Creationism and Human Brain evolution

[mark kennedy]

Genetic recombination also works. Deletion of gene sequences may be loss of information, but perhaps it was the loss of a codon that would code for an amino acid in a protein chain. So if we remove that amino acid and it becomes another substance, possibly a better one, one that may help produce a larger or better brain, that could work. The only implication of "deleterious effect" is removing a gene sequence as related to the production of a protein. But removing or adding an amino acid from a protein chain doesn't say much about whether the protein is beneficial or not. It is the identity of the protein, where it is being used, and the interactions with other substances that is more significant.

Higher recombination can improve fittness by providing more alleles but you are talking about a deletion event. This kind of an indel can be neutral in some cases but the real trick is keeping the reading frame open. Chances it would get out of the transcription check point or be eliminated by genetic drift. The only way of establishing it in the genome is for it to provide a selective advatage. On average the rate would be 3 to 7 nucleotides being established on average for millions of years.

Ever heard of asexual reproduction? All that's required is a single common ancestor. Either it has mutations, or it uses this thing called conjugation, which amounts to sexual reproduction, or more importantly, genetic recombination. Given that we've been around for quite a while, and evolution of primates would have been millions of years ago, it's not difficult to see chaneg in 40 million nucleotides, since we're also considering generations of a reasonable population of primates.

Oh sure, if we are assuming that asexually reproducing organisms can evolve from genomes of thousands of nucleotides to millions suddenly then another 40 million nucleotides is a peice of cake. Going from a simple bacteria to eukaryotes and then later to animalia cells is an enormous leap in the amount of functional genes nessacary. However, I am talking about the differences between us and our supposedly closest living releative.

The precursors of brains is the ganglion. Mutations or genetic recombination resulted in cephalization, the centralizing of a group of ganglion in one region. With natural selection, this would shift the development of the nervous system towards a primitive brain, and eventually, better ones.

Mutations in the genetic recombination will result in lower fittness the vast majority of the time. Then when a beneficial effect is found it is usually as a result of dwindling resources in a small minority of the population. When the populations are introduced to a more suitable environment the mutated stains will lose their advantage and later generations will suffer negative selection. This is how it is directly observed and demonstrated in modern genetics.

 

[mark kennedy]

Well, it is nice to see that Mark can use the PubMed search, or maybe Google Scholar. But what in the world makes you think, Mark, that the genomic sequence of the Chimp is an evolutionary dilemma? From the abstract of the The Chimpanzee Sequencing and Analysis Consortium whoes article you cited:

It is cited and linked in the OP. I also did a thread discussing the paper called 'Chimpanzee Genome completly sequenced' where I had a brief exchange with on of the authors. You can find it here:

http://www.christianforums.com/t2135307-chimpanzee-genome-completly-sequenced.html

 

[AngelusTenebrae]

Higher recombination can improve fittness by providing more alleles but you are talking about a deletion event. This kind of an indel can be neutral in some cases but the real trick is keeping the reading frame open. Chances it would get out of the transcription check point or be eliminated by genetic drift. The only way of establishing it in the genome is for it to provide a selective advatage. On average the rate would be 3 to 7 nucleotides being established on average for millions of years.

I was speaking of the actual proteins they code for, not the actual genes. The genes are only a template from which the proteins are synthesized. If a mutation were benefical, it's like having a sentence with the word, "not" in it, but you mean the opposite. So removing the word "not" would make the sentence function better in terms of meaning.

Oh sure, if we are assuming that asexually reproducing organisms can evolve from genomes of thousands of nucleotides to millions suddenly then another 40 million nucleotides is a peice of cake. Going from a simple bacteria to eukaryotes and then later to animalia cells is an enormous leap in the amount of functional genes nessacary. However, I am talking about the differences between us and our supposedly closest living releative.

Either you meant there was a change in the actual nucleotides, or you meant that 40 million of them were tacked on.

Mutations in the genetic recombination will result in lower fittness the vast majority of the time. Then when a beneficial effect is found it is usually as a result of dwindling resources in a small minority of the population. When the populations are introduced to a more suitable environment the mutated stains will lose their advantage and later generations will suffer negative selection. This is how it is directly observed and demonstrated in modern genetics.

You're giving mutations too much credit. Genetic recombination is a big factor for variation in genes. It doesn't seem like much, and you can't really apply it to humans today because there is virtually no selection. It is why you fail to see genetic recombination doing anything. But breeders and farmers do understand this significance. They selectively breed their animals or plants for desired characteristics.

 

[mark kennedy]

Recombinations are random and they are mutations. Did you mean point mutations?

There is a difference between recombinations during meiosis and things like duplications, transposable elements segmental rearragements and polymorphisms. Recombinations of genes are random during meiosis and higher recombination rates can yeild higher allele rates and generally improve fittness.

The theory of evolution states that all life originated from a single ancestor. Did you miss that part?

No it does not, it is defined as the change of alleles in populations over time.

I'll concede to different origins for eukaryotes and prokaryotes. However, I don't think this is what you are shooting at. Care to give us the objective criteria for determining what does and doesn't belong in the same kind? Are humans and chimps in the Hominidae Kind?

We are classified and in Hominidae but that is largely for organizing classifications. At the simplist level determining common ancestory would be to look at the ability to breed and produce fertile offspring. When looking at differences between the ape and human lineages you would have to look at transposable elements within the functional genes. The only way you would get an objective standard for determining the limits between originally created kinds is to determine the extent to which duplications and polymorphisms can produce a selective advantage.

Why do new world monkeys have nucleotides if they were created separately?

Everything in known biological systems have nucleotides, now you are just being silly.

They were created separately, so why do they share DNA? Birds and bats do not share feathers or nipples, so why say that it makes sense that birds and bats share the same genetic molecule?

I don't know what you are getting at, they share a molecule, so what?

Yes, it's called random mutation.

Actually its called a polymorphism but I guess you aren't interested in the Chimpanzee Genome paper.

Uhh, weren't you the one who said the following:

"The genetic basis is unknown so without a demonstrated or directly observed molecular mechanism you have an a priori assumption."

So not knowing the exact genetic mechanism for brain increases is a problem for evolution but not having any evidence for a supernatural creator is no problem at all? You're joking, right?

At this point we have yet to even discuss the differences between human and chimpanzee brains and the gene sequences involved, which was what the OP was all about. Neither God nor the human soul are objects of scientific investigation but the genetic basis for an unprecedented evolutionary change is.

 

[mark kennedy]

I was speaking of the actual proteins they code for, not the actual genes. The genes are only a template from which the proteins are synthesized. If a mutation were benefical, it's like having a sentence with the word, "not" in it, but you mean the opposite. So removing the word "not" would make the sentence function better in terms of meaning.

I'm known for making typing and grammer errors in my posts, how many of these do you think made better posts. That's why I have an edit button and why cells have cell cycle check points, to edit out mistakes. Take this sentence for instance:

The cat ate the bat not the rat.

Now if you make random changes you will start to get a less comprehensive sentence. This is particularly true if you are randomly inserting a single letter with out rearranging the words, which is the most common way transcript errors make it into the protein coding genes. Bear in mind the amino acids come in groups of three. Care to try a couple of random changes?

edited to add: By the way, I thought you might find this interesting:

"83% of the genes have changed between the human and the chimpanzee—only 17% are identical—so that means that the impression that comes from the 1.2% [sequence] difference is [misleading]. In the case of protein structures, it has a big effect," Sakaki said.

http://www.the-scientist.com/news/20040527/01

Either you meant there was a change in the actual nucleotides, or you meant that 40 million of them were tacked on.

What they did was line up the nucleotide sequences, when there was a break in the sequence it was either a single nucleotide (35 million), if it was 2, 3 or more it was either an insertion or a deletion, thus indels. They were found 5 million indel events, thus the 40 million nucleotide divergance. This included some 3 million bps in the fuctional part of the genome.

You're giving mutations too much credit. Genetic recombination is a big factor for variation in genes. It doesn't seem like much, and you can't really apply it to humans today because there is virtually no selection. It is why you fail to see genetic recombination doing anything. But breeders and farmers do understand this significance. They selectively breed their animals or plants for desired characteristics.

Do you realize that you are the first one to discern the difference between polymorphisms and genetic mutations. The paper I cited and linked in the OP, Initial sequence of the chimpanzee genome and comparison with the human genome, discussed polymorphisms quite a bit. At any rate I don't think that is what you are trying to get at, you are talking about what Darwin called artifical selection. Darwin was thinking about this when he coined the phrase natural selection. It was an unfortunate choice of words since he was talking about the preservation of favored traits. He was comparing artifical selection to changes under nature so that is why he selected the term.

Now, getting to your point. What happens when these plants and animals are breeded for desired traits is genes recombine during meiosis. Certain traits that are recessive (your favorable traits) but when breeded hybrids can have a higher frequency and thus become dominant. The real problem with this is that there is a strong tendancy of the frequency to revert back to the original wild type. Also when these hybrids are breeded for a while they get a genetic bottleneck from inbreeding.

 

[mark kennedy]

There are many unprecedented evolutionary changes. That's kind of what you would expect from a blind process. Why is this one a problem?

This one is unprecedented in it's scope, effect and size. What's more we have the comparative samples right in from of us. Afraid you can't do that with reptile growing feathers and turning into a bird.

Look at the changes seen in dogs. Nothing in nature has ever created such diversity in such a short time.

The divergance between dogs is not that great and it is possible when you take into consideration transposable elements, transcript factors and recombination of genes during meiosis.

Oh, and how did you rule out Leprechauns as another alternative? Flying Spaghetti Monster? Why play God-of-the-Gaps?

Why not explore the only alternative to the single common ancestor model? Seperate lineage.

 

[TeddyKGB]

Why not explore the only alternative to the single common ancestor model? Seperate lineage.

Would that put you on the hook to explain the recurrent laryngeal nerve, appendix, body hair, fingernails, and other assorted oddities that make roughly no sense in the context of a whole-cloth design?

 

[mark kennedy]

Would that put you on the hook to explain the recurrent laryngeal nerve, appendix, body hair, fingernails, and other assorted oddities that make roughly no sense in the context of a whole-cloth design?

The argument and the answer are nothing new.

"laying great stress on the evidential force of imperfection, Haeckel followed Darwin's lead. Throughout his entire corpus, Darwin is never stronger or more bitter in his language than when condemning the failed teleology of theories of creation, which impute imperfect organic design to the direct intent of a rational and benevolent creator."


The Place of Darwinian Theological Themata in Evolutionary Reasoning

 

[Pete Harcoff]

Would that put you on the hook to explain the recurrent laryngeal nerve, appendix, body hair, fingernails, and other assorted oddities that make roughly no sense in the context of a whole-cloth design?

I'm still waiting for a creationist to explain why humans have genes for tails that start to develop, but then another gene causes them to get reabsorbed. Makes no sense from a designer perspective.

 

[mark kennedy]

I'm still waiting for a creationist to explain why humans have genes for tails that start to develop, but then another gene causes them to get reabsorbed. Makes no sense from a designer perspective.

That's not a tail and the OP was at the other end of human anatomy but I'll bite. What gene causes the human tail (rudimentary organ argument?) to emerge?

 

[Pete Harcoff]

That's not a tail and the OP was at the other end of human anatomy but I'll bite. What gene causes the human tail (rudimentary organ argument?) to emerge?

Apparently it's the Wnt-3a and Cdx1 genes. From the 29+ evidences for macroevolution FAQ:

In fact, the genes that control the development of tails in mice and other vertebrates have been identified (the Wnt-3a and Cdx1 genes; Greco et al. 1996; Prinos et al. 2001; Schubert et al. 2001; Shum et al. 1999; Takada et al. 1994). As predicted by common descent from the atavistic evidence, these tail genes have also been discovered in the human genome (Katoh 2002; Roelink et al. 1993). As discussed below in detail, the development of the normal human tail in the early embryo has been investigated extensively, and apoptosis (programmed cell death) plays a significant role in removing the tail of a human embryo after it has formed. It is now known that down-regulation of the Wnt-3a gene induces apoptosis of tail cells during mouse development (Greco et al. 1996; Shum et al. 1999; Takada et al. 1994), and similar effects are observed in humans (Chan et al. 2002). Additionally, researchers have identified a mutant mouse that does not develop a tail, and this phenotype is due to a regulatory mutation that decreases the Wnt-3a gene dosage (Greco et al. 1996; Gruneberg and Wickramaratne 1974; Heston 1951). Thus, current evidence indicates that the genetic cause of tail loss in the evolution of apes was likely a simple regulatory mutation(s) that slightly decreased Wnt-3a gene dosage. Conversely, a mutation or environmental factor that increased dosage of the Wnt-3a gene would reduce apoptosis of the human tail during development and would result in its retention, as an atavism, in a newborn.

I've never seen a creationist account for these. The only thing they attack are the human pseudotails (which are fatty bits). But the T.O. page has an example of a tail with vertebrate and all (and links to more). I've never seen true human tails explained.

 

[TeddyKGB]

The argument and the answer are nothing new.

"laying great stress on the evidential force of imperfection, Haeckel followed Darwin's lead. Throughout his entire corpus, Darwin is never stronger or more bitter in his language than when condemning the failed teleology of theories of creation, which impute imperfect organic design to the direct intent of a rational and benevolent creator."


The Place of Darwinian Theological Themata in Evolutionary Reasoning

Ah, the three bastions of creationist rhetoric.

The "we shamelessly pick and choose which bits to seize upon"...

1. Blind cave fish and flightless birds are examples of genetic degeneration, which creationism is only too happy to countenance.

The "everyone just pretend you didn't hear the words 'recurrent laryngeal nerve'"...

2. How do we know what a flawed design is if we can not comprehend perfect design (and we can not, apparently, because we are not God)?

And the truly bizarre...

Consider, for instance, the question of the creator's proper domain. Many philosophers and theologians take the creator's proper domain to be the entirety of time and space, and furthermore hold that issues of moral value figure ultimately in any theory of creation. If this is so then the finitude of human scientific observation may lead us to infer mistakenly that an organic design (e.g., the panda's pseudothumb) is imperfect, when its imperfection is only apparent, that is, local. On this view, any judgment of perfection or imperfection must be qualified with a proviso that perfection -- defined as divinely created perfection -- can be judged only on the scale of the whole creation. And there is no reason for a creator to optimize one part of the universe at the expense of the whole.

That's right, folks. Believe it or not, the universe would be less perfect if the panda had a true thumb.

Some stuff you just can not make up.

 

[mark kennedy]

Apparently it's the Wnt-3a and Cdx1 genes. From the 29+ evidences for macroevolution FAQ:


I've never seen a creationist account for these. The only thing they attack are the human pseudotails (which are fatty bits). But the T.O. page has an example of a tail with vertebrate and all (and links to more). I've never seen true human tails explained.

I have yet to see the connection between the Wnt-3a and Cdx1 genes and the dorsal cutaneous appendage. Now when you find me the scientific literature that connects the two we can look at the genetic basis for human tails.

STUDY DESIGN: Observational case report. OBJECTIVES: To report a case of dorsal cutaneous appendage or the so-called human tail that was the cause of tethered cord syndrome. SUMMARY OF BACKGROUND DATA: The dorsal cutaneous appendage, or so-called human tail, is often considered to be a cutaneous marker of underlying occult spinal dysraphism. In such cases, there is usually a separate underlying tethering lesion. There have been only three case reports in the literature where this appendage itself was the tethering lesion. The fourth such case is being reported. METHODS: An 11-month-old male child was brought for consultation for a "tail-like" structure in the low back since birth. Examination revealed a subtle thinning of the right lower extremity and a caudal appendage in the lower lumbar region. Plain radiographs revealed spina bifida at S1. MRI revealed a transitional lipoma at L5-S1 with a terminal syrinx. RESULTS: During surgery, a fibrous tract was seen extending from the base of the appendage through the defect in the bone and dura. The tract ended in the transitional lipoma of the cord at L5-S1. Sectioning of the tract and debulking of the transitional lipoma was done. After surgery, there was no change in the neurologic status of the patient. CONCLUSIONS: This case illustrates that the so-called "human tail" or the dorsal cutaneous appendage is not just a marker of underlying occult spinal dysraphism. In rare cases, the appendage itself can be the tethering lesion. In every case of dorsal cutaneous appendage, the surgeon should diligently search for the intraspinal extension of the lesion even if such an extension is not revealed by the MRI.

So-called human tail

 

[TeddyKGB]

I have yet to see the connection between the Wnt-3a and Cdx1 genes and the dorsal cutaneous appendage. Now when you find me the scientific literature that connects the two we can look at the genetic basis for human tails.

Does this mean you have read all the additional links on the page Harcoff referred you to?

 

[Dr.GH]

The argument and the answer are nothing new.

The argument need not be 'new' if it is correct and 'old.'

There are many regions of non-transcribed DNA in the hominid genome. Some thousands of segments bare the unmistakable characteristics of remnants of retroviral insertions. There are recently discovered "retrogenes" which are transcribed but are still non-functional as the gene product is promptly reabsourbed. Those too are largely results of endogenous retroviral insertions.

The more interesting are the totally non-functional, non-transcribed segments. These, lacking any positive selection pressure, and merely a trivial negitive selection presure are totally free to vary according to streight forward stochastic processes. These are the DNA mutations due to random irradiation, random oxidative alteration of base pairs, random copy errors during mitosis.

Comparisons of the shared endogenous retroviral fragments between the apes categorically demonstrate our shared heritage. It is either ignorance of the facts or willful ignorance of the facts to deny this.

Readily availble articles on these sequence data are below.

Fig. 2. Phylogenies of seven HERV loci. Maximum parsimony (MP) trees are shown for each locus. Neighbor-joining (NJ) and maximum likelihood (ML) analyses yielded essentially identical results (data not shown). Insertions and deletions were weighted equal to 1 substitution. Tree searches were performed by using the branch-and-bound option [HERV-K(HML6.17), RTVL-Ia, and RTVL-H] or the exhaustive search option [HERV-K18 and HERV-K(C4)]. Final trees were rooted by designating outgroup sequences. Numbers indicate bootstrap values for major nodes (n = 100). AGM, African green monkey. (A) HERV-K(HML6.17) One of three minimum MP trees of length (L) = 258 aligned HERV-K(HML6.17) sequences. Outgroup LTRs are from a provirus related to HERV-K(HML6.17) found in human BAC110P12 (bases 115, 102 to 122, and 217; accession no. U95626) by [size=-1]BLAST[/size] homology search. (B) Single most-parsimonious tree for the HERV-K18 locus (L = 128). The published HERV-K10 LTR sequences were used as an outgroup (31). (C) Single most-parsimonious tree (L = 199) for the HERV-K(C4) sequences. Two HERV-K(C4)-related solo LTRs were included as outgroups. (D) One of eight equally parsimonious trees (L = 393) for the RTVL-Ia locus. Dashed lines indicate the unexpected placement of the gibbon 5' LTR branch. The outgroup contains RTVL-Ib LTR sequences (14). (E) One of four equally parsimonious trees (L = 372) for the RTVL-Ia locus after excluding the gibbon 5' LTR. (F) One of seven equally parsimonious trees (L = 145) for RTVL-Ha. (G) One of two equally parsimonious trees (L = 126) for RTVL-Hb. The 5' LTR from bonobo was not amplified. (H) One of seven equally parsimonious trees containing both the RTVL-Ha and RTVL-Hb loci (L = 200). Published RTVL-H and RTVL-H2 LTRs were designated as outgroups for rooting the final trees in F, G, and H (36, 37).

I strongly recommend Constructing primate phylogenies from ancient retrovirus sequences which is the source for the figure above.

This is from an an article by Heui-Soo Kim, Osamu Takenaka and Timothy J. Crow "Isolation and phylogeny of endogenous retrovirus sequences belonging to the HERV-W family in primates." "The branching times of the phylogeny should be considered as approximate, and the tree was modified from Steinhuber et al. (1995) , Anderssen et al. (1997) and Medstrand & Mager (1998)." Takenaka et al 1999, focus intently on a single shared retrovirus family to derive a sequence and approximate age for the insertion events. Personally, I think that their data are in better accord with the known fossil data than those genetic reconstructions suggesting a much older branching of the chimp and human lineages.

 

[mark kennedy]

Does this mean you have read all the additional links on the page Harcoff referred you to?

The ones that provided a link are what I looked at but I can go back and take a closer look.

Edited to add: Ok the citations in the debate were a dead end as usual. The so-called human tail is an abnormality the resembles a tail, nothing more.

 

[mark kennedy]

The argument need not be 'new' if it is correct and 'old.'

There are many regions of non-transcribed DNA in the hominid genome. Some thousands of segments bare the unmistakable characteristics of remnants of retroviral insertions. There are recently discovered "retrogenes" which are transcribed but are still non-functional as the gene product is promptly reabsourbed. Those too are largely results of endogenous retroviral insertions...ad infinitum ad nauseum

"Endogenous retroviruses. Endogenous retroviruses (ERVs) have become all but extinct in the human lineage, with only a single retrovirus (human endogenous retrovirus K (HERV-K)) still active24. HERV-K was found to be active in both lineages, with at least 73 human-specific insertions (7 full length and 66 solo long terminal repeats (LTRs)) and at least 45 chimpanzee-specific insertions (1 full length and 44 solo LTRs). A few other ERV classes persisted in the human genome beyond the human−chimpanzee split, leaving 9 human-specific insertions (all solo LTRs, including five HERV9 elements) before dying out."

Initial sequence of the chimpanzee genome and comparison with the human genome

There is only one active retrovirus in the human genome, which translated means all the others mark major divergance in the respective genomes.

 

[TeddyKGB]

Ok the citations in the debate were a dead end as usual. The so-called human tail is an abnormality the resembles a tail, nothing more.

Well, I guess that settles that. It seems real science does not stand a chance when you have an internet connection and 15 minutes to spare.

 

[Pete Harcoff]

Edited to add: Ok the citations in the debate were a dead end as usual. The so-called human tail is an abnormality the resembles a tail, nothing more.

Considering I doubt you actually took the time and resources to actually look up the citations, I find your conclusion a little underwelming.

I also find it odd that you'd call a protrusion from the base of the lower back complete with vertebrae something that just "resembles a tail". Exactly what do you think a tail is?

 

[Dr.GH]

There is only one active retrovirus in the human genome, which translated means all the others mark major divergance in the respective genomes.

I would like to read that reference please. And what is the problem of major diverance to evolutionary theory? OH MY WHATEVER is that creato "macroevolution?" That is certainly one favored form of speciation. There is even some speculation that retroviral inserts provide some input for "major divergance" in the form of non-essential DNA sequences. (I personally think that this is unnecessary, even if possible).