The Coccyx

[xianghua]

After all, if all vertebrates were created de novo from nothing during the creation week, by what logic would this creator put the same embryonic structures in fish and human embryos at any point in the first place?

first: what about the difference in the embryonic stage between some species? have you look at a salamander embryo for instance?


secondly: why the engine in both a car and a truck is in the same place (in most cases in the front)? is this because of a common descent or a common designer?

 

[PsychoSarah]

"A vestigial structure, by definition, has reduced or lost original function."

Even by this definition the coccyx in humans is NOT, since it is neither.

-_- yes, because it lost the function of supporting a tail. That's what the structure does in animals with tails.

 

[ViaCrucis]

first: what about the difference in the embryonic stage between some species? have you look at a salamander embryo for instance?


secondly: why the engine in both a car and a truck is in the same place (in most cases in the front)? is this because of a common descent or a common designer?

Automobiles are not living organisms which reproduce and pass on their genetic information to a succeeding generation.

-CryptoLutheran

 

[PsychoSarah]

so the argument is that if its similar to a tail then its a tail?

-_- it's physiologically indistinguishable from the structure that becomes tails in species with tails, is directed to form by genes associated with tail development, and is dissolved through directed cell death rather than becoming anything. Are you going to argue that the webbing between the fingers and toes of a human embryo isn't actually webbing? Because far more people have been born with that than tails. http://doctorsdemystify.homestead.com/DD2010/simple_syndactyly_both_imrs.JPG

i can actually give you the original paper(if its make any difference):

Feather Development Genes and Associated Regulatory Innovation Predate the Origin of Dinosauria

Ah, this makes a huge difference, actually. Since the genes mentioned in the article are estimated to have originated before the existence of dinosaurs, it is possible that quite a few of them also predate the split between the evolutionary lines of dinosaurs and mammals (note: mammals do not have dinosaur ancestors, the split happened before either group existed). When they mentioned humans, they brought up that humans shared about 7% of the feather genes that chickens have in some form or another (regulatory genes and the like that are also related to feathers, not genes that alone produce them or don't have other functions). This is compared with previous estimates of 5%. So, that makes for a notable difference in actual shared genes, yes. However, again, that doesn't make humans or any other mammal developing feathers spit in the face of evolution any less. Furthermore, plenty of the genes they bring up that aren't present in mammals could have developed prior to the existence of dinosaurs, since the evolutionary lines of mammals and dinosaurs split tens of millions of years before the existence of either group.

Mammals developed hair and fur. There are no selective pressures that would result in mammals with feathers, because fur already covers most of the same basic functions of feathers (aside from, perhaps, attracting a mate, to which I bring up that mammals rarely have sexual selection as extreme as birds). Furthermore, enough of the feather genes just aren't present for the advent of feathers to be repeated in mammals.

 

[xianghua]

Automobiles are not living organisms which reproduce and pass on their genetic information to a succeeding generation.

-CryptoLutheran

so if they was able to to that you will not ocnsidering those cars as a product of design?

 

[xianghua]

-_- it's physiologically indistinguishable from the structure that becomes tails in species with tails,

are you talking about the whole tail? because its very different from a standard tail. a real tail have bones and the abillity to move. a human "tail" doesnt have those traits. so they are very different.

is directed to form by genes associated with tail development,

those genes also associated with others functions. so again; we cant conclude that human have genes for a tail.

and is dissolved through directed cell death rather than becoming anything.

a lots of structures dissolving during the embryo development:

Apoptosis - Wikipedia

Furthermore, enough of the feather genes just aren't present for the advent of feathers to be repeated in mammals.

we can claim for a convergent evolution in the genetic level, or a convergent gene loss (from mammals) or even lgt. anything is possible according to evolution.

 

[ViaCrucis]

so if they was able to to that you will not ocnsidering those cars as a product of design?

If I designed a machine that could reproduce as a living organism with genetic information, it would be known that it was designed, and so the question would be moot anyway. It would be known, because I designed it.

-CryptoLutheran

 

[xianghua]

If I designed a machine that could reproduce as a living organism with genetic information, it would be known that it was designed

true. but what if you will find it on a far planet? do you will conclude design or a natural process in this case?

 

[ViaCrucis]

true. but what if you will find it on a far planet? do you will conclude design or a natural process in this case?

If I found an organism on another planet I'd assume it evolved there.

-CryptoLutheran

 

[xianghua]

If I found an organism on another planet I'd assume it evolved there.

-CryptoLutheran

so if you will find a self replicating robot (or a watch) that made from organic components on another planet you will not conclude design?

 

[Speedwell]

so if you will find a self replicating robot (or a watch) that made from organic components on another planet you will not conclude design?

No. Functional organization is not, in itself, evidence of design.

 

[PsychoSarah]

are you talking about the whole tail? because its very different from a standard tail. a real tail have bones and the abillity to move. a human "tail" doesnt have those traits. so they are very different.

I am talking about comparing embryonic stages, not fully developed organisms. Human embryo tails are structurally practically identical as the embryo tails of species that normally do have fully functional tails. Humans do not have the genes to produce a fully functional tail, and our ancestors have been without tails long before humans existed. However, this doesn't explain away the pointless embryonic tail structure that develops only to later die off.

those genes also associated with others functions. so again; we cant conclude that human have genes for a tail.

-_- the other functions of these genes are irrelevant, since analogous genes could easily be substituted (by a creator) that don't involve the development of a tail doomed to die off.

a lots of structures dissolving during the embryo development:

Apoptosis - Wikipedia

Indeed, and all of those structures are pointless in the end. Why waste time and energy producing structures that are only going to die off in the end? That doesn't sound like an intelligent design in the slightest. I find chicken teeth to be the most unforgivable example of this type of structure. They exist so briefly, that it is genuinely difficult to observe it despite how easy it is to get a hold of chicken embryos.

we can claim for a convergent evolution in the genetic level, or a convergent gene loss (from mammals) or even lgt. anything is possible according to evolution.

-_- no, that is the least accurate statement about evolution I have ever heard. A pig cannot give birth to a human without intelligent intervention. That cannot happen and retain the validity of evolution. Convergent evolution only applies to structures that are outwardly similar but are genetically distinct (and have structural differences, no matter how minor they may seem). Whales being more genetically similar to snakes than mammals would disprove evolution. In fact, MOST imaginable biological developments would defy evolution to a ridiculous extent. The ones that actually happen don't defy the theory in any significant way, though, which is a testament to how accurately the theory represents reality.

 

[xianghua]

However, this doesn't explain away the pointless embryonic tail structure that develops only to later die off.

apoptosis is actually very important to the embrio development:


"n addition to its importance as a biological phenomenon, defective apoptotic processes have been implicated in a wide variety of diseases."

"removing or modifying one component leads to an effect in another. In a living organism, this can have disastrous effects, often in the form of disease or disorder."

so maybe this "tail like" structure isnt a tail at all.

-_- the other functions of these genes are irrelevant, since analogous genes could easily be substituted (by a creator) that don't involve the development of a tail doomed to die off.

what do you mean by that? if it have other function then a tail development even in mouse, we cant claim that its a "tail gene" anymore.

I find chicken teeth to be the most unforgivable example of this type of structure. They exist so briefly, that it is genuinely difficult to observe it despite how easy it is to get a hold of chicken embryos.

even if those are real teeth it will be an evidence for degeneration and not evolution.

Convergent evolution only applies to structures that are outwardly similar but are genetically distinct .

why? a convergent evolution also found in the genetic level . so there is no problem for evolution to evolve feathers twice.

 

[tas8831]

first: what about the difference in the embryonic stage between some species? have you look at a salamander embryo for instance?

Can you be more specific?

Yes, I have seen salamander embryos. They have a pharyngeal apparatus.

secondly: why the engine in both a car and a truck is in the same place (in most cases in the front)? is this because of a common descent or a common designer?

Yes, a common human designer.

What is your point?

What we do NOT see, which would be a more apt analogy, is a truck factory that first builds a car, then removes the back half and straps on a truck bed.

 

[tas8831]

first: what about the difference in the embryonic stage between some species? have you look at a salamander embryo for instance?


secondly: why the engine in both a car and a truck is in the same place (in most cases in the front)? is this because of a common descent or a common designer?

Already replied. And got no response.

 

[AV1611VET]

The common ancestors of all apes lived over 14 million years ago and had already lost their tails. It is of no surprise that we don't have much left for a functional tail in our genes.

Ya ... thanks a lot Ms Nature.

You took our tails from us, and now we have to walk with canes and walkers; not to mention that some fall and can't get up.

Real thoughtful of you.

And speaking of thoughtless, you've amassed quite a following over the years: scientists.

 

[46AND2]

But I have to disagree. Their use of the phrase “not two separate infections” is deceptive, because the same infection, in two similar species during the exact time frame, would produce the exact same results that we observe, and therefore it would not be necessary that they be two “separate” infections at all (they are implying this is a claim that has been made, though I searched and could not find it...if one of you do please post a link) and would thus NOT imply an assumption of common descent.

What does this even mean? The same infection of two separate species? Please explain how this is possible.

 

[tas8831]

Now it is generally accepted as Rational Wiki puts it (atheist equivalent of Answers in Genesis) “If two organisms share the same ERV, in the same location, with the same inactivation mutations, then they almost certainly share them due to common inheritance and not two separate infections.”

But I have to disagree. Their use of the phrase “not two separate infections” is deceptive, because the same infection, in two similar species during the exact time frame, would produce the exact same results that we observe, and therefore it would not be necessary that they be two “separate” infections at all (they are implying this is a claim that has been made, though I searched and could not find it...if one of you do please post a link) and would thus NOT imply an assumption of common descent.

Time out...


Let us look at your 'rebuttal'.

In response to:

"“If two organisms share the same ERV, in the same location, with the same inactivation mutations, then they almost certainly share them due to common inheritance and not two separate infections.”

you write:

"...because the same infection, in two similar species during the exact time frame, would produce the exact same results that we observe,"



When you say "same results", are you referring to the 'the same ERV, in the same location',
or 'the same inactivation mutations'?


I note that the entirety of your rebuttal was merely to state an unsupported opinion regarding a desire to 'improve' phylogenetic trees' (more on that gibberish in a moment).

Please EXPLAIN, without copy-pastes or doctored quotes, HOW, exactly, a viral genome could be inserted at the exact same locus in a chromosome of 2 different species (given that the target integration sites are literally all over the genome*), AND possess the same inactivation mutations, purely randomly.

Let us see you probability calculations, since you also write about how you engaged in all sorts of probability stuff when you 'worked in biotech'. And don't forget to document/justify the numbers you use.

In my humble opinion because researchers seek these alleged ERVs out to form or improve phylogenetic trees, lineal relationship is already a pre-supposed reality before they look (which biases the interpretation).

Humble?

OK...

So, as far as I can tell, the first paper to use ERVs to generate phylogenies was in perhaps 1995.

Papers using coding, non-coding, DNA hybridization, mtDNA, etc., had come out at least 6 years earlier, and those using amino acid sequence data even sooner (more than a decade), and the means to compute their probabilities and such have been under constant development throughout that time.

In fact, a paper came out in 1992 providing DNA-based phylogenies for the human question with exceptionally high statistical support for the trees produced (the paper has been cited 149 times), well before the first ERV paper came out. So why would there be a 'need' to 'improve' anything?

You talk about bias (that is really all you can muster, it seems) - many years ago, a 'professional' creationist showed up on a listserv that I was a member of declaring that investigator bias totally colored the outcomes of even sequence analyses.
So, I challenged him to prove it. I took a data set that I had used for an earlier paper, removed all gaps, numerically coded the taxa identifiers, and scrambled the order of the sequences in the matrix. I provided him links to free alignment and analysis programs, and asked him to do an alignment, run a phylogenetic analysis, and report his findings to the listserv and I would compare his results to my 'biased' ones.

The index card on which I wrote down the codes for the 24 taxa is still hanging on my office wall, yellowed and curling on the edges. It was about 14 years ago.

He refused to test his creationist hypothesis.

Would YOU take the challenge? I will have to update the format of the old file - do you use FASTA in your DNA analyses?





*on a related note, shortly after the big '80% of genome is functional' nonsense from ENCODE came out, I teamed up with a math prof I know to see how many binding sites of known sequence (that was essentially ENCODE's definition of function - binding sites) - and there are a lot of them - are found in a chromosome. So, I had the math prof generate an 'artificial chromosome' of 100 million BPs in length of random sequence, and I downloaded a real chromosome's sequence (about 10 million BPs in length, if I remember), and I analyzed them both for known binding sites - the results stunned me. There were MILLIONS of binding sites (including overlaps, etc.). Point is - I think the odds are going to be very much against a purely random insertions at the same locus in multiple species.

 

[pshun2404]

Okay, one at a time (and I honestly admit I may not have and explanation for all you asked). FASTA is a DNA sequence alignment software package. Other variations like FASTP and FASTN are likewise specific software alignment programs. They are great tools so long as their value regarding truth is honestly presented.

As with any software program it is made by modern man and intelligently designed with a purpose and intent. In this case to align like-sequences can and does create a certain illusion.

Again as a tool for finding these areas it is amazing, but in many areas, say between humans and chimps, there are base pairs (sometimes many) that are skipped over or left compared (showing in one and not the other) that then via the paradigm accepted are interpreted as indels, but only are interpreted as such based on the ancestor of the gaps paradigm. It is thus assumed (according to this paradigm) that they were factually inserted or deleted when we actually have no examples of the insertions not being there then there (hence inserted) or being there and then not (hence deleted). Now in all fairness we do have some demonstrable examples most for MOST we do not.

Just consider homo sapiens. In some early sapiens (say Neandertals) we see that there are genomic differences from modern sapiens. So yes we see some of them as insertions, deletions, mutations, and so on. And this shows us undoubtedly that “Sapiens” have changed over time (but they are all still Sapiens just different sub-species). We can say this with assurance because we have a means to compare early originals to moderns. Now then...

All software packages are programmed for a function which includes the programmer’s intent or purpose. So in trying to prove “similarity” in comparative genomes (between two different creatures) when one of the creatures has base pairs separating two segments and the other does not have these the program creates a gap in one which actually is not there and just as likely was never there in that creature. The opposite is also true. So for me it is not which system, it is about how one “explains” or “interprets” the results.

The way I see it, one does not have to create an explanation so the hypothesis appears to be correct, and we can just view them as they are in their totality (the actual data) and accept these all simply as how we differ. IF one had a sequence of 123987431456 and the other simply has 123456 and we apply a program to separate the second to be 123 then 456 with a six position space in between, first of all it is not true, and secondly THEN if trying to show similarity one has to invent an interpretation to explain away the obvious difference, one is jumping to a huge assumption (that is that the basic paradigm ‘ancestor of the gaps’ is true when in fact it also has not been proven outside of within the history of each creature...humans only from humans, cats only from cats, and so on).

We all know how disruptive the change of one single base pair or a mutation CAN BE in a gene (not always) we already know in that specific creature to exist as is (like in cystic fibrosis or sickle cell) this change IS a mutation or indel. We can observe this IS a mutation because we have the whole healthy individual example of all of us to compare it to. So imagine (which should not be difficult for you) if four or five base pairs are different the amazing differences this might reflect. But to believe dogmatically they are an insertion or deletion relative to the ancestor of the gaps one must show the original in that species to compare this ALLEGED later development to.

Now sure, one does not have to in this field because the unproven ancestor of the gaps is dogmatically already accepted as true. But it may not be true (I did not say it IS not, I said MAY not).

 

[pshun2404]

When you say "same results", are you referring to the 'the same ERV, in the same location',
or 'the same inactivation mutations'?

I am agreeing that this may not have happened via “two separate infections” but the same infection, which occurred in the same area around the same time. So let us say that 250,000 ya a serious viral infection spread all through the jungle effecting chimps and humans living there at that time, maybe even killing off some other creatures.

Both being primates their systems dealt with them the same way and inactivated them by using similar mutations to cause them to cease their effect (in other words their genome did this). Now this may be random (but I will not be dogmatic about that) or may be via the program of the DNA to accomplish this goal (to preserve its integrity as much as possible). Similar systems of DNA re-arrangement nay have place them in this exact spot (to use it or render it useless).