The Coccyx

[pshun2404]

Molecular Biologist, Zachary Williams, of Tufts University says “There are around 30 partial or full length human specific ERVs, and somewhere between 100–200 human specific solo LTRs (ERVs where the flanking LTRs have recombined, excising the coding sequence in between). Almost all of these are in the HERV-K (HML-2) clade, so they are very similar in size and sequence; a solo LTR is about 1 kilobase long, and a full length HML-2 provirus is about 10 kb. 30x10kb+200kb=500 kb, so there’s a max of about 500,000 base pairs of human specific ERV sequence; the vast, vast majority of the rest is also found in chimps.

~8% of the human genome is composed of ERVs (and their relatives the LTR retrotransposons), which would be 240 million bp (8% of 3 billion bp). 500,000 bp is 0.2% of that, so about 99.8% of human ERVs are also found in chimps. We can round down to 99% if you want to be super conservative.

I don’t know how many individual ERVs are in the human genome, and I’m not sure it’s possible to accurately determine. It’s highly dependent on what counts as an individual ERV. Do fragments that originated from the same provirus count as separate fragments? Can you reliably determine which fragments belong together? These are non-trivial problems to overcome, and the answer itself is not particularly useful information.

We can guesstimate a rough minimum by assuming all ERVs are full length (~10kb) and dividing the total amount of ERV sequence (~240,000kb) by that, to get 24,000 ERVs. The vast majority of ERVs are much smaller than 10 kb, so the real number has to be significantly larger.”


So what we really know is that many of the alleged ERVs are SIMILAR (not the same), in some locations there are only small sections and in these sectios there are some differences as to BPs and function, some are located in different sections of each specie’s respective genomes, and some may not actually be ERVs at all (though many others can be stated to be actual ERVs). To obtain a rough estimate (again not exact) this microbiologist admits we must “guesstimate” (use a line of best guess) from among possibilities.

Lines of best guess were often used in lab determinations when I worked in Biotech. A number of different outcomes or probabilities are plotted and then a midlan line or median is assumed (we see the same thing when they dated the Boxgrove bones...different methods, different size and quality of samples, etc., yielded different results...the final number of years old settled for, conveniently (ah-hem!) fall in the range they presupposed to find and this is what is taught in textbooks as the truth)

 

[PsychoSarah]

any reference?

To the fact that humans have genes present for developing tails?

How about the fact that tail development in embryos is normal up to a certain point, after which the tail structure dissolves? Genes regulate body structure, and if the tail structure was the result of random mutation, we wouldn't see it in literally every developing infant. Same goes for if this structure was the result of environmental influences.
Here's a labelled one for body structures https://s-media-cache-ak0.pinimg.com/originals/e2/d3/46/e2d346f03379b8995be827308e019c7a.jpg

humans also have genes for feathers development. does its means that humans evolved from birds?:

http://phenomena.nationalgeographic.com/2014/11/20/your-inner-feather/

What have I told you about using National Geographic as a source? This is not a scientific journal, there are a lot of inaccuracies published in National Geographic.

Also, I have to shake my head at the fact that you thought that the genes mentioned in this article were feather specific. They are not. For example, the article mentions that both humans, fish, and birds have genes relating to the formation of placodes, but unfortunately, the article fails to actually explain what placodes do in animals that aren't birds. Placodes are early embryonic structures that, depending on the other genes present, become teeth, hair follicles, or feathers, or sensory organs. It's a bit of a given that vertebrate animals are going to share quite a few of the same genes that form placodes, since those early embryonic structures can develop into a variety of sensory organs and skin features. Placode genes developed long before the split between mammal and reptile, let alone the much later split between reptile and bird, so it is no shock that all three have some of the same genes relating to placodes.

In addressing the color genes for feathers brought up, yeah, those genes function to color any structure that has keratin in it, which includes the scales of fish and reptiles as well as mammal hair and feathers. However, it is blatantly obvious that humans have only a fraction of these genes that birds have, given the limited range of hair colors for our species compared to birds.

Here's the thing: humans do not share a single gene with birds that isn't also shared between birds and some reptiles. Not a single one. We do share plenty of genes that preceded the split between mammal and reptile, since birds diverged from reptiles later, but certainly not more than reptiles do with birds.

 

[pshun2404]

Carl Zimmer, “We Are Viral from the Beginning,” The Loom , Discover, June 14, 2012, believes ERVs are sections of the genome that “look like” retroviral invasions. And he tells us “most endogenous retroviruses mutate so much they are reduced to genetic baggage, unable to do anything at all.” However, many identified as such do carry the hallmark signs of being or at least having been virus related insertions.

Jonathan P. Stoye, “Koala Retrovirus: A Genome Invasion in Real Time,” Genome Biology 7, no. 11 (2006): 241, doi:10.1186/gb-2006-7-11-241, reveals that ERVs often appear to move around to different places, as a means of explaining why they appear in different places which sometimes causes a problem for comparative genomes. Having said that we KNOW that there are certain ERVS that ARE located in the exact same place across multiple genomes, and YES humans and chimps have the highest correlation.

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.

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).

 

[pshun2404]

More on ERVs:

Madalina Barbulescu et al., “A HERV-K Provirus in Chimpanzees, Bonobos, and Gorillas, but Not Humans,” Current Biology 11 (May 2001): 779–83, doi:10.1016/S0960-9822(01)00227-5, tells us that some of the ERVs found in chimps, bonobos, and gorillas, are not present in humans and many in humans are not found in any of the others (also see Chris T. Yohn et al., “Lineage-Specific Expansions of Retroviral Insertions within the Genomes of African Great Apes but Not Humans and Orangutans,” PLoS Biology 3 (April 2005): e110, 10.1371/journal.pbio). In light of this Molecular Biologist, Dr. Anjeanette Roberts believes “the longer I think about ERVs and viral origins, and as I observe scientific reports identifying various critical functions associated with ERVs and other repetitive genomic elements, I believe it may be profitable for driving scientific inquiry to question some of the underlying assumptions that support ERVs as inarguable signs of common descent.”

A study done by Catriona M. Macfarlane and Richard M. Badge, (“Genome-Wide Amplification of Proviral Sequences Reveals New Polymorphic HERV-K(HML-2) Proviruses in Humans and Chimpanzees that are Absent from Genome Assemblies,” Retrovirology 12 (April 2015): id. 35, doi:10.1186/s12977-015-0162-8) implies we may need to re-think the time element generally assumed because mounting evidence indicates a much more recent insertion event for humans than for chimps at shared ERV insertion sites previously thought to confirm the common ancestry argument.

If that is true in those thy examined it could also be true in other cases (which means the evidence used in these sites no longer can be said to indicate descent). Same insertion, in the same place, yet two different times. Do our similar genomes show a sort of preference where such materials would be placed?

Yale Molecular Biologist Dr. Anjeanette Roberts again enlightens us when she reveals “divergence of long terminal repeat sequences (components of ERVs) SOMETIMES VARIES SIGNIFICANTLY from one species to another at shared sites, even when normalized for mutation rates.”

See how different many of these alleged “same ERVs” and “shared sites” actually are? We get the data, but then we INTERPRET the data (filtered through our presupposition). In many areas we interpret through such a filter. I see it all the time in theology as well, one’s denominational spin making a possibly related string of scriptures say what they already expected to find rather than just letting ALL the passages speak to the issue.

 

[PsychoSarah]

in old world monkeys all in some varieties have it...all in others do not...it is variable in Gibbons...present in Orangutans, variable in gorillas, chimps, and humans...so what. None of this demonstrates the palmaris longus muscle is vestigial. It is an inheritable characteristic within each species but for "vestigial" to fit, it would have to be something there that is now less or left over. Calling it that or interpreting it as that is subjective (again theory based).

A vestigial structure, by definition, has reduced or lost original function. In humans, this muscle does absolutely nothing but take up space, which is why so many people on this planet don't even notice if they have it or not. It makes even less sense for it to be there if it never had a purpose (which it demonstrably does in orangutans and monkeys that swing from tree to tree). Why would people be created with a muscle that they do not and cannot use? In those animals for which it does have a use, the muscle improves grip strength and coordination when swinging from branch to branch or jumping, as well as to retract claws. However, in humans, it does nothing. Heck, in some people, the muscle portion is actually missing, and only the tendon is present. The structure is highly variable, and again, entirely absent in a large portion of the human population. Structures that have function are not like that, they remain consistent and present in an excessive majority of a population because to lack them or to have them be altered is generally a disadvantage. But vestigial structures get all kinds of weird, because as long as they don't end up encroaching upon a structure with function, their shape, size, or presence is entirely irrelevant to survival.

However, the greatest example of a vestigial structure I personally can think of is the arm of the emu. Emu arms have no muscles attached to them at all, so the birds can't move them or even utilize the single, large claw on the arms in any way. In fact, thanks to their feathers, the arms are covered and practically impossible to see, so you can't even argue that these arms are sexually attractive to others of their species.

The worst example of a vestigial structure I can think of is human "wisdom" teeth. After all, it's our actions (brushing our teeth) that mostly prevents these teeth from serving their purpose. If you don't have a full set of teeth when they start to grow in, they probably pop through the gums the vast majority of the time without much issue. Some people have large enough mouths that they pop through anyways. Are wisdom teeth more trouble than they are worth? If you still have all of your teeth, probably. But if you don't, maybe not, they still function as teeth just fine when they grow in correctly. Mandibular second premolars are actually the most common teeth to be "missing" (a person never develops them at all), followed by the maxillary second premolars. Neither of those are the "wisdom" teeth, but rather the second to last molars to grow in.

 

[pshun2404]

I believe wisdom teeth (which are still the exact same size) were designed to fill in where molars would have normally fell out (forever until dentists). In early humans no molars meant difficulty chewing, when the wisdoms came in these would provide a reprise on the need for grinders.

 

[PsychoSarah]

So okay regarding a, which genes are those and how do YOU know that these genes in humans are specified for this function?

I know of two specifically that we share with many distant relatives of ours, including mice: WNT3A and CDX1. The tail human embryos develop is signaled for death partly by the inhibition of the WNT3A gene (plenty of genes exist with the sole purpose of keeping other genes inactive, either temporarily or permanently). The reason why the WNT3A gene stays active long enough for the embryo to develop a tail is that it is also responsible for the direction of developing the spinal chord early on. Yeah, most genes have multiple functions.

We can tell what those genes do in mice because we do morally questionable things to their DNA to find out how messed up they will be if a gene is missing or severely mutated. Those ones are key in tail development.
We can tell that genes are turned on or off during the development of human embryos using a dye that is taken in to DNA in proportion to how active the genes are (the more active the gene, the more it is stained by the dye).

See my later posts which refute this notion. Similar genes, out of sequence (a gene’s expression AND purpose AND function DEPEND ON the codons before and after them...genes express in context not uniquely), organisms requiring different genes to produce same results, and same genes in different organisms producing different results.

Link me to the posts or at least give me a post number so I don't have to dig around to find them.

Organisms REQUIRING different genes for the same result? And you determine this how exactly? Of course, inserting a gene randomly into who knows where without the preceding sequences needed to signal that the gene be activated will not have the typical effect. However, scientists use jellyfish and firefly genes all the time to determine if gene insertion has been successful, as these genes consistently result in at least some parts of the animals glowing, if not their whole bodies. Of course, they aren't always in the same body parts because the genes were inserted into different places, and all cells in your body do not have the same genes active. That's actually what distinguishes cell types the most, which genes they have active.

As for b, the number of vertebrate in humans is 33 at the end of the 8 week period of embryonic development we see “33 or 34 cartilaginous vertebrae arranged in flexion” (see The Journal of Anatomy, 1980 Oct; 131(Pt 3): 565–575, by O’Rahilly, Muller, and Meyer. You can see they are logically similar. Neither of which when the body grows to engulf them indicates a tail (either before or after development). The “APPEARANCE” of a tail is only due to the lack of development of the full body, and the potential vertebrate present in embryos is consistent with what we would expect. None of this is equivalent to repressed or altered tail development. The explanation is given to convince the student of the hypothesis based pre-supposed conclusion (IMO this is not due to bad science just indoctrinated “scientists” which is not the same).

-_- I never said that there were necessarily vertebrae in the human embryo tails. In fact, even among the few people born with tails that's uncommon (and the accounts that claim it are questionable).

Tail formation is controlled by many genes, some of which are missing or just mutated into being without function in humans. I have never stated that humans had every gene necessary for the formation of tails. We don't, which is why humans are never born with functional tails. But I do wonder how you reconcile people having only part of the genes to develop any given structure. Seriously, what would the point of creating people with genes that can't even amount to much when active?

The ALLEGED branchial clefts (gill) are actually pharyngeal (and now called that by most honest anatomists) because we KNOW they do not contain and we NEVER form brachia AND we have known this or some time, yet those pushing the myth still teach it as true (see Langman, J., Medical Embryology, 4th edition, Williams & Wilkins, Baltimore, 1981).

I called them gill flaps because that's what they become in fish. Yes, they become different structures in humans, with the outer flap portion entirely smoothed out and absent later (like the webbing between the developing fingers and toes). However, there is no point to this structure developing analogous to how it does in fish embryos at all, no reason for useless outer flaps.

I am not attempting to be dishonest. Dishonest would be suggesting that human embryos develop gills which are later dissolved. They are not gills, but gill flaps, and they do become other structures in humans than they do fish. The reason they are noteworthy is because that gill flap shape is entirely unnecessary for the human body structures they become later, and is also lost.

That is just for starters as I already post longwinded explanations for my positions and have received rebuke (so I break them up). SO I totally disagree with your conlusion. We DO NOT have genes for the formation of tails or gills (the embryo always and only receives its oxygen from the mothers blood)...

-_- what even is that last bit? We begin to develop lungs long before we exit the womb, so I don't know why you felt it was worth mentioning that developing infants get their oxygen from the mother's blood. Do you think shark embryos don't begin to form gills long before they are born?

If you say we do please share what genes they are and how you know they express for or repress these functions, Thanks

I know the tail ones function to form tails in mice due to the fact that when artificially messed with, the mice don't form tails properly. Most genes DO THE SAME THING REGARDLESS AS TO WHAT ORGANISM THEY ARE PRESENT IN. Those that don't are the EXCEPTION, not the rule. And we find those exceptions pretty fast, given that we use a wide variety of different organisms in genetic studies. Analogous genes are both determined by structure and placement, so it is unfair to think that genome comparisons do not take gene location into account, when they absolutely do.

 

[USincognito]

Or both separate communities of species were infected at the same early time period. Plus, the "Reproductive and Cardiovascular Disease Research Group" points out that if so many of these were actually caused by retro viruses we should see a much larger presentation of cell death which is seemingly absent in both species (http://www.sgul.ac.uk/depts/immunology/~dash/apoptosis/) and over 80% of the ERVs are NOT located in the exact place in the respected genomes but in similar locations. All this says then is that these retroviruses effected apes and humans. Plus some of the same retroviruses are found in pther seemingly unrelated organisms.

There's a problem with the Evolution Dismantled webpage from which you lifted this material without citation.
Are Endogenous Retroviral Sequences (ERVs) Evidence for Evolution? | Evolution Dismantled
The link is broken and the "quote" for footnote [8] must come from the missing page because much of the verbiage is from this paper:
Apoptosis: A Review of Programmed Cell Death
Which has exactly two references to endogenization, neither of which refer to viruses.

 

[USincognito]

my claim was that humans have genes for feathers development in birds. this is a fact.

This is not a fact because we do not have genes for feather development. We have genes that are used for feather development in birds. That is not what you're trying to claim.

now is see that usincognito changed it into "genes for feathers". so its was not my mystake.

Incorrect. It was your mistake not reading what I wrote for comprehension. I very clearly stated that humans do not have genes for feathers and noted that would be required for a violation of the nested hierarchy as you are falsely trying to portray the situation. Again, we have the genes which are used in feather development birds (as do many other mammals and reptiles), we do not have genes used for feather development.

Let my semantic discussion seem obtuse - if X1, Y4 and Z3 genes are used in both mammals and birds, but in mammals they make hair and fingernails, but in birds they make feathers, then we don't have the pathways that make feathers. Here's an example - Hoxd12 plays a role in the formation of the cetacean flipper. It also plays a role in the formation of bird wings. By your "logic", that means whales have "genes for wing development".

They don't.

 

[xianghua]

How about the fact that tail development in embryos is normal up to a certain point, after which the tail structure dissolves? Genes regulate body structure, and if the tail structure was the result of random mutation, we wouldn't see it in literally every developing infant. Same goes for if this structure was the result of environmental influences.

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

What have I told you about using National Geographic as a source? This is not a scientific journal, there are a lot of inaccuracies published in National Geographic.

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

Also, I have to shake my head at the fact that you thought that the genes mentioned in this article were feather specific.

i never said that they are feathers specific. and i already discuss about this in other posts.

 

[xianghua]

In those animals for which it does have a use, the muscle improves grip strength and coordination when swinging from branch to branch or jumping, as well as to retract claws. However, in humans, it does nothing.

dont be so sure:

Assessment of the presence/absence of the palmaris longus muscle in different sports, and elite and non-elite sport populations. - PubMed - NCBI

"The palmaris longus may provide an advantage in certain types of sport that require hand grip, and for elite athletes participating in sports that require a dominant-handed or two-handed cylindrical hand grip."

and yes: some structures may be a true vestigial. but it doesnt prove evolution at all. just a degeneration.

 

[pshun2404]

"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.

 

[xianghua]

"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.

we also dont have genes for making a tail. the wnt3a have several functions even in mouse:

WNT3A - Wikipedia

 

[tas8831]

my claim was that humans have genes for feathers development in birds. this is a fact. now is see that usincognito changed it into "genes for feathers". so its was not my mystake.

Your implication is not a fact.

I stand by my criticism.

 

[tas8831]

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.

Can you explain this?

Why do you think that a retrovirus would insert at one specific site?

Can you explain how retroviral insertions work?

 

[tas8831]

"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.

This is your opinion only.

 

[tas8831]

dont be so sure:

Assessment of the presence/absence of the palmaris longus muscle in different sports, and elite and non-elite sport populations. - PubMed - NCBI

"The palmaris longus may provide an advantage in certain types of sport that require hand grip, and for elite athletes participating in sports that require a dominant-handed or two-handed cylindrical hand grip."

and yes: some structures may be a true vestigial. but it doesnt prove evolution at all. just a degeneration.

And yet, many people do not have one.

Regarding 'degeneration', it seems that this was all brought up in regards to vestigials, not whether or not the palmaris longus was 'evidence' for evolution.

When comparing the musculature of different vertebrates, interesting patterns become apparent - patterns that one only looking for ways to dismiss science will never see. Take the trapezius. In humans, it is considered one muscle, with its origin essentially along the vertebral column, from the neck to the lower thoracic regions, inserting onto the scapula and clavicle, receiving innervation from 2 sources. It has 3 distinct functional fiber groups.

Comparing it to the cat - same innervation, same origins, same insertions (except that cats have rudimentary clavicles not attached to the scapulae). Yet, there are 2 distinct muscles, each with a different name (clavotrapezius and spinotrapezius). Why? Because of the orientation of the scapula relative to the vertebral column - it is rotated roughly 90 degrees relative to the orientation of the human scapula (quadruped v. biped) . Such 'splitting/merging' of muscles is pretty common across the vertebrates.

 

[tas8831]

We DO NOT have genes for the formation of tails or gills (the embryo always and only receives its oxygen from the mothers blood)...

We do, however, have the genes for producing the pharyngeal apparatus, as do fish, as do birds, as do dogs, etc.


Which is really the point - that all vertebrate embryos possess pharyngeal apparatus at some early stage of their development is indicative of a shared ancestral genetic architecture.

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?

 

[USincognito]

"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.

It is neither a reduced nor non-functioning tail?

Please explain the extensor coxxygis muscle then.

 

[tas8831]

Excellent post. A couple points of clarification/expansion.

We can tell what those genes do in mice because we do morally questionable things to their DNA to find out how messed up they will be if a gene is missing or severely mutated.

We also know, contrary to the repetitive, embellished diatribes of Jeff Tomkins, that there is 'junkDNA' in genomes - 3% has been removed in mice and they show no ill effects..
Poor mice.

Those ones are key in tail development.
We can tell that genes are turned on or off during the development of human embryos using a dye that is taken in to DNA in proportion to how active the genes are (the more active the gene, the more it is stained by the dye).

In addition, developmental genes are parts of cascades - one gene product sets up concentration gradients (or even non-gene products, like folic acid) that initiates or alters the expression of others genes, whose products do the same, and so on, ultimately producing, say, a bird wing. Tweaking a gene or two in this cascade can end up producing a bat wing, or a human hand.

This is why those writing about the "genes for feathers" and "genes for tails" are really only exhibiting the limits of Google/creationist website expertise, not their in-depth knowledge of the subject. But I digress.

Organisms REQUIRING different genes for the same result? And you determine this how exactly?

That one seemed a bit suspect to me also.

However, there is no point to this structure developing analogous to how it does in fish embryos at all, no reason for useless outer flaps.

I am not attempting to be dishonest. Dishonest would be suggesting that human embryos develop gills which are later dissolved. They are not gills, but gill flaps, and they do become other structures in humans than they do fish. The reason they are noteworthy is because that gill flap shape is entirely unnecessary for the human body structures they become later, and is also lost.

Which is, when taken in their appropriate context, really good evidence FOR shared ancestry.

The arches in the pharyngeal apparatus in both fish and humans (and stoats and wombats and...) contain nerves, cartilage, and blood vessels - in fish, they do in fact become the gills (gill arches), pretty much as is; in humans, most of the blood vessels degenerate or anastomose to others, producing the vasculature of the neck and parts of the face, the cartilages degenerate or fuse to become a couple of structures in the face/neck, etc.

To me, a student of developmental biology (among other things), this actually shows what a little tweaking - and not even necessarily to the actual genes themselves, but also to the regulatory sequence - can do.