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Author Topic:   Genetic 'Bottlenecks' and the Flood
Mammuthus
Member (Idle past 4033 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 31 of 59 (41457)
05-27-2003 11:38 AM
Reply to: Message 20 by Alec
05-25-2003 10:30 PM


There has been talk of animals not having evidence of a population bottleneck. What genomes have been mapped that do not? Also, wouldn't the bottleneck be for about 5,000 years ago, the supposed time of the Flood? I do know that Mitochondrial Eve has been dated back to about 6000 years, using faster, actualy measured mutation rates, in an artice in Science.

M: That study was disputed
Nat Genet 1998 Feb;18(2):109-10 Related Articles, Links

Comment on:
Nat Genet. 1997 Apr;15(4):363-8.

Mitochondrial mutation rate revisited: hot spots and polymorphism.

Jazin E, Soodyall H, Jalonen P, Lindholm E, Stoneking M, Gyllensten U.

Regardless, the other examples you provided like elephant seals and cheetahs are known to have undergone recent bottlenecks because of hunting pressure...and they don't coalesce to 5 or 6K years ago i.,e
Curr Biol 2000 Oct 19;10(20):1287-90 Related Articles, Links

An empirical genetic assessment of the severity of the northern elephant seal population bottleneck.

Weber DS, Stewart BS, Garza JC, Lehman N.

Department of Biological Sciences, University at Albany, State University of New York, 12222, USA.

A bottleneck in population size of a species is often correlated with a sharp reduction in genetic variation. The northern elephant seal (Mirounga angustirostris) has undergone at least one extreme bottleneck, having rebounded from 20-100 individuals a century ago to over 175,000 individuals today. The relative lack of molecular-genetic variation in contemporary populations has been documented, but the extent of variation before the late 19th century remains unknown. We have determined the nucleotide sequence of a 179 base-pair segment of the mitochondrial DNA (mtDNA) control region from seals that lived before, during and after a bottleneck low in 1892. A 'primerless' PCR was used to improve the recovery of information from older samples. Only two mtDNA genotypes were present in all 150+ seals from the 1892 bottleneck on, but we discovered four genotypes in five pre-bottleneck seals. This suggests a much greater amount of mtDNA genotypic variation before this bottleneck, and that the persistence of two genotypes today is a consequence of random lineage sampling. We cannot correlate the loss of mtDNA genotypes with a lowered mean fitness of individuals in the species today. However, we show that the species historically possessed additional genotypes to those present now, and that sampling of ancient DNA could elucidate the genetic consequences of severe reductions in population size.

In any case, population genetic studies of hundreds of species of plants and animals have been done and there is no indication of a common bottleneck much less one that happened at a time corresponding to the mythical flood.


This message is a reply to:
 Message 20 by Alec, posted 05-25-2003 10:30 PM Alec has not yet responded

  
Alec
Inactive Member


Message 32 of 59 (41752)
05-29-2003 10:04 PM


Crashfrog:

quote:
That doesn't make sense. It takes far, far longer for a species to lose functionality (the adaptation to multiple salinity environments) than it does to gain it because there's no selection pressure for losing things unless their presence is somehow detrimental.

Exactly. In the creation model, the farther back you go in history (towards creation), the more genetically diverse organisms are. They were created with ultimate genetic diversity, and adaptation by natural selection--becoming specialized for an environment--only limits genetic variation. Therefore, because fish, etc., have become adapted to certain, specialized environments does not mean they didn't have this capability in the past and, as some evidence shows, does not mean that such variation is non-existent today.

quote:
Why would fishes have lost their adaptation to multiple salinities? What's the disadvantage in having it?

Why are there pseudogenes in the genome--what's the disadvantage in having real genes? You see the flaw in your argument? Mutations are not always driven by environmental factors, though I believe they certainly can be. Mutations are almost always known for their detrimental effects, and even though it would be advantageous for the organism to keep its function, a mutation can change that.

quote:
Fish may have lost the ability to adapt to different salinities but it would have taken a lot longer than 4000 years. There's just no selection pressure for it.

I'll discuss the speed of mutation, etc., in a moment. As for the selection pressure--if a species of fish has taken up freshwater lakes as its habitat, adaptation to multiple salinities would be irrelevant. And if the ability to cope with multiple salinities is advantageous is this certain situation, why don't we find more fish with this ability today?

quote:
In a vast, churning miasma? I don't find that reasonable.
There's a thread here <www.evcforum.net/cgi-bin/dm.cgi?action=page&f=7&t=43&p=4 -->www.evcforum.net/cgi-bin/dm.cgi?action=page&f=7&t=43&p=4">http://www.evcforum.net/cgi-bin/dm.cgi?action=page&f=7&t=43&p=4> that discusses how the flood would have had to have been simultaneously incredibly violent to deposit sedimentary layers in the way we see them, yet also pretty calm to allow a 600-year-old man and his boat full of animals to survive. The flood explanation just isn't self-consistent.

The original issue was over population genetics, and I certainly don't know much about geology. The Flood was violent, probably accompanied by volcanic activity and the like. The dimensions of the ark, I have read, are such so that it could still righten itself if it was tipped 60 degrees. The dimensions are the optimum for ships--used today, if fact. I don't know what this has to do with self consistency. The Bible says the Flood would destroy what was on the face of the Earth, which it did--and the vessel which 8 humans were saved on was built to task.

quote:
Are you sure about this? I don't see how a founder population of two (or even seven) could have any significant amount of genetic diversity - certainly not enough to explain the diversity we see today. ... In a population of two, any selection at all ends the species.

Many genes are pleiotropic--they affect many different traits [Ridley 1999, p. 66]. This can account for rapid diversification. The opposite is also true: some single traits are affected by many different genes. This can aid rapid diversification also. Think of genes not as written-in-stone codes, by highly interactive bits of DNA. For example, "jumping genes" (transposons), can move to different parts on the same chromosome, or another chromosome altogether. Supressor genes can move, thus possibly either turning a gene on, or another off, or both. They may even play a part in antibiotic resistance. It is possible that the cell may be able to control transposition, also. As far as such polymorphism arising quickly, Woodmorappe [1996, p. 192] again cites a relevant example: "A very small number (probably a single pair) of macaques had been introduced to Mauritius island by Dutch sailors some 400 years ago. the presently-large population exhibits low MtDNA diversity when compared with the macaques on the Philippines. Yet (H), the average heterozygosity, as measured by allozymes, is greater than that found among the macaques on the Philippines." He cites the following reference: S.H. Lawler, et al.. 1995. Mitochondrial DNA of the Mauritian macaques (Macaca fascicularis): an example of the founder effect. American Journal of Physical Anthropology 96:133-141.

In addition to this, I mentioned splice variants in my last message, which opens a whole new world of possibilities. Therefore, "exons may be combined in alternative ways, creating distinct but related mRNAs... The resulting proteins may differ only slightly [in shape] but nevertheless have entirely distinct roles [Zweiger 2001, p. 48]." This shows the fine-tuning of a proteins shape (which determines its function). Other complex processes have been discovered--for example, protein encoding by both DNA strands, not just the one. This "rasies new questions regarding genome complexity and evolution [Labrador et al. 2001]."

Of course, mtDNA can also mutate very quickly. Just eight days ago, Nature published an article on this very fact. MtDNA was extracted from white-footed mice (in museums) which were caught in the Chicago area in 1855. They compared five collection sites, using a 340-bp polymorphic region. Only one mouse today had the A haplotype. Quote, "We found a consistently similar directional change of mouse genotype over this period at each of five collection sites that were separated by 10-70 km. The genotype most common 100 years ago is no extremely rare, indicating that the mammalian mitochondrial genome can undergo rapid evolution [Pergams et al. 2003]." Besides showing that mutation can happen very fast, this could also have significant results for the molecular clock.

Another example: "Recent studies were prompted by the curious case of a 'Benny', a hybrid between two different species--the tall swamp wallaby and the tubby tamar wallaby. Benny's chromosomes were found to have been seriously disfigured. Some of the centromeres... were tne times as long as normal; part of an arm of chromosome 2 has been moved to chromosome 7, and part of the X chromosome had been reversed. Analysis of Benny's DNA showed that it was "dramatically under-mathylated'. Methylation of DNA is a mahor method of controlling gene expression, so 'dramatically under-methylated DNA' means DNA that is 'out of control'. The researcher involved called it 'very extreme, and quite shocking'. ... Benny's experience led to the idea that perhaps a similar mechanism [as jumping genes from retorovirus DNA] has influenced wallaby speciation. A follow-up study of the Queensland rock hoppers turned up trumps. Dramatic changes of a similar kind were found, leading to an equally dramatic conclusion--'something that we thought might take 50 million years might take 5 minutes instead [Williams 2003]." The reference he cited is as follows: D. Fox, Wallaby nations, New Scientist, 3 August 2002, pp. 32-35.

So, fast genetic change is known to take place. As to any selection at all of pairs ending life, perhaps much of that did happen. Inbreeding depression may have been less severe in the past, also, as animals would have been more genetically diverse. Also, animals could have been interbreeded to remove all of the un-fit organisms, thus ensuring that death due to inbreeding depression would not happen. Numerous possibilities exist.

quote:
Plate tectonics - ever heard of it? Mount Everest used to be a lot shorter. Used to be under a sea, in fact. (Plates colliding, and all.) I'll wager that you certainly don't find any contemporary sea life on the top of Everest. No whales, for instance.

However, marine fossils on top of Everest are a direct prediction of the creation model, too. I honestly don't know about the whales part.

quote:
We don't have to map the genomes of every animal. We just have to map the genome of one animal that would have had to have been on the ark to disprove the ark story. I haven't looked, and I'm no geneticist, but I'd be very surprised indeed if there wasn't a mammal (for instance) with no recent genetic bottleneck.

I really don't know if an example exists or not. Cattle are an interesting example:

quote:
Another interesting detail comes from a mitochondrial Eve study in cattle. The mtDNA sequences point to at least 200 000 years fro the most recent common ancestor of cattle. This date was calculated by using convetional values for mtDNA substitution rates [emphasis mine; this is important] derived from human mitochondrial Eve studies and paleontological divergence dates of cattle and bison. On the other hand, archaeological evidence indicates no domesitcations earlier that 10 000 years BP. To resolve this conflict, Luftus et al. postulated independent domestication events of callt.e However, if Loftus's phylogenetic tree of cattle is correct and domestication was recent, about 23 substitutions would have occurred in the sequenced 915 bp D-loop regions during the past 10 000 years, which corresponds to 2.5 substitutions/site/million years. The similarity to Parsons' calues is striking, even if evolutionary rates in man and cattle are probably different. Perhaps it is worth rethinking domestication history of cattle with Parsons' high subsititution rates in mind [Loewe and Scherer 1997].

So a recent domestication of cattle is possible based on actual, measured mutation rates. Really, there is so much debate over the molecular clokc in the scientific literature that I don't believe anything can be known at all for sure at the moment.

In humans, the mutation rate has been found using the assumption that (a) humans diverged from chimps, and (b) this took place 5 million years ago (which is a debate in and of itself). By finding the differences between humans and chimps, an avergae mutation rate per year is found using the 5 million year assumption. Significant to note is that when mutation rates are actually measured, the rate seems much more rapid in many organisms [Gibbons 1998, Pergams et al. 2003].

quote:
The flood model raises way more questions than it addresses, is self-contradictory, and simply fails to be reasonable. I don't really see how it can be taken as anything but a myth.

Okay.

NosyNed:

quote:
It seems to me that this crys out for quantification. How long, days, hours, weeks in "gradually" in the first one? ANd how "sudden" is the second?

I really don't know the exact figures--they can be found in Comparitive Biochemistry and Physiology 28:1427. And I think it is self-evidence how sudden the global deluge was.

quote:
Certainly, we understand that evolution can happen pretty quickly under some circumstances. But there are at least a couple of problems with the idea.
1) The raw speed of the speciation. I've seen some creationist sites that have "kind" at the family level. For there to be no historic record of this happening the full range of speciation would have to have been complete sometime well before 2000 years ago.
2) Why did it stop? There is no suggestion of a mechanism that can turn on and off that extremely.
I'm afraid that an arm waving explanation like this isn't going to hold up under any kind of close examination.

Firstly, I specified my "arm-waving" above, as well as answered that such mechanisms exist today. I really don't at all understand what you're trying to say in your first point.

Mammuthus:

I will have to see if I can find the Nature Genetics article you cited.

quote:
Regardless, the other examples you provided like elephant seals and cheetahs are known to have undergone recent bottlenecks because of hunting pressure...and they don't coalesce to 5 or 6K years ago i.,e
Curr Biol 2000 Oct 19;10(20):1287-90 Related Articles, Links

What do they coalesce to, and how are we certain of hunting pressure as the cause? I don't have access to that journal. Also, as I previously stated, I don't believe the molecular clock can be heavily relied on at the moment (especially old ages) in light of evidence of rapid mutation rates, such as that discussed in Pergams et al..

quote:
A bottleneck in population size of a species is often correlated with a sharp reduction in genetic variation.

The example of macaques I give above could contradict this statement. Additionally, a bottleneck can cause a rare genotype to be expressed by eliminating the more common genotypes.

Sorry, but I'm out of time. Exams next week--gotta study.

-Alec

References:

Gibbons, Ann, "Calibrating the Mitochondrial Clock," Science 279(5347):28-29, 2 January 1998.

Labrador, Mariano, "Protein Encoding by Both DNA Strands," Nature 409(6823):1000, 22 February 2001.

Loewe, Laurence, and Siegfried Scherer, "Mitochondrial Eve: The Plot Thickens," Trends in Ecology and Evolution 12(11):422-423, 11 November 1997.

Pergams, Oliver R.W., et al., "Rapid Change in Mouse Mitochondrial DNA," Nature 423(6938):397, 22 May 2003.

Ridley, Matt, Genome (Perennial, 1999).

Williams, Alexander R., "Jumping Paradigms," TJ 17(1):19-21, 2003.

Woodmorappe, John, Noah's Ark: A Feasibility Study (ICR, 1996).

Zweiger, Gary, Transducing the Genome (McGraw-Hill, 1999).


Replies to this message:
 Message 33 by crashfrog, posted 05-29-2003 10:58 PM Alec has not yet responded
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crashfrog
Inactive Member


Message 33 of 59 (41755)
05-29-2003 10:58 PM
Reply to: Message 32 by Alec
05-29-2003 10:04 PM


Therefore, because fish, etc., have become adapted to certain, specialized environments does not mean they didn't have this capability in the past and, as some evidence shows, does not mean that such variation is non-existent today.

I don't think you understand my objection. My point is that, since there's no pressure to lose temperance to changing salinity, there's no way most fish would have lost it in only 4000 years or so. That kind of genetic change takes far, far longer.

The mechanisms of mutation and natural selection are very well understood, and unless you can posit a potential survival advantage for an inability to tolerate different salinities, those mechanisms preclude such a change from happening in anything close to 4000 years.

Mutations are almost always known for their detrimental effects, and even though it would be advantageous for the organism to keep its function, a mutation can change that.

Actually they're almost always known for their neutral effects, for instance the four to fifty mutations you have, somewhere in your genetic code.

You're proposing that all species of fish have salinity-temperance pseudogenes? That appears to be your argument. I don't know how salmon (for instance) deal with changing salinity. I don't know what kind of genes that it takes.

If you do, please fill me in. I'm really not a biologist, just a reasonable person.

As for the selection pressure--if a species of fish has taken up freshwater lakes as its habitat, adaptation to multiple salinities would be irrelevant.

Exactly my point. If the trait is neutral with respect to the environment, we should see a lot more fish with it. If there's no reason to select for or against it, it should tend to continue in the population until random mutation disables it. That takes a lot longer than 4000 years.

Are you seeing my point with this? 4000 years isn't enough time for most species of fish to lose that trait. Since they don't have it now, either they lost it far, far longer than 4000 years ago, or else they never had it. My bet is the second choice. Most fish never were adapted to multiple salinities, therefore they wouldn't have survived a global flood. Since we have fish today we can assume, then, that the global flood never happened.

The dimensions of the ark, I have read, are such so that it could still righten itself if it was tipped 60 degrees.

As well as broken in half had it sailed into the trough of a large wave.

The dimensions are the optimum for ships--used today, if fact.

Boats built today are made from steel. Also they have keels. There's a hundred reasons why Noah's ark would have floundered in a violent sea.

However, marine fossils on top of Everest are a direct prediction of the creation model, too.

Sure. On the other hand, plate tectonics is supported by a host of other data, including GPS which comfirms the rising of mountains and the sliding of plates. Your flood story is supported by no evidence at all.


This message is a reply to:
 Message 32 by Alec, posted 05-29-2003 10:04 PM Alec has not yet responded

  
Mammuthus
Member (Idle past 4033 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 34 of 59 (41952)
06-02-2003 10:52 AM
Reply to: Message 32 by Alec
05-29-2003 10:04 PM


quote:
Another example: "Recent studies were prompted by the curious case of a 'Benny', a hybrid between two different species--the tall swamp wallaby and the tubby tamar wallaby. Benny's chromosomes were found to have been seriously disfigured. Some of the centromeres... were tne times as long as normal; part of an arm of chromosome 2 has been moved to chromosome 7, and part of the X chromosome had been reversed. Analysis of Benny's DNA showed that it was "dramatically under-mathylated'. Methylation of DNA is a mahor method of controlling gene expression, so 'dramatically under-methylated DNA' means DNA that is 'out of control'. The researcher involved called it 'very extreme, and quite shocking'. ... Benny's experience led to the idea that perhaps a similar mechanism [as jumping genes from retorovirus DNA] has influenced wallaby speciation. A follow-up study of the Queensland rock hoppers turned up trumps. Dramatic changes of a similar kind were found, leading to an equally dramatic conclusion--'something that we thought might take 50 million years might take 5 minutes instead [Williams 2003]." The reference he cited is as follows: D. Fox, Wallaby nations, New Scientist, 3 August 2002, pp. 32-35.

Um, this is a case of differential methylation in a non-fertile hybrid..this is known for Drosophila as well i.e. hybrid dysgenesis caused by transposons called P elements. However, this does not imply an increase in mutation...the tranposons can serve as a species barrier..not as magic diversifier or a way of speeding up the mutation rate.

quote:
Mammuthus:

I will have to see if I can find the Nature Genetics article you cited.

quote:
--------------------------------------------------------------------------------
Regardless, the other examples you provided like elephant seals and cheetahs are known to have undergone recent bottlenecks because of hunting pressure...and they don't coalesce to 5 or 6K years ago i.,e
Curr Biol 2000 Oct 19;10(20):1287-90 Related Articles, Links
--------------------------------------------------------------------------------

What do they coalesce to, and how are we certain of hunting pressure as the cause? I don't have access to that journal. Also, as I previously stated, I don't believe the molecular clock can be heavily relied on at the moment (especially old ages) in light of evidence of rapid mutation rates, such as that discussed in Pergams et al..


Um..the paper you cite does not show an increased mutation rate. It just shows that there was selection either for or against one of the two mtDNA haplotypes in mice in the Chicago area. Both types are still present. And this does not actually address the coalescence time since the last common ancestor of the haplotypes which would have preceded the bottleneck event that was recorded.

If you hypothesize that ALL animals in the world were reduced to a single breeding pair, their would be genetic evidence of such a bottleneck in ALL species regardless of the rate of the molecular clock. This is not the case...not even in primates that are closely related to us like chimps which have 4 times the genetic diversity as Homo sapiens in both mtDNA and nuclear markers. They do not show evidence of a any severe bottleneck much less one the magnitude of proponents of the ark myth.

cheers,
M

[This message has been edited by Mammuthus, 06-02-2003]


This message is a reply to:
 Message 32 by Alec, posted 05-29-2003 10:04 PM Alec has not yet responded

  
Alec
Inactive Member


Message 35 of 59 (46775)
07-21-2003 8:13 PM


Crashfrog and Mammuthus,

I'm sorry, I intended to respond to this and then forgot completely.

Firstly, I've read the study by Jazin et al., and Thomas Parsons and Mitchell Holland responded to their criticisms and explained why the results of their study may have not been in line with their own. Additionally, the results of the original Parsons study has seemed to be confirmed in more recent research (for example, Tully et al. 2000).

Crashfrog:

quote:
I don't think you understand my objection. My point is that, since there's no pressure to lose temperance to changing salinity, there's no way most fish would have lost it in only 4000 years or so. That kind of genetic change takes far, far longer.

New species of, say, salmon have arisen under the observation of humans. I don't think this kind of change requires that long of a time. We really can't know; some evidence does suggest rapid speciation after a bottleneck.

quote:
The mechanisms of mutation and natural selection are very well understood, and unless you can posit a potential survival advantage for an inability to tolerate different salinities, those mechanisms preclude such a change from happening in anything close to 4000 years.

Since when do mutations need a selective advantage to occur and proliferate? If a species of fish was living in fresh water, mutation affecting salinity tolerance would be more like 'genetic drift', perhaps unaffected by natural selection, unless it was in favor of an only-salty environment. There would be selection of the only-fresh water fish over the fish more adapted to multiple salinities.

quote:
Actually they're almost always known for their neutral effects, for instance the four to fifty mutations you have, somewhere in your genetic code.

According to one of my newer textbooks, "most mutations are deleterious, but the neutral theory asserts that the selective advantages or disadvantages of most molecular mutations are so small that selection on them is too weak to offset the influences of genetic drift (Purves et al. 2001)." So I suppose you're right in the sense that the negative effects of most mutations are so small as to seem neutral.

As far as the whole salinity issue, I must admit I was taken off-guard and hardly know anything about it; I'm trying to be a reasonable person also .

Mammuthus:

quote:
If you hypothesize that ALL animals in the world were reduced to a single breeding pair, their would be genetic evidence of such a bottleneck in ALL species regardless of the rate of the molecular clock. This is not the case...not even in primates that are closely related to us like chimps which have 4 times the genetic diversity as Homo sapiens in both mtDNA and nuclear markers. They do not show evidence of a any severe bottleneck much less one the magnitude of proponents of the ark myth.

We haven't even mapped the chimp genome yet, said to be our most recent ancestor. Other animals also have much higher mutation rates, for example rodents and perhaps hominids other than humans [Eyre-Walker and Keightley, 1999]. The difference between species, for example, human/chimp DNA similarity, depends on what is being compared; for exmaple, when indels are included in the comparison of the major histocompatibility complex, the similarity drops to 86.7 from the commonly touted ~98% [Anzai et al. 2003]. Indeed, "Sequence divergence estimates between human, chimpanzee and gorilla nuclear genome do not adequately respresent fine changes in genome organization [Hacia 2001]."

I'm sorry but I'm leaving in a few minutes and I must go now; I will check with this forum again soon!

-Alec

References

Tatsuya Anzai, et al., "Comparative Sequencing of HUman and Chimpanzee MHC Class I Regions Unveils Insertions/Deletions as the Major Path to Genomic Divergence," PNAS 100(13):7708-7713, 24 June 2003.

Adam Eyre-Walker and Peter D. Keightley, "High Genomic Deleterious Mutation Rates in Hominids," Nature 397(6717):344-347, 28 January 1999.

Joseph G. Hacia, "Genome of the Apes," Trends in Genetics 17(11):637-645, November 2001.

William K. Purves, et al., Life: The Science of Biology (Sinauer and WH Freeman, 2001), pp. 439-440.

Lois A. Tully, et al., "A Senitive Denaturing Gradient-Gel Electrophoresis Assay Reveals a High Frequency of Heteroplasmy in Hypervariable Region 1 of the Human mtDNA Control Region," Am. J. Hum. Genet. 67(2):432-443, August 2000.


Replies to this message:
 Message 36 by crashfrog, posted 07-21-2003 8:21 PM Alec has not yet responded
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crashfrog
Inactive Member


Message 36 of 59 (46776)
07-21-2003 8:21 PM
Reply to: Message 35 by Alec
07-21-2003 8:13 PM


Since when do mutations need a selective advantage to occur and proliferate?

Well, they don't of course. The point that I was making (that you appear to have missed again) is that mutations don't proliferate at the rate that they would have to in order to eliminate salinity tolerance in most fish in under 4000 years without some kind of selective advantage.

As far as the whole salinity issue, I must admit I was taken off-guard and hardly know anything about it; I'm trying to be a reasonable person also

I realize that. As far as I'm concerned, I haven't heard anything to counter it. Fish simply wouldn't lose a tolerance for changing salinity in only 4000 years unless there was a major selective advantage in doing so. Otherwise it would have taken millions of years to lose through genetic drift.

[This message has been edited by crashfrog, 07-21-2003]


This message is a reply to:
 Message 35 by Alec, posted 07-21-2003 8:13 PM Alec has not yet responded

  
PaulK
Member
Posts: 13228
Joined: 01-10-2003
Member Rating: 1.9


Message 37 of 59 (46818)
07-22-2003 4:12 AM
Reply to: Message 35 by Alec
07-21-2003 8:13 PM


Just on the chimps, I have to point out that :

1) Chimpanzees are NOT our ancestors - they are our closest LIVING relatives.

2) The similarity between the human and chimpanzee genomes has nothing to do with the genetic diversity found within the chimpanzee species.
So why are you responding to the point that chimpanzees do not show the genetic bottleneck implied by the ark story by talking about the similarities between human and chimpanzee genes ?


This message is a reply to:
 Message 35 by Alec, posted 07-21-2003 8:13 PM Alec has not yet responded

    
Mammuthus
Member (Idle past 4033 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 38 of 59 (46826)
07-22-2003 5:18 AM
Reply to: Message 35 by Alec
07-21-2003 8:13 PM


Hi Alec,

I missed this so sorry for the late response.

There is a difference between the mutation rate and the genetic diversity among primates. However, the mutation rate is still irrelevatn to the point I made...if there was a world wide flood in biblical times, regardless of the mutation rates, you would see a coalescence of genetic diversity at that point due to the genetic bottleneck. This is not observed. Elephants don't show this, whales don't..the mammalian model of bottlenecks, the cheetah does not, elephant seals do not, chimps don't..., fish do not, plants don't.
Sequencing of genomes is entirely irrelevant to the study of genetic bottlnecks in its current form. What does the sequencing of a single representative individual tell you about the population gentic history of the species? Nothing. The types of studies that do are smaller scale sequencing projects of loci like mtDNA or micro and mini satellite markersī, SNP studies of lots of individuals of a species...and none of these are consistent with a flood induced bottleneck.

cheers,
M


This message is a reply to:
 Message 35 by Alec, posted 07-21-2003 8:13 PM Alec has not yet responded

  
Rrhain
Member
Posts: 6173
From: San Diego, CA, USA
Joined: 05-03-2003
Member Rating: 2.5


Message 39 of 59 (46847)
07-22-2003 6:50 AM
Reply to: Message 35 by Alec
07-21-2003 8:13 PM


Alec writes:

quote:
According to one of my newer textbooks, "most mutations are deleterious, but the neutral theory asserts that the selective advantages or disadvantages of most molecular mutations are so small that selection on them is too weak to offset the influences of genetic drift (Purves et al. 2001)."

Um, I have this book (though it's the second edition from 1987). And I was taught biology by Dr. Purves at Harvey Mudd.

I can state with certainty that he would be quite dismayed that you are using his text as some sort of indication that evolution has some fundamental problems that indicate a global flood.

If you like, I can email him and ask him for his opinion. Here's a more complete view:

The origin of genetic variability is mutation (Chapter 12). Most mutations are known to be harmful or neutral, but if the environment changes, previously neutral or deleterious alleles may become advantageous. Therefore, the amount of 'nonadaptive' variation in populations may have important biological consequences.

From Chapter 12, "Nucleic Acids as the Genetic Material":

Some mutations do involve extensive chemcial changes in the structure of DNA. Others, called point mutations, change only a single nucleotide in the genetic information. Point mutations can generally revert, that is, they can mutate back to the original form. Extensive mutations may be rearrangements (which change the position or direction of a DNA segment without actually removing any genetic information) or deletions (in which a segment of DNA is irretrievably lost).

All mutations are rare events. The observed frequencies of mutations are different for different organisms and for different genes within a given organism. Usually the frequency of mutation is lower than 1 mutation per 104 genes per DNA duplication, and someties the frequency is as low as 1 mutation per 109 genes per duplication. The majority are point mutations resulting from the substitution of one nucleotide during the synthesis of a new DNA strand.

The text then goes on to discuss the various types of point mutation (transition, transversion, frame-shift), and then compares the effects:

It is small wonder that a frame-shift mutation is so disruptive. An organism carrying such a mutant gene can only survive only if the gene product affected is not an essential part of the cellular machinery or if the organism also carries another copy of the gene in its normal form. This situation is different from that applying to base-substitution mutations. Often base-substitution mutations change the genetic message so that one amino acid is substituted for another in the protein. Such a missense mutation may sometimes cause the protein to be completely nonfunctional, but often the effect is only to reduce its functional efficiency. on rare occasions the functional efficiency is even improved. Individuals carrying issense mutations may survive even though the affected protein is absolutely essential to life.

In short, Purves is not saying what you are making him out to say.

------------------
Rrhain
WWJD? JWRTFM!


This message is a reply to:
 Message 35 by Alec, posted 07-21-2003 8:13 PM Alec has not yet responded

    
Alec
Inactive Member


Message 40 of 59 (46992)
07-23-2003 3:16 AM


quote:
Chimpanzees are NOT our ancestors - they are our closest LIVING relatives.

True. We are said to have diverged from them about 6 million years ago, so I guess 'ancestor' just came out. I will try to be more careful with my words, because I agree that makes a difference.

quote:
So why are you responding to the point that chimpanzees do not show the genetic bottleneck implied by the ark story by talking about the similarities between human and chimpanzee genes?

Mammuthus spoke of "primates that are closely related to us like chimps." I thought that perhaps the information would be relevant. It really doesn't have a great deal to do with genetic bottlenecks though, I agree.

quote:
There is a difference between the mutation rate and the genetic diversity among primates. However, the mutation rate is still irrelevatn to the point I made...

I was discussing mutation rates in the mitochondrial genome because you cited the Jazin et al. study before as if it somehow discredited the Parsons study. At least that's the impression I had until I read it, and I wished to clarify.

quote:
...if there was a world wide flood in biblical times, regardless of the mutation rates, you would see a coalescence of genetic diversity at that point due to the genetic bottleneck.

Firstly, I was in part discussing mutation rates because of the previos mtEve discussion. Additionally, if mutation rates are faster in an animal, they will become more genetically diverse faster. The study I cited on hominid mutation rates regarded nuclear DNA.

quote:
This is not observed. Elephants don't show this, whales don't..the mammalian model of bottlenecks, the cheetah does not, elephant seals do not, chimps don't..., fish do not, plants don't.

Really, I've only studied the human genome and don't know much about other animals. I take your word for it.

quote:
Sequencing of genomes is entirely irrelevant to the study of genetic bottlnecks in its current form. What does the sequencing of a single representative individual tell you about the population gentic history of the species? Nothing. The types of studies that do are smaller scale sequencing projects of loci like mtDNA or micro and mini satellite markersī, SNP studies of lots of individuals of a species...and none of these are consistent with a flood induced bottleneck.

Linkage disequilibrium and low genetic diversity is, to my knowledge, the reason for the inference of a bottleneck in human history. I really don't know what to say because I'm not sure about everything you're referring to. What I think you should do is pick a study in a journal that I can go and read, and we can discuss it. Right now I do not know of any examples so I am in a difficult situation.

quote:
I can state with certainty that he would be quite dismayed that you are using his text as some sort of indication that evolution has some fundamental problems that indicate a global flood.

That is not what I was doing at all, but I do not doubt he would be dismayed. I simply stated that most mutations are deleterious and was challenged, and cited his textbook as evidence. The more complete view you cited is good. However, whether or not mutations are usually 'bad or good' does not really form the basis of my present arguments, nor did I intend for it to be the issue; I simply clarified my position. I'm not sure what you believe I'm 'making him out to say,' and I would like to know so that I could perhaps clarify further. That issue came up while we were discussing how fish could have lost adaptation to multiple salinities. Another stated that "Actually they're almost always known for their neutral effects, for instance the four to fifty mutations you have, somewhere in your genetic code." and I answered that. The only thing I intended for the quote was to show that mutations are most often deleterious (in other words, exactly what it stated). Therefore, the only misconception that could arise is if the quote is wrong, which I doubt. I certainly didn't make the claim that his quote somehow gives an 'indication that evolution has some fundamental problems'--that's a bit far out, I would say. Additionally, I did not claim that his quote in any way 'indicate[s] a global flood'. Therefore, I believe contacting William K. Purves is largely unecessary; however, if you believe that would aid this discussion you of course may do so.

Regards,
Alec


  
Alec
Inactive Member


Message 41 of 59 (46993)
07-23-2003 3:20 AM


Also, Mammuthus, it is I who should be apologizing. I have trouble finding the time to get on here and provide anything resembling a thorough response; I do appreciate your promt-ness and will attempt to do my best also.

-Alec


Replies to this message:
 Message 42 by Mammuthus, posted 07-23-2003 5:24 AM Alec has not yet responded

  
Mammuthus
Member (Idle past 4033 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 42 of 59 (47005)
07-23-2003 5:24 AM
Reply to: Message 41 by Alec
07-23-2003 3:20 AM


Hi Alec,
No problem....sometimes I bail out of here completely for lack of time myself.

I have selected a few articles that I hope you can get access to regarding several of the species I mentioned...I will post the abstracts along with them.

Humans have a long genetic history, the cheetah bottleneck correlates with the mass extinctions at the end of the Pleistocene..elephant seals were hunted almost to extinction recently so looking at ancient DNA one can see that they were more diverse prior to this (not surprisingly), I will try to find some info on cervids in north America since they apparently started to increase at the end of the Pleistocene.

Annu Rev Genomics Hum Genet. 2000;1:361-85. Related Articles, Links

Genetic perspectives on human origins and differentiation.

Harpending H, Rogers A.

Department of Anthropology, University of Utah, Salt Lake City, Utah 84112, USA.

This is a review of genetic evidence about the ancient demography of the ancestors of our species and about the genesis of worldwide human diversity. The issue of whether or not a population size bottleneck occurred among our ancestors is under debate among geneticists as well as among anthropologists. The bottleneck, if it occurred, would confirm the Garden of Eden (GOE) model of the origin of modern humans. The competing model, multiregional evolution (MRE), posits that the number of human ancestors has been large, occupying much of the temperate Old World for the last two million years. While several classes of genetic marker seem to contain a strong signal of demographic recovery from a small number of ancestors, other nuclear loci show no such signal. The pattern at these loci is compatible with the existence of widespread balancing selection in humans. The study of human diversity at (putatively) neutral genetic marker loci has been hampered since the beginning by ascertainment bias since they were discovered in Europeans. The high levels of polymorphism at microsatellite loci means that they are free of this bias. Microsatellites exhibit a clear almost linear diversity gradient away from Africa, so that New World populations are approximately 15% less diverse than African populations. This pattern is not compatible with a model of a single large population expansion and colonization of most of the Earth by our ancestors but suggests, instead, gradual loss of diversity in successive colonization bottlenecks as our species grew and spread.

Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3172-6. Related Articles, Links

Dating the genetic bottleneck of the African cheetah.

Menotti-Raymond M, O'Brien SJ.

Biological Carcinogenesis and Development Program, National Cancer Institute, Frederick, MD 21702.

The cheetah is unusual among fields in exhibiting near genetic uniformity at a variety of loci previously screened to measure population genetic diversity. It has been hypothesized that a demographic crash or population bottleneck in the recent history of the species is causal to the observed monomorphic profiles for nuclear coding loci. The timing of a bottleneck is difficult to assess, but certain aspects of the cheetah's natural history suggest it may have occurred near the end of the last ice age (late Pleistocene, approximately 10,000 years ago), when a remarkable extinction of large vertebrates occurred on several continents. To further define the timing of such a bottleneck, the character of genetic diversity for two rapidly evolving DNA sequences, mitochondrial DNA and hypervariable minisatellite loci, was examined. Moderate levels of genetic diversity were observed for both of these indices in surveys of two cheetah subspecies, one from South Africa and one from East Africa. Back calculation from the extent of accumulation of DNA diversity based on observed mutation rates for VNTR (variable number of tandem repeats) loci and mitochondrial DNA supports a hypothesis of an ancient Pleistocene bottleneck that rendered the cheetah depauperate in genetic variation for nuclear coding loci but would allow sufficient time for partial reconstitution of more rapidly evolving genomic DNA segments.

Curr Biol. 2000 Oct 19;10(20):1287-90. Related Articles, Links

An empirical genetic assessment of the severity of the northern elephant seal population bottleneck.

Weber DS, Stewart BS, Garza JC, Lehman N.

Department of Biological Sciences, University at Albany, State University of New York, 12222, USA.

A bottleneck in population size of a species is often correlated with a sharp reduction in genetic variation. The northern elephant seal (Mirounga angustirostris) has undergone at least one extreme bottleneck, having rebounded from 20-100 individuals a century ago to over 175,000 individuals today. The relative lack of molecular-genetic variation in contemporary populations has been documented, but the extent of variation before the late 19th century remains unknown. We have determined the nucleotide sequence of a 179 base-pair segment of the mitochondrial DNA (mtDNA) control region from seals that lived before, during and after a bottleneck low in 1892. A 'primerless' PCR was used to improve the recovery of information from older samples. Only two mtDNA genotypes were present in all 150+ seals from the 1892 bottleneck on, but we discovered four genotypes in five pre-bottleneck seals. This suggests a much greater amount of mtDNA genotypic variation before this bottleneck, and that the persistence of two genotypes today is a consequence of random lineage sampling. We cannot correlate the loss of mtDNA genotypes with a lowered mean fitness of individuals in the species today. However, we show that the species historically possessed additional genotypes to those present now, and that sampling of ancient DNA could elucidate the genetic consequences of severe reductions in population size.

: Mol Biol Evol. 2001 Feb;18(2):214-22. Related Articles, Links

Global patterns of human DNA sequence variation in a 10-kb region on chromosome 1.

Yu N, Zhao Z, Fu YX, Sambuughin N, Ramsay M, Jenkins T, Leskinen E, Patthy L, Jorde LB, Kuromori T, Li WH.

Department of Ecology and Evolution, University of Chicago, 1101 East 57th Street, Chicago, IL 60637, USA.

Human DNA variation is currently a subject of intense research because of its importance for studying human origins, evolution, and demographic history and for association studies of complex diseases. A approximately 10-kb region on chromosome 1, which contains only four small exons (each <155 bp), was sequenced for 61 humans (20 Africans, 20 Asians, and 21 Europeans) and for 1 chimpanzee, 1 gorilla, and 1 orangutan. We found 52 polymorphic sites among the 122 human sequences and 382 variant sites among the human, chimpanzee, gorilla, and orangutan sequences. For the introns sequenced (8,991 bp), the nucleotide diversity (pi) was 0.058% among all sequences, 0.076% among the African sequences, 0.047% among the Asian sequences, and 0.045% among the European sequences. A compilation of data revealed that autosomal regions have, on average, the highest pi value (0.091%), X-linked regions have a somewhat lower pi value (0.079%), and Y-linked regions have a very low pi value (0.008%). The lower polymorphism in the present region may be due to a lower mutation rate and/or selection in the gene containing these introns or in genes linked to this region. The present region and two other 10-kb noncoding regions all show a strong excess of low-frequency variants, indicating a relatively recent population expansion. This region has a low mutation rate, which was estimated to be 0.74 x 10 per nucleotide per year. An average estimate of approximately 12,600 for the long-term effective population size was obtained using various methods; the estimate was not far from the commonly used value of 10,000. Fu and Li's tests rejected the assumption of an equilibrium neutral Wright-Fisher population, largely owing to the high proportion of low-frequency variants. The age of the most recent common ancestor of the sequences in our sample was estimated to be more than 1 Myr. Allowing for some unrealistic assumptions in the model, this estimate would still suggest an age of more than 500,000 years, providing further evidence for a genetic history of humans much more ancient than the emergence of modern humans. The fact that many unique variants exist in Europe and Asia also suggests a fairly long genetic history outside of Africa and argues against a complete replacement of all indigenous populations in Europe and Asia by a small Africa stock. Moreover, the ancient genetic history of humans indicates no severe bottleneck during the evolution of humans in the last half million years; otherwise, much of the ancient genetic history would have been lost during a severe bottleneck. We suggest that both the "Out of Africa" and the multiregional models are too simple to explain the evolution of modern humans.


This message is a reply to:
 Message 41 by Alec, posted 07-23-2003 3:20 AM Alec has not yet responded

  
Alec
Inactive Member


Message 43 of 59 (48044)
07-30-2003 12:36 PM


Mammuthus,

I don't have access to the journals Molecular Biology and Evolution or Current Biology. I looked at the one by Harpending and Rogers but it was too long for me to photocopy in the few minutes I had at the college last night. I found the cheetah one, also, and will read it as soon as I can. I do remind you though, that this is dated to 1993. Even the Harpending and Rogers one was written before the completion of the HGP. Additionally, when I looked through it I did not see the mention of a lack of bottlenecks in other animals, which is what I thought we were tlaking about--perhaps I missed it (most likely).

I'll try to be as punctual as possible! Many thanks!

-Alec


Replies to this message:
 Message 44 by Mammuthus, posted 07-31-2003 5:31 AM Alec has not yet responded

  
Mammuthus
Member (Idle past 4033 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 44 of 59 (48139)
07-31-2003 5:31 AM
Reply to: Message 43 by Alec
07-30-2003 12:36 PM


Hi Alec,
When you come back I can summarize the findings of the MBE and Current Biology articles...it really sucks that they don't make archive files free....but that is a beef that I and a lot of other scientists have with academic publishing.

Anyway back on topic...the 1993 paper is still relevant and has not been refuted. I will point out two things...the HGP is irrelevant to the study of genetic bottlenecks. The sequence is a map of where all the genes, pseudogenes, telomeres, centromeres etc are...it says nothign about any sequences variation in the population.

Second, you won't find a paper about lack of bottlenecks...you will find papers about the high genetic diversity, relationships to other species, and timing of splits of one group from another. Papers on bottlenecks only show up when it is noticed that there is a lot less genetic diversity in a species than expected or relative to other related species. This usually comes out when one is studying the population genetics of a group for some other reason.

I'll look around and see if I can find some review articles on the subject so you don't have to go chasing around after individual papers.

cheers,
M


This message is a reply to:
 Message 43 by Alec, posted 07-30-2003 12:36 PM Alec has not yet responded

  
Alec
Inactive Member


Message 45 of 59 (48264)
07-31-2003 9:46 PM


Mammuthus,

quote:
...the HGP is irrelevant to the study of genetic bottlenecks

Didn't the HGP complete a SNP map, which is used to find LD, which provides evidence of human bottlenecks?

quote:
Second, you won't find a paper about lack of bottlenecks...you will find papers about the high genetic diversity

Well then, high genetic diversity. I would think that studies would publish about low-ranging LD, though.

quote:
I'll look around and see if I can find some review articles on the subject so you don't have to go chasing around after individual papers.

Thank you I'm leaving for Idaho for a week tomorrow, I may or may not have time to get back on before then. I do plan on lots of reading! See you...

-Alec


Replies to this message:
 Message 46 by sfs, posted 08-27-2003 11:12 PM Alec has not yet responded

  
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