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Old 10-04-2002, 11:33 AM   #11
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David H:
Since only about 2% of the human genome is composed of genes that are actually expressed most mutations have little affect on anything. Genes that are really needed are "conserved" by natural selection. Mutations are believed to bring only a 1 % change in the genome of higher eukaryotes every 10 million years. So there is no impending doom from accumulation of mutations IMO. If you think about it, if there never were any mutations we would all be cynobacteria or somthing living in a deep sea vent.
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Old 10-04-2002, 11:43 AM   #12
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Quote:
Originally posted by Wyz_sub10:
<strong>GeoTheo,

You accept evolution, don't you? I thought you have said you did. If so, I think pangloss was looking for a creationist response to this. If you accept evolution, you'll probably have no problem with evolution adding information (which has been a cornerstone issue for creationism).</strong>
Well good luck finding one that will respond. I am an evolutionist, but somtimes play the devils advocate in these types of threads because I get bored wating for worthy creationists to show up.
I suspect most conservative Christians entering a biology program nowadays are converted to theistic evolution by their sophmore year. Perhaps they just keep quiet about it in Church.
If someone can ace courses like molecular genetics and understand everything while still maintaining alternative explanations in their head that can equally explain all the data from a perspective of special creation, my hat is off to them they are truly a genius. Hopefull one such genius will show up.
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Old 10-04-2002, 11:54 AM   #13
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I don't personally think humans have anymore genetic information per sethan yeast just going by the size of our genomes. Doesn't seem very flattering does it?
I think what happened is mammals used some of the same genes other organisms have in different ways in order to build these big brains we have.
To increase genetic info wouldn't each organism need to come up with more and more amino acids?
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Old 10-04-2002, 12:18 PM   #14
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Quote:
Originally posted by GeoTheo:
<strong>I don't personally think humans have anymore genetic information per sethan yeast just going by the size of our genomes. Doesn't seem very flattering does it?
</strong>
I think it's pretty safe to say that humans have more genetic information than yeasts. I don't know the numbers off hand, but we have far more functional genes than yeasts do, and the number of functioning genes times their functional length is probaby the only useful back-of-the-envelope measure of genetic information that I can think of. But creationists never spell out exactly what they mean by "information". The definition changes to suit the argument.

Nevertheless, under the definition I've given above, increases in genetic information have been observed many times under laboratory conditions, opperating by known mechanisms, and can be readily inferred from phylogeny. The "no new information" argument should be put up there with the "no transitional fossils" argument.

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Old 10-04-2002, 12:28 PM   #15
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Quote:
Originally posted by GeoTheo:
<strong>I don't personally think humans have anymore genetic information per sethan yeast just going by the size of our genomes. Doesn't seem very flattering does it?</strong>
The yeast genome is about 13,000kb. The human genome is about 3,000,000kb. Yeast have 6-10,000 genes, humans have 30-40,000 genes.
Quote:
<strong>
I think what happened is mammals used some of the same genes other organisms have in different ways in order to build these big brains we have.
To increase genetic info wouldn't each organism need to come up with more and more amino acids?</strong>
No. That's like claiming that in order for a novelist to write a new book, he needs to invent some new letters.

We also have about the same number and type of genes as a mouse, yet most of us have brains bigger than those of mice.
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Old 10-04-2002, 12:57 PM   #16
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Quote:
davidH:
You know to me it seems as if the DNA code is getting progressively "eaten away at" by mutations.
It may "seem" that way to you, but I cannot see any reason to think so.
Quote:
I know evolution relies on mutation giving more information,
What is "information" in this context, and how do you "know" that "relies on mutation giving more information"?
Quote:
but is that what is happening at this present moment in time?
Without a meaningful definition of "information", how can one address this?
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There are now thousands of genetic disorders/diseases due to mutations and yet relatively few (if any) mutations that are benefical [sic].
There are reasons that we might expect that, under current circumstances, deleterious mutations might be more common than beneficial ones in humans. That being said, please explain why you think that this is actually the case.
Quote:
Would it not be logical to assume that once the population reaches the maximum that the environment can support, that these harmful mutations will eventually wipe humanity off the earth?
No. Even assuming that you are correct about the numbers of mutations, it does not follow that these mutations would kill off all humans. I also do not see the relevance of the carrying capacity here.
Quote:
Let me explain myself.

Harmful mutations are removed by natural selection.
And, often, by genetic drift.
Quote:
At the moment these are far more abundant than any benefical [sic] mutations of humans
An unsupported claim, but one which we can accept for argument's sake.
Quote:
- if indeed there are any that have occurred.
I think that it is pretty obvious that they have, but this seems to be irrelevant to the discussion here.
Quote:
So all organisms with harmful mutations are removed (all those genetic diseases that now abound).
??? Are you suggesting that everyone who has an allele (gene) that is deleterious will immediately die? Are you aware that only 1% of the alleles responsible for cystic fibrosis are found in people who suffer from cystic fibrosis?
Quote:
If for every 100 harmful mutations there is one benefical [sic] mutation, then the odds of the carriers of the benefical [sic] mutation surviving the harmful mutations are low.
Even if we grant your "if", this is a non-sequiter: it does not follow that the odds of such a carrier surviving would then be "low". If you disagree, please explain.
Quote:
For the benefical mutations won't make us immune to the thousands of harmful mutations that abound.
Harmful mutations will not generally harm us when they are in others, harmfull mutations will not always harm us when they are in us, and harmful mutations that do harm us do not necessarily kill us.
Quote:
That being the case
You have not established that it is.
Quote:
wouldn't we genetically go down hill - even the slight peaks of any benefical mutations that happened to occur wouldn't make a difference to the downward trend?
No. All you need is a few to survive and reproduce. You don't need all those deleterious mutation-laden individuals to reproduce. By the way, virtually all humans carry deleterious alleles.
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That's how I tend to see it happening anyway.
Fair enough, but with all due respect your knowledge of genetics is limited. Why would you think that geneticists are wrong?
Quote:
With industry increasing the rate of harmful mutations seems to increase and as industry is set to keep on growing this mutations will still occur.
It may well be that there is a general increase in mutation rates, but on the other hand there is no evidence that I am aware of that this is the case. However, mutations certainly do occur. The average human has several new ones.
Quote:
Everything seems to point to human's genetic code getting progressively worse with genetic diseases abounding...
I do not see anything pointing that way.
Quote:
Any thoughts on this? What does the medical trend show - an increase in the amount of genetic conditions over the last decades?

It would be interesting to see this researched.
This would be difficult to study, given that observed changes in reported cases could be due to changes in diagnoses, increased survival of people with genetic diseases, gene flow among populations, etc. It would still be interesting to look at, of course, from the point of view of tracking mutagens in our environment.

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Old 10-04-2002, 12:59 PM   #17
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BTW, here are a few relevant referrences to "genetic information" increases. We used to have an ongoing thread at antievolution.org, and then a server crash wiped out most of it.
Quote:
Kellogg EA., Root hairs, trichomes and the evolution of duplicate genes. Trends Plant Sci 2001 Dec;6(12):550-2.

Michael Conlon J., The origin and evolution of peptide YY (PYY) and pancreatic polypeptide (PP). Peptides 2002 Feb;23(2):269-78.

Briscoe AD., Functional diversification of lepidopteran opsins following gene duplication. Mol Biol Evol 2001 Dec;18(12):2270-9.[below in examp. GET]

Inoue K, Dewar K, Katsanis N, Reiter LT, Lander ES, Devon KL, Wyman DW, Lupski JR, Birren B., The 1.4-Mb CMT1A duplication/HNPP deletion genomic region reveals unique genome architectural features and provides insights into the recent evolution of new genes. Genome Res 2001 Jun;11(6):1018-33.

Brown CJ, Todd KM, Rosenzweig RF (1998) Multiple duplications of yeast hexose transport genes in response to selection in a glucose-limited environment. Mol Biol Evol 1998 Aug;15(8):931-42 Nature 387, 708 - 713 (1997)

Van de Peer Y, Taylor JS, Braasch I, Meyer A., The ghost of selection past: rates of evolution and functional divergence of anciently duplicated genes. J Mol Evol 2001 Oct-Nov;53(4-5):436-46.

Hoshino A, Johzuka-Hisatomi Y, Iida S., Gene duplication and mobile genetic elements in the morning glories. Gene 2001 Mar 7;265(1-2):1-10.

Eichler EE., Recent duplication, domain accretion and the dynamic mutation of the human genome. Trends Genet 2001 Nov;17(11):661-9.

Araki H, Inomata N, Yamazaki T., Molecular evolution of duplicated amylase gene regions in Drosophila melanogaster: evidence of positive selection in the coding regions and selective constraints in the cis-regulatory regions. Genetics 2001 Feb;157(2):667-77.

O'Malley BW, Stein JP, Means AR., The evolution of a complex eucaryotic gene. Metabolism 1982 Jul;31(7):646-53.

Sidow A., Gen(om)e duplications in the evolution of early vertebrates. Curr Opin Genet Dev 1996 Dec;6(6):715-22

T. J. Vision, D. G. Brown, S. D. Tanksley, The Origins of Genomic Duplications in Arabidopsis. Science 290, 2114 (2000).

Friedman R, Hughes AL., Pattern and timing of gene duplication in animal genomes. Genome Res 2001 Nov;11(11):1842-7.

Gilbert W, de Souza SJ, Long M., Origin of genes. Proc Natl Acad Sci U S A 1997 Jul 22;94(15):7698-703.
Full text: <a href="http://www.pnas.org/cgi/content/full/94/15/7698" target="_blank">http://www.pnas.org/cgi/content/full/94/15/7698</a>

Domon C, Steinmetz A., Exon shuffling in anther-specific genes from sunflower. Mol Gen Genet 1994 Aug 2;244(3):312-7.

Huang CH, Kikuchi M, McCreary J, Blumenfeld OO., Gene conversion confined to a direct repeat of the acceptor splice site generates allelic diversity at human glycophorin (GYP) locus. J Biol Chem 1992 Feb 15;267(5):3336-42.

Holmes N, Parham P., Exon shuffling in vivo can generate novel HLA class I molecules. EMBO J 1985 Nov;4(11):2849-54.

Jones JM, Huang JD, Mermall V, Hamilton BA, Mooseker MS, Escayg A, Copeland NG, Jenkins NA, Meisler MH., The mouse neurological mutant flailer expresses a novel hybrid gene derived by exon shuffling between Gnb5 and Myo5a. Hum Mol Genet 2000 Mar 22;9(5):821-8.

Harayama S., Artificial evolution by DNA shuffling. Trends Biotechnol 1998 Feb;16(2):76-82.

Jelesko JG, Harper R, Furuya M, Gruissem W., Rare germinal unequal crossing-over leading to recombinant gene formation and gene duplication in Arabidopsis thaliana. Proc Natl Acad Sci U S A 1999 Aug 31;96(18):10302-7.

Kolkman JA, Stemmer WP., Directed evolution of proteins by exon shuffling. Nat Biotechnol 2001 May;19(5):423-8.

Ostermeier M, Benkovic SJ., Evolution of protein function by domain swapping. Adv Protein Chem 2000;55:29-77.

Patthy, La´szlo ´, Genome evolution and the evolution of exon-shuffling —a review. Gene 238 ( 1999) 103–114.

Hiller R, Hetzer M, Schweyen RJ, Mueller MW., Transposition and exon shuffling by group II intron RNA molecules in pieces. J Mol Biol 2000 Mar 24;297(2):301-8.

De Chateau M, Bjorck L., Protein PAB, a mosaic albumin-binding bacterial protein representing the first contemporary example of module shuffling. J Biol Chem 1994 Apr 22;269(16):12147-51.

de Chateau M, Bjorck L., Identification of interdomain sequences promoting the intronless evolution of a bacterial protein family. Proc Natl Acad Sci U S A 1996 Aug 6;93(16):8490-5.

Dwyer DS., Assembly of exons from unitary transposable genetic elements: implications for the evolution of protein-protein interactions. J Theor Biol 1998 Sep 7;194(1):11-27.

Hughes DC., MIRs as agents of mammalian gene evolution. Trends Genet 2000 Feb;16(2):60-2.

Moran JV, DeBerardinis RJ, Kazazian HH Jr., Exon shuffling by L1 retrotransposition. Science 1999 Mar 5;283(5407):1530-4.

Eickbush T., Exon shuffling in retrospect. Science 1999 Mar 5;283(5407):1465;1467.

Li X, Scaringe WA, Hill KA, Roberts S, Mengos A, Careri D, Pinto MT, Kasper CK, Sommer SS., Frequency of recent retrotransposition events in the human factor IX gene. Hum Mutat 2001 Jun;17(6):511-9.

Ried K, Rao E, Schiebel K, Rappold GA., Gene duplications as a recurrent theme in the evolution of the human pseudoautosomal region 1: isolation of the gene ASMTL. Hum Mol Genet 1998 Oct;7(11):1771-8.

Enright AJ, Ouzounis CA., Functional associations of proteins in entire genomes by means of exhaustive detection of gene fusions. Genome Biol 2001;2(9):RESEARCH0034

Doolittle RF., Do you dig my groove? Nat Genet 1999 Sep;23(1):6-8.

Zuckerkandl E., Intrinsically driven changes in gene interaction complexity. I. Growth of regulatory complexes and increase in number of genes. J Mol Evol 2001 Oct-Nov;53(4-5):539-54.

Zuckerkandl E., Neutral and nonneutral mutations: the creative mix--evolution of complexity in gene interaction systems. J Mol Evol 1997 Apr;44(4):470.

Hayashi CY, Lewis RV., Spider flagelliform silk: lessons in protein design, gene structure, and molecular evolution. Bioessays 2001 Aug;23(8):750-6. [many related articles]

Long M, Langley CH, Natural selection and the origin of jingwei, a chimeric processed functional gene in Drosophila. Science 1993 Apr 2;260(5104):91-5 [many related articles]

Begun DJ., Origin and evolution of a new gene descended from alcohol dehydrogenase in Drosophila. Genetics 1997 Feb;145(2):375-82

Betran E, Ashburner M., Duplication, dicistronic transcription, and subsequent evolution of the Alcohol dehydrogenase and Alcohol dehydrogenase-related genes in Drosophila. Mol Biol Evol 2000 Sep;17(9):1344-52.

Nurminsky DI, Nurminskaya MV, De Aguiar D, Hartl DL., Selective sweep of a newly evolved sperm-specific gene in Drosophila. Nature 1998 Dec 10;396(6711):572-5. [related articles]

Brosius J., RNAs from all categories generate retrosequences that may be exapted as novel genes or regulatory elements. Gene 1999 Sep 30;238(1):115-34.

Kuryshev VY, Skryabin BV, Kremerskothen J, Jurka J, Brosius J., Birth of a gene: locus of neuronal BC200 snmRNA in three prosimians and human BC200 pseudogenes as archives of change in the Anthropoidea lineage. J Mol Biol 2001 Jul 27;310(5):1177-8. [and related articles]

Rhoads DM, Levings CS 3rd, Siedow JN., URF13, a ligand-gated, pore-forming receptor for T-toxin in the inner membrane of cms-T mitochondria. J Bioenerg Biomembr 1995 Aug;27(4):437-45. [and related articles]

Courseaux A, Nahon JL., Birth of two chimeric genes in the Hominidae lineage. Science 2001 Feb 16;291(5507):1293-7.

Lloyd Demetrius, Directionality principles in thermodynamics and evolution Proc. Natl. Acad. Sci. USA Vol. 94, pp. 3491-3498, April 1997

Taylor JS, Van de Peer Y, Meyer A., Genome duplication, divergent resolution and speciation. Trends Genet 2001 Jun;17(6):299-301.

Christoph Adami*, , Charles Ofria ,§, and Travis C. Collier, Evolution of biological complexity Proc. Natl. Acad. Sci. USA, Vol. 97, Issue 9, 4463-4468, April 25, 2000.
Ohta T., Mechanisms of molecular evolution. Philos Trans R Soc Lond B Biol Sci 2000 Nov 29;355.

Patthy L., Exon shuffling and other ways of module exchange. Matrix Biol 1996 Nov;15(5):301-10; discussion 311-2.

Soltis DE, Soltis PS., Polyploidy: recurrent formation and genome evolution. TRENDS IN ECOLOGY AND EVOLUTION 1999 Sep;14(9):348-352.

Ohta T., Evolution of gene families. Gene 2000 Dec 23;259(1-2):45-52.
That's only a partial list. I lost everything that was catelogued on the antievolution,org thread. So there's lots of additional and especially recent examples that could be added to this list.

theyeti
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Old 10-04-2002, 01:21 PM   #18
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Hello everyone,

I just attended a seminar about transposons, but rather than hijack this thread, I started a new one <a href="http://iidb.org/cgi-bin/ultimatebb.cgi?ubb=get_topic&f=58&t=001492" target="_blank">HERE</a>.

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[ October 04, 2002: Message edited by: scigirl ]</p>
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Old 10-04-2002, 01:36 PM   #19
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Peez,

The relevance of the carrying capacity is there - I should have explained why I thought so.

Why is marriage discouraged amoung family? Reason is because children born are more likely to suffer from a genetic disease. Not to go into details I will leave it at that.

Thus if the carrying capacity is reached we have a relatively "fixed" number of individuals present and the number from which to choose a mate will no longer increase.

As mutations are continually occurring genetic diseases will increase in concentration in ratio to the population that is "fixed".
Therefore as time goes on the concentration will increase and partners will have a higher probablity of meeting someone else with the same faulty genes....exactly the same as the danger of having children with someone related to you.

This is just my thoughts and how I view it, I could be wrong probably am but that's just what I think.
I mean think of the thousands of genetic disorders that are around, do they remain constant or have they increased since the beginning of time?


Quote:
Since only about 2% of the human genome is composed of genes that are actually expressed most mutations have little affect on anything.
And yet look at all the genetic disorders that we have today...
Also do mutations occur randomly throughout the whole 100% or are they more concentrated in the 2% that are actually expressed.

Quote:
Mutations are believed to bring only a 1 % change in the genome of higher eukaryotes every 10 million years. So there is no impending doom from accumulation of mutations IMO.
If you think about it, if there never were any mutations we would all be cynobacteria or somthing living in a deep sea vent.
Mutations are BELIEVED to bring about..... Not good at all, that means faith and that means that estimate of 1% change every 10million years could be way off mark.

"If you think about it, if there never were any mutations we would all be cynobacteria...."

Maybe this isn't the best kind of reasoning to use, for it's said that mutations made us what we are - you can't argue this and say - if it wasn't mutations then we wouldn't be here today.
Circular reasoning if you follow my drift.

Peez,

Quote:
??? Are you suggesting that everyone who has an allele (gene) that is deleterious will immediately die? Are you aware that only 1% of the alleles responsible for cystic fibrosis are found in people who suffer from cystic fibrosis?
Again sorry peez, maybe it will make more sense now that I explained what I was getting at when I mentioned carrying capacity.
If the concentration of these alleles increases in the population then it would be logical to assume that partners are more likely to have these alleles and hence the problems begin..

Most of us will have some defective allele and it's when we have a child with someone else who also has this same defective allele that the children are at risk.

Yo, I have a question here. Do mutations only occur "naturally" when a sperm and egg meet - right at the start of our lives? - You know what I mean.

A truthful answer please;

Is the DNA code of man improving or not - based on the facts that we have at present? If it's both then which way is the balance - towards getting "better" or getting "worse"?
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Old 10-04-2002, 02:12 PM   #20
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DavidH,

One way our genome DOES get rid of mutations is through homologous recombination during meiosis.

I talk a little bit about this <a href="http://iidb.org/cgi-bin/ultimatebb.cgi?ubb=get_topic&f=58&t=001492" target="_blank">here</a> if you want to wade through it. . . .

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