same designer, same design.

[matthewgar]

Well all heard the explanation for homology, and genetics for why closly related species appear to be related, why humans share so much of the same DNA and genes with other apes and such. That because many of the genes in apes have the same function in humans of course they would look simular, like how a chevy truck and a GM truck look simular since they serve a simular purpose and so on.

And people focus on both sides on the simularities and such, but has there ever been good explanation for the many simularities that are both remnants of old genes, broken genes, or non effecting changes that are found along many lines that evolution expects. Read a good book called Relic of Eden, wich spends more time focusing on the evidence for evolution that we shouldn't expect to see if everything was created in their present form, or present kind.

Things like genes that copy themselves and will randomly get reinserted back into the genome being found in the same locations that fit evolution. Gorilla's have some that neither chimpanzee's and humans have, and humans have some they share with chimpanzee's but not gorilla's, and there are even some that humans and chimpanzee's have independantly of each other. This is found in all related species and we contain some along with many other mamals, though the further from a species the extra genes tend to decay till unreconizable.

There are inversions where entire sections of a chromosone flip, it has no effect on the genes themselves since the start and stop codones are still there, and has no effect on the organism but we share many of these with other apes and quiet a few that are shared with chimpanzee's that again arn't found in gorilla's.

You have broken genes we no longer use, humans, pigs and other simular species have the genes to produce vitamin C, but at some point in our past it was broken, most likly when we were getting Vitamin C from our enviorment, you have genes like for smell in humans, 4% of our genome is devoted to scent, but majority of them are broken, dolphins have genes for scent yet don't use them. There is a gene for a protein that apes use that strenghtens the muscles in their jaws and gives them their incredible bite, we have that gene still in our genome but it's broken, and if it was still functioning it would cause us unable or having a harder time to speak.

So these plus many more I'm sure others could mention are what we find, and mean genetics show evolution and common descent, it's not just the parts that are simular it's the differences, also how many convergences despite looking the same and having the same effects and purposes don't end up looking the same genetic or even under the skin. The squid and human eye both evolved independantly yet the squid eye is superior despite having the same function and the same use.

 

[matthewgar]

no responses from creationists? Or anyone have other examples of where same designer same design doesn't adequatly explain what we see?

And just a interesting tidbit I learnt a bit ago, while only 2% of our encoding DNA is different, 50-70% of our genes are different in small ways. The gene that controls brain/skull size that has 142 base pairs, only changed about 2 base pairs between the time that chickens and chimpanzee's broke off and went down their respective lines, but 11 basepairs changed from when chimpanzee's and humans broke off, wich is one of the leading changes that made us human.

 

[Papias]

Well, I guess it's hard to argue with a complete and correct opening post!

You listed some great examples where the DNA evidence clearly supports evolution, and shows that the "common design" argument simply shows a lack of understanding of the evidence, where much of the evidence for common descent cannot be explained by the common design argument.

One good example I didn't see in your OP (did I just miss it?) was Chromosome 2. Common design wouldn't make a vestigial centromere and two end to end vestigial telomeres, yet that's what we all carry trillions of copies of in every part of our bodies.

Papias

 

[matthewgar]

Well, I guess it's hard to argue with a complete and correct opening post!

You listed some great examples where the DNA evidence clearly supports evolution, and shows that the "common design" argument simply shows a lack of understanding of the evidence, where much of the evidence for common descent cannot be explained by the common design argument.

One good example I didn't see in your OP (did I just miss it?) was Chromosome 2. Common design wouldn't make a vestigial centromere and two end to end vestigial telomeres, yet that's what we all carry trillions of copies of in every part of our bodies.

Papias

It's a great example, but I left it out because I'm rather dubious of it's signifcance in refuting common designer argument. Since if were using the same deisgner argument, then of coruse we would have had two more chromosones that fused together at some point early on. It works to refute the miss number of chromosones between apes and humans, but there are easy arguments to make against it being proof of common descent. No way of showing from the fusion that it wasn't simply 2 human chromosones that fused after god created us. Combined with the other evidence it might work but not enough on it's own.

If I'm wrong then feel free to correct me :>

 

[Papias]

Yeah, it does get complicated, and is not as easy to explain, nor with as straightforward possible past histories (as you point out), so it's not as clear.

Papias

 

[shernren]

Spelling it as "similar" will up your credibility just that wee bit more.

But yeah, I agree.

 

[Greg1234]

no responses from creationists?

No need. Psuedo genes,Vestigial structures, and junk DNA has been debunked with modern science.

And just a interesting tidbit I learnt a bit ago, while only 2% of our encoding DNA is different, 50-70% of our genes are different in small ways. The gene that controls brain/skull size that has 142 base pairs, only changed about 2 base pairs between the time that chickens and chimpanzee's broke off and went down their respective lines, but 11 basepairs changed from when chimpanzee's and humans broke off, wich is one of the leading changes that made us human.

Chickens becoming people, bacteria becoming chickens and the like is based on inference. Inference based on bacteria remaing bacteria and random mutation being sterile.

 

[matthewgar]

No need. Psuedo genes,Vestigial structures, and junk DNA has been debunked with modern science.


Chickens becoming people, bacteria becoming chickens and the like is based on inference. Inference based on bacteria remaing bacteria and random mutation being sterile.

*chuckles* you do know, that none of these are junk DNA, we know exactly what they do, and they don't do them. Show some evidence against inversions, duplicating genes, ERV's and many other examples. You have to explain away why non effecting random events would be copied across multiple species if they are not related.

And again your strawman idea of evolution arn't even worth responding too, show you understand evolution then we can discuss what is real or not.

 

[Greg1234]

*chuckles* you do know, that none of these are junk DNA, we know exactly what they do, and they don't do them. Show some evidence against inversions, duplicating genes, ERV's and many other examples. You have to explain away why non effecting random events would be copied across multiple species if they are not related.

And again your strawman idea of evolution arn't even worth responding too, show you understand evolution then we can discuss what is real or not.

The idea first stems that the copy of a gene is the result of a stochastic event. Given that a mutation within the gene is also random. The insertion of this random sequence back into the genome is not an issue, neither does the utilization of genes by organisms evidence for common ancestry. The utilization of the similar codes for a similar phenotypic trait is also not evidence for common ancestry as the genotype will reflect similarities. The idea that the locations of genes is random is based on the presumption that gene location does not play a factor. But the distribution of genes across the genome, would most likely be the subjected to the coding which enticed the duplication of the gene in the first place. There are some indications that the location of genes does in fact play a functional role in the organism. This may involve the expression of genes within the genome.

In the case of inversions, this is not evidence of common ancestry. The start and stop codons still being in place may mean that the gene is not changed but expression may be. A gene does not code for one protein, and the movement of a gene, or a gene flip (180 degrees) may have an effect not only on type of protein but the type of expression of the same one. You must first assume that the flipping a change in positional reference has no effect on the expression of that gene. But we are seeing that this may not be the case, as with the spollR gene

A short excerpt:
"The SpoIIR protein is required for the activation of the transcription program directed by

E in the mother cell. The spoIIR locus is located at 324°, near the origin of replication (0/360°). We show here that movement of spoIIR to 28° had little effect on sporulation. However, movement to regions not in the origin-proximal part of the chromosome substantially reduced sporulation efficiency. At 283° sporulation was reduced to less than 20% of the level obtained when spoIIR was at its natural location, and movement to 190° reduced sporulation to about 6% of that level. These positional effects were also seen in the transcription of a spoIIR-lacZ fusion. In contrast, movement of other spo-lacZ fusions from 28° to 190° had little effect on their expression. These results suggest that spoIIR is the subject of "positional regulation," in the sense that the chromosomal position of spoIIR is important for its expression and function."

The usage of "positional regulation" is not automatically the result of a common decent.

The use of retro viral like sequences stems firstly from the idea of Junk DNA, and that the waste land that it is, remains as the store house. But seeing that "Junk" DNA is actually purposeful, and that insertions are actually directed, this is not conclusive of common decent.

The real question is how you built a man from bacteria through random mutation when tests indicate results to the contrary.

 

[shernren]

as with the spollR gene:

A short excerpt:
"The SpoIIR protein is required for the activation of the transcription program directed by

E in the mother cell. The spoIIR locus is located at 324°, near the origin of replication (0/360°). We show here that movement of spoIIR to 28° had little effect on sporulation. However, movement to regions not in the origin-proximal part of the chromosome substantially reduced sporulation efficiency. At 283° sporulation was reduced to less than 20% of the level obtained when spoIIR was at its natural location, and movement to 190° reduced sporulation to about 6% of that level. These positional effects were also seen in the transcription of a spoIIR-lacZ fusion. In contrast, movement of other spo-lacZ fusions from 28° to 190° had little effect on their expression. These results suggest that spoIIR is the subject of "positional regulation," in the sense that the chromosomal position of spoIIR is important for its expression and function."

Just a comment on this. What is happening is that the chromosome of the organism of interest (a Bacillus) is a ring chromosome. Thus, the position of the spoIIR locus is specified in degrees corresponding to where it is along the ring chromosome relative to the origin.

A change of 180 degrees thus isn't a "flip"; it means that the gene sequence has been moved halfway along the ring, retaining the same order of nucleotides that it originally had. It has not been inverted; to my knowledge (though I may be wrong) the inversion of a sequence would be very unlikely to code for anything meaningful, as DNA and RNA have "forward" and "backward" directions that are chemically distinct.

 

[matthewgar]

The idea first stems that the copy of a gene is the result of a stochastic event. Given that a mutation within the gene is also random. The insertion of this random sequence back into the genome is not an issue, neither does the utilization of genes by organisms evidence for common ancestry. The utilization of the similar codes for a similar phenotypic trait is also not evidence for common ancestry as the genotype will reflect similarities. The idea that the locations of genes is random is based on the presumption that gene location does not play a factor. But the distribution of genes across the genome, would most likely be the subjected to the coding which enticed the duplication of the gene in the first place. There are some indications that the location of genes does in fact play a functional role in the organism. This may involve the expression of genes within the genome.

In the case of inversions, this is not evidence of common ancestry. The start and stop codons still being in place may mean that the gene is not changed but expression may be. A gene does not code for one protein, and the movement of a gene, or a gene flip (180 degrees) may have an effect not only on type of protein but the type of expression of the same one. You must first assume that the flipping a change in positional reference has no effect on the expression of that gene. But we are seeing that this may not be the case, as with the spollR gene

A short excerpt:
"The SpoIIR protein is required for the activation of the transcription program directed by

E in the mother cell. The spoIIR locus is located at 324°, near the origin of replication (0/360°). We show here that movement of spoIIR to 28° had little effect on sporulation. However, movement to regions not in the origin-proximal part of the chromosome substantially reduced sporulation efficiency. At 283° sporulation was reduced to less than 20% of the level obtained when spoIIR was at its natural location, and movement to 190° reduced sporulation to about 6% of that level. These positional effects were also seen in the transcription of a spoIIR-lacZ fusion. In contrast, movement of other spo-lacZ fusions from 28° to 190° had little effect on their expression. These results suggest that spoIIR is the subject of "positional regulation," in the sense that the chromosomal position of spoIIR is important for its expression and function."

The usage of "positional regulation" is not automatically the result of a common decent.

The use of retro viral like sequences stems firstly from the idea of Junk DNA, and that the waste land that it is, remains as the store house. But seeing that "Junk" DNA is actually purposeful, and that insertions are actually directed, this is not conclusive of common decent.

The real question is how you built a man from bacteria through random mutation when tests indicate results to the contrary.

First off ERV"s are random and not directed, they appear so due to the fact that if they are inserted into a sperm or egg cell, and add themselves to the middle of say a major protein the fetus never survives. But yes the junk DNA is still quiet junk, some of it is better known, but there is alot that just doesn't do anything, and we say this because we know what that does or doesn't do. You guys have taken a qoute that says we better understand that there is less junk DNA and then taken it to mean there is none, you guys need to stop quote mining and such.

As for the duplication of the gene, your missing the point, chimpanzee's and humans share many *though chimpanzee's have a new duplicating gene that we don't* of the same genes in the SAME LOCATIONS. Not just ones that are whole, but *gasp* Ones that are broken, ones that show simular decays in duplications that predate the split, though not all are 100%.

Same design, same designer fails to explain why random elements, even if they have potential to be more directed end up being overlapping for large chunks. That be like you covering up half of a dart board so every other section is covered in hard metal, so that when I throw 10 darts only 4 stick, then I duplicate that onto another board, so each board has 4, then you throw 10, and I throw 10 more at mine, the first 4 will be in the same places, but any that hit in the last 10 arn't. But we can see that 4 of them statisticly couldn't be random even though there is a higher chance they will hit certain areas of the dart board. Where they hit in those areas is still random.

 

[Mallon]

I never liked the "same design, same designer" argument. It never made sense to me. If similarities suggest a common designer, do dissimilarities suggest different designers? Do a cat and a dog share a common designer because of their shared similarities, and a snail a different designer because it is relatively unlike the other two species?

 

[Greg1234]

First off ERV"s are random and not directed,

ERV insertions go through a purification process which starts with deliberate selection.

But yes the junk DNA is still quiet junk,

Darwinist literature. Not its not.

As for the duplication of the gene, your missing the point, chimpanzee's and humans share many *though chimpanzee's have a new duplicating gene that we don't* of the same genes in the SAME LOCATIONS. Not just ones that are whole, but *gasp* Ones that are broken, ones that show simular[*similar] decays in duplications that predate the split, though not all are 100%.

So a chimp and a human duplicate a gene. Broken genes are said to be broken through comparisons with other genes of the same sequence and comparing their function. A genetic expression often utilizes the linguistic component called homonyms. Which means that a single gene can code for many different proteins although exhibiting the same sequence. Much like "bank" can mean an embankment, or a place where money is kept. In DNA, a single gene can encode for as much as 50 proteins. This is because DNA can make decisions acting as a bio-computer.

Same design, same designer fails to explain why random elements

Just given. And im not an adherent to random mutation.

 

[Greg1234]

Just a comment on this. What is happening is that the chromosome of the organism of interest (a Bacillus) is a ring chromosome. Thus, the position of the spoIIR locus is specified in degrees corresponding to where it is along the ring chromosome relative to the origin.

A change of 180 degrees thus isn't a "flip"; it means that the gene sequence has been moved halfway along the ring, retaining the same order of nucleotides that it originally had. It has not been inverted; to my knowledge (though I may be wrong) the inversion of a sequence would be very unlikely to code for anything meaningful, as DNA and RNA have "forward" and "backward" directions that are chemically distinct.

If movement is not the flip he meant then this was already given in gene location. A flip having a similar effect.

 

[matthewgar]

If movement is not the flip he meant then this was already given in gene location. A flip having a similar effect.

When I say flips having no effect refers to this.

Start-> gene -> end codes the same as dne <- eneg <- tarts, since were talking three dimensionally here. If you take four blocks and spell it gene then flip then look at them from 180 degree's they will show both gene and eneg. Least thats how I'm understanding it, what matters is where the gene is started to code from not wich direction it is. The same proteins are formed in the same order regardless of wich way it faces.