Genetics and Genesis

sfs · Apr 11, 2007

lucaspa said:
I think you misread the article. Going back to the original journal, the ASPM gene was evolving in the period 2 million years agoto 200,000 years ago. Not 5800 years ago.

Wrong original paper. The post was referring to Mekel-Bobrov et al (Science 309:1720-2), which claims evidence for ongoing selection at ASPM. I think the paper is wrong, but that is what it says.

gluadys · Apr 11, 2007

mark kennedy said:
I'm going to stray a little but I want to make this as clear as I can. I have no problem with the Canadian Black Bear and the Arctic Polar Bear having a common ancestor, I don't think any Creationist would. They live in fairly close proximity to one another but one is black and the other white.

Just think about it for a minute, does their common ancestor really have time for the accumulation of missense mutations to start having a beneficial effect? For one thing the deleterious effects will manifest and there will be a restriction of gene flow from a bottleneck in order for them to be fixed.

This last paragraph, especially the last sentence, makes no sense at all. Could you please clarify a few things?

What do you mean when you ask if their common ancestor has time for mutations to accumulate to a beneficial effect?

It almost sounds as if you thought of the common ancestor as a single bear with only one lifetime in which to accumulate mutations. (Though, of course, most mutations accumulated during its lifetime would be somatic and not inheritable anyway.)

I am sure you realize the common ancestor was a population, not an individual. And that this population existed over many generations. So then, you say, the deleterious effects would manifest. Now it sounds as if you think the deleterious effects would manifest in every individual in the population. Why would that happen? Even if a deleterious effect did manifest in every member of the population, would it be the same deleterious effect, or would there be different deleterious effects in different individuals. Surely it would likely be different effects in different individuals.

Finally, since you seem to agree that natural selection does purge deleterious mutations from populations, even though you don't have much confidence in positive selection, on what basis would deleterious effects accumulate? Obviously, some individuals might inherit two or three alleles that produce deleterious effects, but will they then successfully pass on these genes to another generation? And won't independent assortment even then split them up so that they are separated in their offspring? But what would force the accumulation of deleterious effects in all members of the population? In fact, will not purging selection maintain a population that is mostly free of deleterious mutations, rather than permitting an accumulation of them? The only mutations that will accumulate are those that are not subject to purging selection, i.e. mostly neutral mutations.

Finally, can you define the terms "gene flow" and "bottleneck" as you are using them here, because the don't fit any definition I know of these terms. Using the definitions I know, the sentence is pure gobbledygook.

shernren · Apr 12, 2007

mark kennedy said:
A directly observed or demonstrated molecular mechanism capable of altering the amino acid sequence in a highly conserved gene involved in the development of the human brain. With a beneficial effect of course.

There are twelve possible single base substitutions:

A -> T
A -> C
A -> G
T -> A
T -> C
T -> G
C -> T
C -> A
C -> G
G -> A
G -> T
G -> C

Which of these do you want to know the chemical mechanism for?

All these chemical mechanisms are capable of altering a highly conserved gene.

It is also quite easy to show that they are beneficial. Show me the sequence of the chimpanzee ASPM gene, and show me the sequence of the human ASPM gene. Now, the right set of the molecular mechanisms above will change the chimpanzee gene into the human gene, which will be by your standards a beneficial change.

So, do you accept that the ASPM gene is under positive selection?

mark kennedy · Apr 13, 2007

lucaspa said:
I think you misread the article. Going back to the original journal, the ASPM gene was evolving in the period 2 million years ago to 200,000 years ago. Not 5800 years ago.

The scenario is it stated 5-7 mya, accumulated neutral effects until about 2.5 million years ago when it sprang into effect.

"The size of human brain tripled over a period of

2 million years (MY) that ended 0.20.4 MY ago. This evolutionary expansion is believed to be important to the emergence of human language and other high-order cognitive functions, yet its genetic basis remains unknown. An evolutionary analysis of genes controlling brain development may shed light on it. ASPM (abnormal spindle-like microcephaly associated) is one of such genes, as nonsense mutations lead to primary microcephaly, a human disease characterized by a 70% reduction in brain size. Here I provide evidence suggesting that human ASPM went through an episode of accelerated sequence evolution by positive Darwinian selection after the split of humans and chimpanzees but before the separation of modern non-Africans from Africans. Because positive selection acts on a gene only when the gene function is altered and the organismal fitness is increased, my results suggest that adaptive functional modifications occurred in human ASPM and that it may be a major genetic component underlying the evolution of the human brain. " http://www.genetics.org/cgi/content/abstract/165/4/2063

Did you really read that? A gene characterized by a microcephaly (literally small brain) is evidence that Darwinian evolution accumulated mutations for millions of years before they took effect and triples the size of the brain. That despite the fact they have no idea what the molecular mechanism is.

But there are cities built in Asia that are twice as old!
3. WG Solheim II, An earlier agricultural revolution. Scientific American, April 1972 in Scientific American, The Origins of Technology.

Based on what exactly?

This is one of the more popular Talmudic interpretations. Adam and Eve were not the first people, but the first JEWISH people.

That is absurd, the Jewish line started with Abraham not Adam. The term Jew did not even emerge until sometime after Dispersion. I don't know where you are getting your information but you should really try to stick to science.

Ah, but if you look, those "sons of God" were not mortal. Remember, in Genesis 5 God has to limit the lifespans of the offspring of matings between human women and the "sons of God", because those offspring were apparently immortal.

You would seem to be making a random assertion about the Nephilim.

From the Strong's:

גּבּר גּבּור
gibbôr gibbôr
ghib-bore', ghib-bore'
Intensive from the same as H1397; powerful; by implication warrior, tyrant: - champion, chief, X excel, giant, man, mighty (man, one), strong (man), valiant man.

You might consider studying the Holy Bible a little before making these strange speculations about what it means. Nephilim as it is sometimes translated means mighty, it is translated this way 136 times. They were violent, that is what the word is actually communicating and there is nothing indicating that they were immortal.

Deamiter · Apr 13, 2007

mark kennedy said:
Did you really read that? A gene characterized by a microcephaly (literally small brain) is evidence that Darwinian evolution accumulated mutations for millions of years before they took effect and triples the size of the brain. That despite the fact they have no idea what the molecular mechanism is.

A few corrections -- first of all, the gene characterized by microcephaly is not evidence of Darwinian evolution, the differences between the gene in humans and the gene in other apes strongly suggest positive selection. Further, it's interesting that you keep saying they have no idea what the "molecular mechanism" is, but they know very well what mechanisms cause mutations. The quote does not say that the genetic basis for ASPM genes is unknown -- it's saying that we do not fully understand what differences between us and chimps allow higher cognative functions. ASPM is certainly a good candidate as part of the evolution of the human brain, but we know enough about genetics to be certain that it's not the only gene affecting brain size, nor is brain size it's only function!

This really says nothing against evolution as creationists have no more idea what the genetic basis for higher cognative functions is than evolutionary scientists! The key here is that it's not saying, "we have no idea where these mutations came from" it's saying "We don't know exactly what caused the increase in cognative ability, but this ASPM gene is a good candidate for the following reasons."

It's particularly interesting that you keep skipping over the many mutations that are not deleterious by claiming that none can be positive... when we only have enough data to have identified 32 and only 2 weren't studied precisely because they had caused microcephaly! It's similar to saying, "you can't show me which gene mutated to cause fingernails, therefore they couldn't have evolved" when the only reason nobody can identify the gene is that sequencing is still extremely expensive.

mark kennedy · Apr 13, 2007

lucaspa said:
Not always. And, in fact, not even very often. Very few mutations are out and out deleterious.

Even fewer are adaptive.

Among the mutations that affect a typical gene, different kinds produce different impacts. A very few are at least momentarily adaptive on an evolutionary scale. Many are deleterious. Some are neutral, that is, they produce no effect strong enough to permit selection for or against; a mutation that is deleterious or advantageous in a large population may be neutral in a small population, where random drift outweighs selection coefficients. The impact of mutation is quite different in different DNA sequences. It is maximal in a conventional gene or exon, and at least transitorily less in a gene whose function is required rarely or is redundant. If adaptive mutations are rare, as seems to be the case, then rates of DNA sequence evolution are driven mainly by mutation and random drift, as KIMURA 1983A has argued. In this case, the proportion of neutral mutations at a site or locus is the ratio of its rate of evolution to that of a region that can be considered neutral, such as a pseudogene. Most newly arisen mutations in functional genes are deleterious, but the fraction may approach zero for spacer DNAs such as introns and intergenic regions. Of course, some protein evolution certainly results from favorable mutations, and to this extent the neutral fraction is overestimated. (Rates of Spontaneous Mutation, Drake et al, Genetics, Vol. 148, 1667-1686, April 1998)

What you focus on only is cases of purifying selection. Once an allele is such that it is at maximal fitness, then of course any change in it is going to decrease fitness. But remember, the allele didn't start out that way. It started out at lesser fitness and then mutated to what we see now.

That will never work, they have to accumulate with neutral effect for millions of years.

Not even most times. Most mutations are silent. They change the 3rd codon, which is usually redundant, and give the exact same protein when translated to amino acids.

Other mutations are conservative. They may change the amino acid, but the new one has very similar chemical properties to the old one and the protein folding does not change. For instance, change leucine to isoleucine and the protein doesn't change in its 3-D structure.

Notice I am not now nor have I ever argued anything to the contrary.

Yes. Limb development. After all, the arrangement of a humerous, radius and ulna, 5 wrist bones, and carpals are highly conserved across all vertebrate lineages.

Skeleton structures are more conserved then a gene involved in the regulation of mitotic spindle orientation in proliferating cells of the neuroepithelium? I'll tell you what, we will get back to that one.

http://www.hhmi.org/news/lahn.html
"For each species, the researchers identified changes in the ASPM gene that altered the structure of the resulting protein, as well as those that did not affect protein structure. Only those genetic changes that alter protein structure are likely to be subject to evolutionary pressure, Lahn said. Changes in the gene that do not alter the protein indicate the overall mutation rate - the background of random mutations from which evolutionary changes arise. Thus, the ratio of the two types of changes gives a measure of the evolution of the gene under the pressure of natural selection."

The measure of natural selection is a ratio and the jump from ape to human was a dramatic one with no known molecular mechanism to account for it.

Figure 3 Hum. Mol. Genet. -- Evans et al.

From the original paper by Lahn and colleagues in Science:

"Phylogenetic analysis of ASPM has revealed strong positive selection in the primate lineage leading to Homo sapiens (3–5), especially in the past 6 million years of hominid evolution in which ASPM acquired about one advantageous amino acid change every 350,000 years (4). "

This test also reveals that, on average, ASPM fixed one advantageous amino acid change in every 300 000–400 000 years since the human lineage diverged from chimpanzees some 5–6 million years ago. (Adaptive Evolution of ASPM a Major Deteriminant of a Cerebral Cortex, Human Molecular Genetics 2004)

Want to know the really interesting part, for at least half that time these accumulated mutations had no effect on the size of the brain.

Because the brain size of a typical microcephaly patient is comparable with those of early hominids such as the 2.3- to 3.0-MY-old Australopithecus africanus (430 g) I hypothesize that ASPM may be one of the genetic components underlying the human brain expansion. (Evolution of the Human ASPM Gene, a Major Determinant of Brain Size, Genetics 2003)

I thought positive selection was when there was an advantage so it was preserved. This scenario seems to think that neutral mutations accumulated steadily for millions of years and our ancestors still had a little head. Then from 2.5 mya to 1.9 mya it literally doubles in size.

You can look at the papers referenced for the specific advantageous amino acid changes.

You can't find a molecular mechanism or a dimes worth of proof it's possible but you can sure find the assumption made throughout.

"The unusually high frequency of haplotype 63 is strongly suggestive of positive selection (8). We tested the statistical significance of the possibility of positive selection using coalescent modeling (7). The frequency of haplotype 63 is notably higher in Europeans and Middle Easterners (including Iberians, Basques, Russians, North Africans, Middle Easterners, and South Asians), as compared with other populations (table S1). We therefore focused on this group to take advantage of its relatively simple and homogeneous demographic structure (9). Because 7 of the 50 Europeans and Middle Easterners were homozygous for haplotype 63, we tested the probability of obtaining 7 or more homozygotes (among 50) for a single haplotype across a 62.1-kb region containing 122 segregating sites (the number of polymorphic sites found in Europeans and Middle Easterners). ... These parameters produced a highly significant departure from the neutral expectation (P < 0.00001). "

Not genetic drift, but positive selection.

Positive selection of neutral effects from random mutations that only cause sever reduction in brain size and fitness produced this dramatic adaptive giant leap.

Figure 1. Phylogeny of ASPM in primates. The great ape lineages are highlighted in red, and the ape lineages leading to humans in bold. The Ka/Ks ratios of individual segments of the phylogenetic tree are indicated.
Hum. Mol. Genet. -- Evans et al.

No. That's a false premise. Humans and chimps differ by less than 2% of their amino acid sequences in expressed genes. Since there have been 7 million years since the split and we take a generation time of 20 years, that works out to 350,000 generations. In one experiment with fruit flies, a different species was produced by natural selection after only 5 years or 2500 generations. This species differed from the original by over 3% in expressed genes. There have been over 100 times the number of generations between us and the apes. Plenty of time.

No, false assumption. The advantages did not express themselves for millions of years so they had no reason to accumulate.

19% of the total 1019 indels are of sizes that are multiples of three nucleotides. A simulation was then performed for 20,000 replications with the inferred ASPM coding sequence of the common ancestor of humans and chimpanzees. Under no functional constraints, the substitution rate is identical to the mutation rate and mutations are assumed to be random. An ORF is interrupted when an indel of a size that is not a multiple of three nucleotides or a nonsense point mutation occurs...Human ASPM has 28 coding exons, spanning 62 kb in chromosome 1p31 and encoding a huge protein of 3477 amino acids.... A gene may occasionally exhibit dN/dS > 1 when a large fraction of nonsynonymous mutations are advantageous and are driven to fixation by positive selection. I estimated the dN/dS ratio for ASPM in each of the three tree branches (Fig 2), using a maximum-likelihood method, and found that dN/dS is lowest in the orangutan branch (0.43), higher in the chimpanzee branch (0.66), and highest in the human branch (1.03). (Evolution of the Human ASPM Gene, a Major Determinant of Brain Size, Genetics 2003)

Positive selection is inferred despite the fact that the gene is currently under strong purifying selection, the only known effects of mutations in this gene are neutral or deleterious and there is no known molecular mechanism for producing them.

That's a false "if". See the references to the Science article.

Here, I'll list them:

3. J. Zhang, Genetics 165, 2063 (2003).[Abstract/Free Full Text]
4. P. D. Evans et al., Hum. Mol. Genet. 13, 489 (2004).[Abstract/Free Full Text]
5. N. Kouprina et al., PLoS Biol. 2, E126 (2004). [CrossRef] [Medline]
6. S. L. Gilbert, W. B. Dobyns, B. T. Lahn, Nat. Rev. Genet. 6, 581 (2005). [CrossRef] [ISI] [Medline]

I've read them, more then once.

OK, here are some:
{snip the cut and pace PubMed search results}

Don't you think I have tried that, for hours at a time before asking an evolutionist? You haven't changed a bit but nice to see you again just the same.

Xaero · Apr 13, 2007

Mark, did you really read post No.40 from sfs and No. 43 from shernren?

Mark Kennedy said:
Did you really read that? A gene characterized by a microcephaly (literally small brain) is evidence that Darwinian evolution accumulated mutations for millions of years ...

Through bad mutations geneticists can discover the functions of certain genes for the first time, thats why bad mutations are detected easier - they cause a
conspicuous malforming of an organ. Small beneficial steps are harder to detect in our lifetime.
But like Deamiter said, it isn't the only gene coding for the brain, there are others and they are still under positive selection today. (A Map of Recent Positive Selection in the Human Genome)

... before they took effect and triples the size of the brain.

Because of the benefit of social behavior (and therefore the need for a complex brain) + a better diet, the brainsize could finally start to get real big . (Molecular Insights into Human Brain Evolution)

sfs said:
I'll just note that you have once again failed to respond to my challenge: what is your alternative explanation for the tree we see in nonfunctional differences between species?

Earlier i posted a thread about LINE-1 (mostly inactive transposable elements) which shows that the common accepted clade of mammalian relationships is correct:
http://www.christianforums.com/t489...t-phylogenetic-tree-of-placental-mammals.html. Genetics totally supports Evolution.

sfs said:
Molecular mechanisms for adaptive change that don't involve missense mutations are well known: mutations to regulatory regions.

As a recent paper states: (Rate of Evolution in Brain-Expressed Genes in Humans and Other Primates) genes coding for protein sequences have been under slowed down evolution while more changes happened in regulatory genes.

shernren said:
Which of these do you want to know the chemical mechanism for?

Many molecular mechanisms of mutations are well known. For example i mentioned the C->T deamination on methylated CpG sites. Also T->A mutation could happen during replication because of the abundance of ATP inside cells. Others are depurination or tautomerism. (http://en.wikipedia.org/wiki/Mutations#Causes_of_mutation)

Deamiter · Apr 14, 2007

Mark, could you quickly explain what you mean by "molecular mechanism" or "genetic mechanism?" Are you using these terms interchangably? Can you give an example of what this mechanism might look like?

It confuses me because sometimes you seem to suggest that scientists don't know the mechanism for mutations, and other times it seems that you're saying they don't know which mutations caused a particular trait. In literature, I usually see "we don't know the genetic mechanism" when they're saying they don't have a complete understanding of how every gene works to affect every trait -- not that they have absolutely no clue what some of the genes do and what some traits are controlled by. In short, you seem to be using it to say scientists have no idea, whereas scientists usually use it to say their understanding is preliminary.

I'm just curious because you seem to use it as a catch-all to say that scientists don't have a clue. It'd be nice to know precisely in what way you are using the phrase so we can all understand exactly what you are claiming scientists don't know since you seem to use the term somewhat differently than I've seen in journals.

mark kennedy · Apr 14, 2007

Deamiter said:
Mark, could you quickly explain what you mean by "molecular mechanism" or "genetic mechanism?" Are you using these terms interchangably? Can you give an example of what this mechanism might look like?

I can show you what one looks like but it's hard for me to explain what they are and how they work. I'm still trying to piece it together and many, if not most of these debates make it even harder since you end up fielding arguments that are irrelevant.

Project description:

The chloroplasts of higher plants perform oxygenic photosynthesis resulting in the transfer of light energy into chemical form, which is the basis of heterotrophic life on Earth. Photosynthesis may be dived into two sets of reactions: light reactions taking place in the thylakoid membranes, and carbon fixation reactions in soluble stroma. To ensure immaculate primary production under a wide spectrum of environmental conditions, the structure and function of photosynthetic machinery must be extremely dynamic. The molecular mechanisms behind these dynamic changes remain largely uncharacterised, although detailed knowledge of these reactions is of utmost importance for understanding the adaptation on organism level. The aim of our study is to resolve molecular adaptation mechanisms of the photosynthetic machinery and to reveal how the information about the prevailing physiological state in the chloroplast is mediated to the nucleus (retrograde signalling). Retrograde signalling mechanisms and adaptation of the photosynthetic machinery to environmental cues

Principal investigator:
Paula Mulo, Ph.D.

I turned a corner at some point and now I'm primarily interested in known molecular mechanisms for adaptation as opposed to the ones the logically follow Darwinian and naturalistic assumptions.

It confuses me because sometimes you seem to suggest that scientists don't know the mechanism for mutations, and other times it seems that you're saying they don't know which mutations caused a particular trait. In literature, I usually see "we don't know the genetic mechanism" when they're saying they don't have a complete understanding of how every gene works to affect every trait -- not that they have absolutely no clue what some of the genes do and what some traits are controlled by. In short, you seem to be using it to say scientists have no idea, whereas scientists usually use it to say their understanding is preliminary.

I don't know how much a transcript error, deletion, insertion, point mutation or rearrangement can help adapt organisms over time. It's difficult for me to track down but I get the impression that I have stumbled into a very complicated world of exploration.

I'm just curious because you seem to use it as a catch-all to say that scientists don't have a clue. It'd be nice to know precisely in what way you are using the phrase so we can all understand exactly what you are claiming scientists don't know since you seem to use the term somewhat differently than I've seen in journals.

The researchers looking into the molecular mechanisms for the evolution of the brain are at a lost to explain how the human brain tripled in size except to say that it was an extraordinary leap in adaptive evolution. The comparisons I keep bringing up are leading me to conclude that they have no explanation for how the human brain evolved from that of apes.

I want to look more closely at adaptations at a molecular level before I make any sweeping statements about them. Not just because of the criticism I will no doubt draw in these debates but because practice does not make perfect, it makes permenant. I do think that there are variables in the amino acid sequences but I'm still trying to figure out what they are and what controls them.

Hope that clears up some of the confusion.

Grace and peace,
Mark

Deamiter · Apr 14, 2007

The researchers looking into the molecular mechanisms for the evolution of the brain are at a lost to explain how the human brain tripled in size except to say that it was an extraordinary leap in adaptive evolution. The comparisons I keep bringing up are leading me to conclude that they have no explanation for how the human brain evolved from that of apes.

Are you honestly suggesting that because scientists do not yet know which mutations caused which morphological changes, the known mechanisms by which mutations happen cannot explain the morphological changes?

The molecular mechanism for mutations are known and these can account for evolutionary adaptations. It seems like you take the acknowledgement that we do not understand the effects of each and every section of DNA to mean that scientists do not understand how changes to the DNA can accumulate.

Or are you claiming that there are specific differences between humans and other apes that cannot be explained by known mechanisms that cause mutations?

shernren · Apr 15, 2007

mark kennedy said:
I turned a corner at some point and now I'm primarily interested in known molecular mechanisms for adaptation as opposed to the ones the logically follow Darwinian and naturalistic assumptions.

So you're essentially becoming a Lamarckian.

mark kennedy said:
I don't know how much a transcript error, deletion, insertion, point mutation or rearrangement can help adapt organisms over time. It's difficult for me to track down but I get the impression that I have stumbled into a very complicated world of exploration.

Firstly, "transcript errors" have nothing to do with mutations. It's high time you get your terminology and conceptual understanding correct. Secondly, are you simply trying to say there are no such things as beneficial mutations?

mark kennedy said:
The researchers looking into the molecular mechanisms for the evolution of the brain are at a lost to explain how the human brain tripled in size except to say that it was an extraordinary leap in adaptive evolution. The comparisons I keep bringing up are leading me to conclude that they have no explanation for how the human brain evolved from that of apes.

But "an extraordinary leap in adaptive evolution" is the explanation for how the human brain evolved from that of apes, unless you have any good evidence to show that adaptive evolution cannot occur.

mark kennedy · Apr 15, 2007

shernren said:
So you're essentially becoming a Lamarckian.

No shernren, I'm a Mendelian.

Firstly, "transcript errors" have nothing to do with mutations.

In biology, mutations are changes to the base pair sequence of genetic material (either DNA or RNA). Mutations can be caused by copying errors in the genetic material during cell division and by exposure to ultraviolet or ionizing radiation, chemical mutagens, or viruses, or can occur deliberately under cellular control during processes such as meiosis or hypermutation.

Mutation, Wilipedia

In the living cell, DNA undergoes frequent chemical change, especially when it is being replicated (in S phase of the eukaryotic cell cycle). Most of these changes are quickly repaired. Those that are not result in a mutation. Thus, mutation is a failure of DNA repair.

Kimbal Biology Pages

It's high time you get your terminology and conceptual understanding correct.

Unbelievable....

Secondly, are you simply trying to say there are no such things as beneficial mutations?

No, what I have been saying for better then a year:

Among the mutations that affect a typical gene, different kinds produce different impacts. A very few are at least momentarily adaptive on an evolutionary scale. Many are deleterious. (Rates of Spontaneous Mutation, John W. Drake et al. Genetics Vol. 148, 1667-1686, April 1998)

Are you saying that random mutations are the mechanism that evolved the human brain from the size, density and complexity of an apes?

But "an extraordinary leap in adaptive evolution" is the explanation for how the human brain evolved from that of apes, unless you have any good evidence to show that adaptive evolution cannot occur.

That's not how it works, if there is no directly observed or demonstrated mechanism that it repeatable, then it's not science, it's supposition. Even an a priori assumption is permissible but it has to make predictions. Guess what a mutation effecting a neural gene like the ASPM does every time it is expressed in the phenotype?

Just let me know when your ready for a formal debate.

shernren · Apr 15, 2007

mark kennedy said:
In biology, mutations are changes to the base pair sequence of genetic material (either DNA or RNA). Mutations can be caused by copying errors in the genetic material during cell division and by exposure to ultraviolet or ionizing radiation, chemical mutagens, or viruses, or can occur deliberately under cellular control during processes such as meiosis or hypermutation.
Mutation, Wilipedia

In the living cell, DNA undergoes frequent chemical change, especially when it is being replicated (in S phase of the eukaryotic cell cycle). Most of these changes are quickly repaired. Those that are not result in a mutation. Thus, mutation is a failure of DNA repair.
Kimbal Biology Pages

(emphasis added) Now pray tell, precisely what is "transcription"? You are not using standard definitions of biological terms, and thus it's about as easy to talk to you about biology as it is to talk about theology with someone who thinks that the Trinity is a character from The Matrix.

mark kennedy said:
Are you saying that random mutations are the mechanism that evolved the human brain from the size, density and complexity of an apes?

Why not? If you want to disprove it, it's as simple as:

1. show that it is chemically impossible for the common ancestor's ASPM gene to undergo mutations that transform it into the Homo sapien ASPM gene.

2. show that even if those mutations are chemically possible, it is then biologically impossible for such a mutation to spread through the Homo sapien population.

Those are very simple ways to prove that you are correct.

Deamiter · Apr 15, 2007

mark kennedy said:
That's not how it works, if there is no directly observed or demonstrated mechanism that it repeatable, then it's not science, it's supposition. Even an a priori assumption is permissible but it has to make predictions. Guess what a mutation effecting a neural gene like the ASPM does every time it is expressed in the phenotype?

Looks like your assumption is even less supported! When we see microcephaly in humans, we often examine the genome to see what has caused it. But there is extremely little data on the ASPM gene from those without microcephaly.

So... because microcephaly is often caused by a mutation to this gene, you've concluded that all mutations to this gene cause microcephaly?

We know that mutations can account for each and every difference between the ASPM in humans and other apes. How is hypothesizing that some mutations to ASPM are beneficial any less supported than claiming that each and every mutation to ASPM causes microcephaly when our sample size is almost exclusively made up of those WITH microcephaly (for obvious reasons)?!?

gluadys · Apr 15, 2007

shernren said:
Firstly, "transcript errors" have nothing to do with mutations. It's high time you get your terminology and conceptual understanding correct.

Yes, your terminology is often very confusing. I am still waiting for an answer to my post #42 on bears, accumulating mutations, bottlenecks and gene flow.

Also on what information you expect to get from a molecular mechanism for adaptive evolution.

shernren · Apr 15, 2007

Deamiter said:
Looks like your assumption is even less supported! When we see microcephaly in humans, we often examine the genome to see what has caused it. But there is extremely little data on the ASPM gene from those without microcephaly.

So... because microcephaly is often caused by a mutation to this gene, you've concluded that all mutations to this gene cause microcephaly?

We know that mutations can account for each and every difference between the ASPM in humans and other apes. How is hypothesizing that some mutations to ASPM are beneficial any less supported than claiming that each and every mutation to ASPM causes microcephaly when our sample size is almost exclusively made up of those WITH microcephaly (for obvious reasons)?!?

By his reasoning, suppose I see someone flip a coin a few times and all the time get tails. I should therefore conclude that this coin cannot flip heads. Furthermore, if I see any coin on a table heads up, I should conclude that since the previous coin cannot be flipped heads up, this coin must not have been flipped into that position but must have been placed there deliberately.

This is the exact same reasoning that goes into mark's "Since one or two mutations of the human ASPM gene are deleterious, it is impossible for any mutation of any ASPM gene to be beneficial."

mark kennedy · Apr 16, 2007

shernren said:
(emphasis added) Now pray tell, precisely what is "transcription"? You are not using standard definitions of biological terms, and thus it's about as easy to talk to you about biology as it is to talk about theology with someone who thinks that the Trinity is a character from The Matrix.

I think I know what your problem is, you don't understand basic biology. You don't know what transcription is even though the central dogma of biology has been DNA-transcription-RNA-translation since Watson and Crick demonstrated the structure of the double helix.

The central dogma of molecular biology was first enunciated by Francis Crick in 1958[1] and re-stated in a Nature paper published in 1970:[2]

The central dogma of molecular biology deals with the detailed residue-by-residue transfer of sequential information. It states that such information cannot be transferred back from protein to either protein or nucleic acid.

In other words, 'once information gets into protein, it can't flow back to nucleic acid.'

The dogma is a framework for understanding the transfer of sequence information between sequential information-carrying biopolymers, in the most common or general case, in living organisms. There are 3 major classes of such biopolymers: DNA and RNA (both nucleic acids), and protein. There are 3×3 = 9 conceivable direct transfers of information that can occur between these. The dogma classes these into 3 groups of 3: 3 general transfers (believed to occur normally in most cells), 3 special transfers (known to occur, but only under abnormal conditions), and 3 unknown transfers (believed to never occur). The general transfers describe the normal flow of biological information: DNA can be copied to DNA (DNA replication), DNA information can be copied into mRNA, (transcription), and proteins can be synthesized using the information in mRNA as a template (translation). Central dogma of molecular biology

It staggers the imagination that you could make such gross fundamental errors in two consecutive posts and still talk to me like I'm the one who doesn't understand Biology.

Simply astonishing...

Why not? If you want to disprove it, it's as simple as:

1. show that it is chemically impossible for the common ancestor's ASPM gene to undergo mutations that transform it into the Homo sapien ASPM gene.

You don't know what a mutation is, you don't know what a transcription error is and you have not read a word of any of the peer reviewed scientific literature quoted, cited and linked in the thread. Now you want me to prove, that something you don't understand, is impossible?

You think I'm studying evolution don't you? I'm not, I'm studying evolutionists like you.

2. show that even if those mutations are chemically possible, it is then biologically impossible for such a mutation to spread through the Homo sapien population.

Those are very simple ways to prove that you are correct.

You have made two gross fundamental errors and have yet to realize it. You have completely abandoned the evidence and the proper use of basic biological terminology so there is no basis for proving or disproving anything to you.

I have seen evolutionist arguments implode before but this one is a classic case of begging the burden of proof on your hands and knees.

Unbelievable...

mark kennedy · Apr 16, 2007

Deamiter said:
Looks like your assumption is even less supported! When we see microcephaly in humans, we often examine the genome to see what has caused it. But there is extremely little data on the ASPM gene from those without microcephaly.

I don't need an assumption, I have the comparisons of genomic DNA samples of 14 human (Homo sapiens) individuals of different geographic origins (2 African Pygmies, 3 African Americans, 4 Europeans, 2 Southeast Asians, 1 Chinese, 1 Pacific islander, and 1 South American), from one chimpanzee (Pan troglodytes) and one orangutan (Pongo pygmaeus).

Nothing need be assumed, the level of divergence comes down to a simple ratio.

So... because microcephaly is often caused by a mutation to this gene, you've concluded that all mutations to this gene cause microcephaly?

No, I have concluded that they are mostly neutral and that the ones with effects expressed in the phenotype are deleterious. I can say this conclusively because no beneficial effect has ever been directly observed or demonstrated. Also the fact that researchers openly admit they have no clue what molecular mechanism could produce such an alteration of highly conserved sequences means it's not scientific to say that one exists.

We know that mutations can account for each and every difference between the ASPM in humans and other apes. How is hypothesizing that some mutations to ASPM are beneficial any less supported than claiming that each and every mutation to ASPM causes microcephaly when our sample size is almost exclusively made up of those WITH microcephaly (for obvious reasons)?!?

We know nothing of the sort, we know what happens when mutations are introduced into the 28 exons of the huge protein coding gene and it's either nothing or microcephaly (literally small brain). We also know the mutation rate would have to be 1 x 10-9/site/year. We also know that all of these imaginary indels would have had to be in sizes that are multiples of three nucleotides or they would disrupt an Open Reading Frame (ORF).

I just happen to be the only one who thinks this is not only impossible but a fantasy of mythic proportions.

mark kennedy · Apr 16, 2007

gluadys said:
Yes, your terminology is often very confusing. I am still waiting for an answer to my post #42 on bears, accumulating mutations, bottlenecks and gene flow.

You guys are confused by the terms mutation, transcription error and now bottlenecks and gene flow.

A population bottleneck (or genetic bottleneck) is an evolutionary event in which a significant percentage of a population or species is killed or otherwise prevented from reproducing, and the population is reduced by 50% or more, often by several orders of magnitude.

Population bottlenecks increase genetic drift, as the rate of drift is inversely proportional to the population size. They also increase inbreeding due to the reduced pool of possible mates (see small population size).

http://en.wikipedia.org/wiki/Population_bottleneck

Also on what information you expect to get from a molecular mechanism for adaptive evolution.

Now you are asking about what I expect to learn about adaptive evolution from molecular mechanisms that produce adaptive traits.

Give me a break...

Deamiter · Apr 16, 2007

A bit cranky today are we mark?

No, I have concluded that they are mostly neutral and that the ones with effects expressed in the phenotype are deleterious. I can say this conclusively because no beneficial effect has ever been directly observed or demonstrated.

Your definition of the word "conclusive" seems t be nonstandard. You have 14 examples of an ASPM gene and from those you "can say conclusively" that all mutations to ASPM are neutral or deleterious. In your words... "... unbelievable."

By his [mark kennedy's] reasoning, suppose I see someone flip a coin a few times and all the time get tails. I should therefore conclude that this coin cannot flip heads. Furthermore, if I see any coin on a table heads up, I should conclude that since the previous coin cannot be flipped heads up, this coin must not have been flipped into that position but must have been placed there deliberately.

This is the exact same reasoning that goes into mark's "Since one or two mutations of the human ASPM gene are deleterious, it is impossible for any mutation of any ASPM gene to be beneficial."

Genetics and Genesis

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Legend

you are not reading this.

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I just follow Christ.

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Regular Member

I just follow Christ.

Natura non facit saltum

I just follow Christ.

you are not reading this.

Natura non facit saltum

you are not reading this.

I just follow Christ.

Legend

you are not reading this.

Natura non facit saltum

Natura non facit saltum

Natura non facit saltum

I just follow Christ.

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