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Living Fossils Destroy Evolution


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#41 MarkForbes

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Posted 28 February 2011 - 01:15 AM

...Gene duplication does not add novel information to the genome....

But that's the argument that Richard Dawkins is using :D :
http://www.skeptics....tion-challenge/
So why can't you simply accept it :D ?

I agree they are dodging the issue:
http://answers.yahoo...01122444AAfErT3

What's really interesting about Richard Dawkins approach is that he's mentioning computers in his argument.

..DNA carries information in a very computer-like way, and we can measure the genome’s capacity in bits too, if we wish. DNA doesn’t use a binary code, but a quaternary one...



#42 Spectre

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Posted 28 February 2011 - 05:46 AM

But that's the argument that Richard Dawkins is using  :D  :
http://www.skeptics....tion-challenge/

He even admits that very little of the genome is actually used. If gene duplication is the only way that mutations occur, then darwinism has a serious issue. There are actually scientific papers in the works by secular scientists to challenge darwinism. Creationists also have papers lined up for publication as well. Gene duplication is simply a means to preserve information on the genome. The mutations themselves are always a result of a loss of information on a duplicated gene. If this is the case, then abiogenesis and natural selection can not work together in evolution because the DNA that is used to tinker and cause mutations today would never be able to arise.

In summary, no matter how much information is used on the genome, the percentage of the genome that is used does not increase. Mutations are actually a loss of relevant information that is actually used by the genome. This is the problem that materialistic evolutionists ignore.


why can't you simply accept it  :D ?

My parents taught me not to listen to fools. :)

I agree they are dodging the issue:
http://answers.yahoo...01122444AAfErT3 What is really interesting about Richard Dawkins approach is that he's mentioning computers in his argument.

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And who said that no one can learn anything from Creationists? It's ironic that people accuse Creationists of using these type of arguments as "strawmans." Materialistic evolution is nothing but the largest double standard in history.

Great links, thanks for sharing!

#43 Calypsis4

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Posted 28 February 2011 - 07:57 AM

He even admits that very little of the genome is actually used. If gene duplication is the only way that mutations occur, then darwinism has a serious issue. There are actually scientific papers in the works by secular scientists to challenge darwinism. Creationists also have papers lined up for publication as well. Gene duplication is simply a means to preserve information on the genome. The mutations themselves are always a result of a loss of information on a duplicated gene. If this is the case, then abiogenesis and natural selection can not work together in evolution because the DNA that is used to tinker and cause mutations today would never be able to arise.

In summary, no matter how much information is used on the genome, the percentage of the genome that is used does not increase. Mutations are actually a loss of relevant information that is actually used by the genome. This is the problem that materialistic evolutionists ignore.

My parents taught me not to listen to fools. :D


Amen!

My parents didn't teach me to not listen to fools. I had to learn that on my own.

#44 JoshuaJacob

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Posted 28 February 2011 - 12:38 PM

How can something that is a duplicate of something else be new information? Unless you are trying to say that the duplicate is in some way new information, which is kinda like cutting off your nose to spite Your face.

#45 MarkForbes

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Posted 28 February 2011 - 02:39 PM

How can something that is a duplicate of something else be new information? ....

If I understand the evolutionists argument correctly, they try to make a combined argument. And that is duplication + a series of mutations that end up producing something useful.

Imagine the initial genetic code is TOWER.
First Duplication and you will get: TOWER TOWER
Then a series of mutations and you get the following:
TOWER POWER
TOWER POKER
etc.

There are a few problems with that. One of those is that for complex novel subsystems to arise you need to have a couple of fitting meaningful changes at one, and often they are interdependent. For many things, this is virtually impossible to happen.

#46 Spectre

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Posted 28 February 2011 - 03:30 PM

If I understand the evolutionists argument correctly, they try to make a combined argument. And that is duplication + a series of mutations that end up producing something useful.

Imagine the initial genetic code is TOWER.
First Duplication and you will get: TOWER TOWER
Then a series of mutations and you get the following:
TOWER POWER
TOWER POKER
etc.

There are a few problems with that. One of those is that for complex novel subsystems to arise you need to have a couple of fitting meaningful changes at one, and often they are interdependent. For many things, this is virtually impossible to happen.

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And again, I want to reiterate and contribute to Mark's point.

This is what we observe in evolution, gene duplications and errors produce mutations that may or may not be useful. If this is the only way mutations happen, abiogenesis and materialistic evolution as a whole, including natural selection has a very serious problem. Gene duplication is an example of micro evolution and speciation. Materialistic evolutionists again attempt to present this observation of evolution at speciation or below as an argument for observing evolution past speciation.

#47 Mitch

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Posted 28 February 2011 - 06:23 PM

How can something that is a duplicate of something else be new information? Unless you are trying to say that the duplicate is in some way new information, which is kinda like cutting off your nose to spite Your face.

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If a gene has duplicated, one copy of which has mutated, then both length and variety will have been added to the genome. How can that not amount to an increase in information on the genome?

#48 Mitch

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Posted 28 February 2011 - 06:31 PM

I read the rules, you should of too or you are willfully ignorant of them.

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If you think I've broken a rule complain to a Mod, otherwise stick to the issues. Making insinuations about rule-breaking, telling people what they "deserve" and implying evolutionary biologists are fools (post 42) is not an adult discussion and not worthy of my free time.

#49 Spectre

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Posted 28 February 2011 - 06:53 PM

If you think I've broken a rule complain to a Mod, otherwise stick to the issues.  Making insinuations about rule-breaking, telling people what they "deserve" and implying evolutionary biologists are fools (post 42) is not an adult discussion and not worthy of my free time.

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The principle point is I fully addressed your arguments but you failed to address mine. I even posted an excerpt from a paper in a scientific journal that disagrees with your interpretation of mutations on the genome.(In which you never commented on it and continued on with your logical fallacies.)

If you weren't equivating the entire time and using basically conjecture throughout the debate I wouldn't of mentioned the rules. By what you deserve I meant I was giving you too much leeway for even arguing natural selection with you when abiogenesis is an even weaker subject.

I apologize that you feel offended but we have MANY evos that come here and try to shift the goal posts during arguments and it just gets old. I am not trying to be harsh to you, I am just telling you exactly how things are, no sugarcoating applied.

#50 AFJ

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Posted 28 February 2011 - 07:36 PM

We know gene duplication occurs and we know mutations occur.  How could a gene that has duplicated, one of copy of which has mutated, not amount to an increase of information on the genome? What specifically that I believe in is supernatural?  Mutations that add to the genome?  The answer is gene duplication (which has been observed), we've discussed that.

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Mitch,
Below is a partial list of regulatory enzymes which regulate our bodies. Each one of them have at least 25 copies (not new genes), and some have thousands. Why is it that you insist this is some kind of evolution? It's just like ribosomes--the cell has thousands of them so translation can take place. The body constantly needs many of these enzymes and regulatory factors, so they are designed because that is what it takes for homeostasis.

Furthermore, the duplicated genes were here already, when they were discovered within the last century. No one saw their beginning.

Divergence, or the creation of new genes by duplication is assumed to have happened in the past. No one is observing this happen right now. Because two species have different genes, it is assumed these took place millions of years ago, and that it was a mutation in a duplication of of gene. Note evolution is already assumed instead of creation of dupicated genes, like the ones in the list below.

Look here. The author most assuredly tells us divergence took place 35 million years ago in drosyphylia. All these things are based on assumed mutation rates and that the different genes, are "new genes" that happened a certain time ago. Of the which they have not a shred of evidence--only the differing genes--which they assume said process of gene duplictation took place. No rates given, or how they arrived at those rates. No one saw this happen, but we are just supposed to swallow this swill. Oh, and the kicker--those who object to their theory are religiously motivated. No--I object because the science they use is wacky assumption. NO proof at all.


Transcription Factors Sterol Regulatory Element Binding ProteinATF4[1][5] Activating transcription factor 4
BTF3[1][5]
E2F4[1]
ERH (gene)[1][5] Enhancer of rudimentary homolog of drosophila (which in turn is the first enzymatic step in pyrimidine synthesis. Regulated by MITF)
HMGB1[1][5] High mobility group box binds DNA
ILF2[1]
IER2[1] formerly ETR101 Immediate Early Protein
JUND[1][5]
LTBP4[1]
LMO1[1] Rhombotin 1
MYC[1][5] also considered an oncogene when mutated regulates transcription of 15% of all genes
PAX8[1]
PHF1[1][5] Plant homology domain
PTTG1IP[1]
SREBF1[1] Sterol Regulatory Element Binding Protein Smith Magenis
TBP[6] aka TATA-binding protein or GTF2D or TFIID
TCEB2[1][5] Elongin
TCOF1[1] interacts with UBF to translate rRNA

Repressors
ANF91, HPF7, HTF10 [1] Kruppel Associated Box domain
ID3 (gene)[1] inhibits DNA binding
PUF60[1][5]
NFKBIA[1][5] Suppresses NF-kappa
RING1[1]

RNA Splicing
Small nuclear ribonucleoprotein-associated proteins B and B'ADAR[1]
BAT1[5]
FBL[1] Fibrillarin
HNRPD[1][5]
HNRPK[1][5]
PTBP1[1]
PABPN1[1]
SFRS3[5]
SFRS9[1]
SFNRPA[1]
SNRPB[1][5]
SNRPD[5]
SNRPD2[1][5]
SNRPG[1]

Translation Factors
EIF1[1][5] aka SUI1
EIF3C[1] formerly EIF3S8
EIF3D[1] formerly EIF3S4
EIF3F[1] formerly EIF3S5
EIF3I[1] formerly EIF3S2
EIF3G[1] formerly EIF3S7
EIF4A2[1]
EIF4G2[1]
TUFM[1] Tu translational elongation factor mitochondrial

tRNA Synthetases
KARS[1]
RARS[5]
SARS[1]
VARS2[1][5]
YARS[1]

RNA Binding Protein
PABPC1[1] PolyA Binding Protein
ELAVL3[1]
[edit] Ribosomal ProteinsRPL3[1]
RPL5[1][5]
RPL8[1]
RPL9[5]
RPL10[1][5]
RPL11[1]
RPL12[5]
RPL13[1][5]
RPL13A[1][5] Introns contain genes for small nucleolar RNAs U32, U33, U34, and U35
RPL14[1][5]
RPL15[1]
RPL17[1]
RPL18[1]
RPL19[1]
RPL25[5]
RPL27[1]
RPL29[1]
RPL30[5]
RPL32[1]
RPL34[1]
RPL35[1][5]
RPL36[1]
RPL37[1][5]
RPL38[1]
RPL40[5] transcribed with ubiquitin (see FAU (gene))
RPLP1[1]
RPLP2[1]
RPS2[1]
RPS5[5]
RPS9[1]
RPS10[1]
RPS11[1]
RPS12[1]
RPS13[1][5]
RPS14[1][5]
RPS15[1]
RPS16[1][5]
RPS18[1]
RPS19[1][5]
RPS20[5]
RPS23[5]
RPS24[1]
RPS25[1][5]
RPS26[5]
RPS27[5] transcribed with ubiquitin (see FAU (gene))
RPS28[5]
RPS30[1] transcribed with ubiquitin as the FAU (gene)
RPN1[1][5] Ribophorin anchors the ribosome to rough endoplasmic reticulum
MRPL9[1][5]

RNA Polymerase
POLR2A[1]
POLR2E[5]
POLR2J[5]
POLR2L [7]

Protein ProcessingCyclophilin
A[6] Serine-threonine phosphatase inhibitor involved in protein folding
CANX[1][5] Folding of glycoproteins within endoplasmic reticulum
CAPNS1[1][5] Calpain protease
NACA[1][5] Nascent polypeptide associated complex alpha polypeptide
PFDN1[1] Prefoldin 1
PFDN5[1] Prefoldin 5
SNX3[1] Sorting nexin
SNX17[5]
SNX27[5]
SSR2[1] Protein translocation in ER
SUMO2[1][5] Protein targeting

Heat Shock Proteins
HSPA8[1][5]
HSP90AB1[1]
HSBP1[1]

Nucleosome remodeling
HIST1H2BC[1]
H2AFY[1] Histone 2 Subfamily
H2AFZ[1][5] essential for embryogenesis
H3F3A[1][5] H3 Histone Famiy

Cell Cycle
ARHGAP1[1]
ARHGDIA[1][5]
CENPB[1] Centromere protein B
CTBP1[1][5]
cyclophilin
CCND3[1]
GAS1[1][5] Blocks entry into S phase
PPP2CB[1] Negative regulator of growth and cell division
PPP2R1A[5] Negative regulator of growth and cell division
RAD9[1]
KIAA0174[1][5] or IST1 homolog (locates to central dividing line of dividing cells)

Apoptosis
DAD1[1][5] Defender against cell death
DAP (gene)[1]
DAXX[1] Death Associated Protein 6
OncogenesARAF[1]
MAZ (gene)[1][5]
MYC[1][5] also considered a transcription factor
SAFB[1]
RAB1A[1]

DNA Repair/Replication
Ku80[1] aka XRCC5
MCM3AP[1] possibly a primase
[edit] MetabolismPRKAG1[1] Senses energy level and inactivates HMGCoA reductase and Acetyl CoA Carboxylase

Carbohydrate Metabolism
PRKCSH[1][5] Glucosidase 2, subunit beta (activated by PKC)
B4GALT2[1]
GUSB[6] Beta Glucuronidase Sly syndrome
Chitinase[1]
Phosphogluconate dehydrogenase[1]
GSK3A[1]
hexokinase rate limiting step? no reference
H6PD[1][5]
Glucose-6-phosphate isomerase[1]
Phosphofructokinase 1[5]
Aldolase A[5]
Aldolase C[1]
Triosephosphate isomerase[5]
GAPDH[1][5][6]
Phosphoglycerate kinase[1][5][6]
Phosphoglycerate mutase[5]
Enolase[5]
PKM2[1][5] Pyruvate kinase, muscle
Lactate dehydrogenase[1]
LDHB[1] Lactate dehydrogenase
TALDO1[1][5] Transaldolase in pentose shunt
Transketolase[1]
TSTA3[1] Mannose metabolism
[edit] Citric Acid CycleSDHA[1] Succinate Dehydrogenase subunit A
MDH1[1][5] Malate dehydrogenase
[edit] Lipid MetabolismGM2A[1] not highly expressed constitutively
HADHA[1] Trifunctional protein subunit alpha
HADHB[1][5] Trifunctional protein subunit beta


Amino Acid MetabolismCOMT[1]
Catechol-O-methyl transferase
GGTLA1[1] Gamma glutamyl transferase-like 1
PHGDH[1][5] Phosphoglycerate dehydrogenase (first and rate-limiting step of serine biosynthesis)
ODC1[1]
TPMT[1]

Nucleotide Synthesis
IMPDH2[1][5] Guanine Nucleotide biosynthesis

NADH Dehydrogenase
NDUFA1[1]
NDUFA2[1]
NDUFA7[1]
NDUFB7[1]
NDUFC1[1]
NDUFS5[1]
NDUFV2[1]
DIA1[1]

Cytochrome C Oxidase
(Note that COX1, COX2, and COX3 are mitochondrially encoded)

COX4I1[1]
COX5A[1]
COX5B[1][5]
COX6A1[1]
COX6B1[1][5]
COX7A2L[1]
COX7C[1]
COX8[1]
CYC1[1]
UQCRC1[1]
UQCRH[1]
UQCRQ[1][5] see Cytochrome C1




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