There are over fourteen hundred novel genes expressed in humans but not in chimps.” Jerry Coyne – ardent and ‘angry’ neo-Darwinist – professor at the University of Chicago in the department of ecology and evolution for twenty years. He specializes in evolutionary genetics. http://www.evolutionnews.org/2012/05/from_jerry_coyn060271.html
bornagain77
August 11, 2012
August
08
Aug
11
11
2012
01:28 PM
1
01
28
PM
PDT
Also, it looks like the post about 1470 from yesterday, "Dewitt's Reconstruction of Skull 1470" has been removed? https://uncommondescent.com/intelligent-design/dewitts-reconstruction-of-skull-1470/JoeCoder
August 11, 2012
August
08
Aug
11
11
2012
12:26 PM
12
12
26
PM
PDT
@Bibliography77 :P The 80% protein difference--how are they calculating that? If a protein of 400aa length is different by 1-2 aa's, but still has the same function and structure, is it considered different?JoeCoder
August 11, 2012
August
08
Aug
11
11
2012
12:24 PM
12
12
24
PM
PDT
somewhat related notes:
Guy Walks Into a Bar and Thinks He's a Chimpanzee: The Unbearable Lightness of Chimp-Human Genome Similarity Richard Sternberg May 14, 2009 Excerpt: One can seriously call into question the statement that human and chimp genomes are 99% identical. For one thing, it has been noted in the literature that the exact degree of identity between the two genomes is as yet unknown (Cohen, J., 2007. Relative differences: The myth of 1% Science 316: 1836.). ,,, In short, the figure of identity that one wants to use is dependent on various methodological factors. http://www.evolutionnews.org/2009/05/guy_walks_into_a_bar_and_think020401.html
Sternberg further notes here:
How The Junk DNA Hypothesis Has Changed Since 1980 Richard Sternberg October 8, 2009 Excerpt: A surprising finding of ENCODE and other transcriptome projects is that almost every nucleotide of human (and mouse) chromosomes is transcribed in a regulated way. Most of the RNAs produced are various nonprotein-coding transcripts that are copied from both strands in a cell type-, tissue type-, or developmental stage-specific manner. These RNAs belong to a number of different functional classes and new categories are being discovered all the time. Further, these nonprotein-coding transcriptional units extend into and arise from protein-coding segments. Many also map to the regions between protein-coding loci. The RNA map of the mammalian genome has moreover been demonstrated to be hierarchical and far from random. ,,, Instead of 90% of the human or fly genome being junk, it seems that 90% or more of chromosomal DNA has some kind of specific developmental function, given the available data. Indeed, the emerging picture is that the species-specific nonprotein-coding regions encode numerous RNAs that help to shape the phenotype in ways that we are only beginning to understand. This is especially true for the transposable element fraction of human chromosomes -- about 50% of our DNA -- much of which is arranged and expressed in a taxon-specific manner. Part of the reason for why a human is not a chimp is not a cow is not a whale, then, is that each species has its own set of sui generis "genes" -- genomic texts specifying unique RNAs or even proteins that are used in embryogenesis. http://www.evolutionnews.org/2009/10/how_the_junk_dna_hypothesis_ha026421.html
and indeed we find 'to our surprise' that Sternberg is correct in his observation:
Eighty percent of proteins are different between humans and chimpanzees; Gene; Volume 346, 14 February 2005: The early genome comparison by DNA hybridization techniques suggested a nucleotide difference of 1-2%. Recently, direct nucleotide sequencing confirmed this estimate. These findings generated the common belief that the human is extremely close to the chimpanzee at the genetic level. However, if one looks at proteins, which are mainly responsible for phenotypic differences, the picture is quite different, and about 80% of proteins are different between the two species. http://www.ncbi.nlm.nih.gov/pubmed/15716009
which is not really that surprising when we consider the definition of a what gene actually is has changed dramatically:
The Extreme Complexity Of Genes - Dr. Raymond G. Bohlin - video http://www.metacafe.com/watch/8593991/
and:
Multidimensional Genome - Dr. Robert Carter - video (Notes in video description) http://www.metacafe.com/w/8905048
Yet a 80% difference in proteins, though it flows naturally from ID based reasoning, is extremely problematic for Darwinists to explain (as if the 1% hypothetical genetic difference was not problematic enough):
More from Ann Gauger on why humans didn’t happen the way Darwin said - July 2012 Excerpt: You don’t have to take my word for it. In 2007, Durrett and Schmidt estimated in the journal Genetics that for a single mutation to occur in a nucleotide-binding site and be fixed in a primate lineage would require a waiting time of six million years. The same authors later estimated it would take 216 million years for the binding site to acquire two mutations, if the first mutation was neutral in its effect. Facing Facts But six million years is the entire time allotted for the transition from our last common ancestor with chimps to us according to the standard evolutionary timescale. Two hundred and sixteen million years takes us back to the Triassic, when the very first mammals appeared. One or two mutations simply aren’t sufficient to produce the necessary changes— sixteen anatomical features—in the time available. At most, a new binding site might affect the regulation of one or two genes. https://uncommondescent.com/intelligent-design/more-from-ann-gauger-on-why-humans-didnt-happen-the-way-darwin-said/
Further notes:
Collected notes on the severe limits found for the ability of proteins to ‘randomly’ evolve to new functions, for new binding sites, for new domain-domain interactions, and for new ORFan proteins: https://docs.google.com/document/d/11VRNz03ox-vXauBTVonqmRM7amD5CbUWwu6wxr2ABr4/edit
further note: Here is a entire video by Dr. Carter on the 'multi-dimensional' genome:
The Multi-dimensional Genome--impossible for Darwinism to account for-- by Dr Robert Carter - presentation starts approx. 12:00 minute mark - video http://www.youtube.com/watch?v=K3faN5fU6_Y
bornagain77
August 11, 2012
August
08
Aug
11
11
2012
06:43 AM
6
06
43
AM
PDT
There is also this study:
“Dr. Leakey produced a biased reconstruction (of 1470/ Homo Rudolfensis) based on erroneous preconceived expectations of early human appearance that violated principles of craniofacial development,” Dr. Timothy Bromage http://www.geneticarchaeology.com/research/Mans_Earliest_Direct_Ancestors_Looked_More_Apelike_Than_Previously_Believed.asp
bornagain77
August 9, 2012
August
08
Aug
9
09
2012
04:33 PM
4
04
33
PM
PDT

Leave a Reply