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Evolution is a farce: Evidence

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posted on Jan, 6 2015 @ 11:43 PM
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a reply to: Noinden


Not at all. Lets use the BRCA 1 and BRCA 2 gene correlation with certain types of breast cancer as an example,


But this same gene when mutated in mice, does not increase the risk of cancer. Alternatively when this gene is deleted from the mouse it has a lethal effect on embryonic development, but when both copies are mutated in humans apparently it has no effect, allowing the embryo to grow normally into adulthood.

It seems then, that any given gene can have vastly different effects depending on the genetic background it finds itself in, amongst many other [epigenetic] factors that come into play.




posted on Jan, 7 2015 @ 01:11 PM
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a reply to: PhotonEffect

Mice and humans are not the same species. Why would one assume they have the same effect. Breasts in primates are much different tissues than in other mammals (lets stick to only mammals).

You want another example, how about the gene for lactose tolerance (the LCT gene). It can be dated to having mutated in a helpful manner to Humans to around the same time as we were domesticating cattle (and other species we milk). Its a direct genotype to phenotype correlation as well. As a lactose intolerant, I can assure you it is also notable.

Just because something is not simple, does not mean a theory is wrong. We are barely over a decade into sequencing large genomes, and only now approaching useful time frames. What once took a decade and millions of dollars can now be a few days and a few thousand. Having actually sequenced a few human genomes, that few days seems like forever, but I was assured I needed to be patient
Mind you as someone who came from chemistry to bioinformatics, I was used to a different time frame.



posted on Jan, 7 2015 @ 06:04 PM
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a reply to: Noinden

Mice and humans are not the same species. Why would one assume they have the same effect.

Because it's the same gene; the same sequence of base pairs. Right? Otherwise what's the point of comparing genomes and making a big to do about how we share 98% ourselves with the chimp?


You want another example, how about the gene for lactose tolerance (the LCT gene). It can be dated to having mutated in a helpful manner to Humans to around the same time as we were domesticating cattle (and other species we milk).

The timing isn't surprising to me. The organism plays an important role in its own evolution. Plenty of data to support the bi-lateral feed back loops between environment > organism > cells > dna > and back up....I don't think for a second that the LCT mutation was random. My opinion of course...

Just because something is not simple, does not mean a theory is wrong.

It's not the complexity that makes it wrong. It's the interpretations of the evidence.
edit on 7-1-2015 by PhotonEffect because: (no reason given)



posted on Jan, 7 2015 @ 07:17 PM
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a reply to: PhotonEffect

What I feel you are missing here, is despite a high level of similarity the human genome is still very distinct from that of mice. Thus a single gene BRCA 1, will most likely be interacting with other genes in a different manner. Cell apoptosis (cell death) in the mouse, due to mucking about with BRCA genes is not that surprising. It just means that that gene holds a slightly different role in the mouse. No biggie.

As for the LCT gene, you would be a IDer? Because its a natural mutation, and follows the path of migration of domestication quite nicely.



posted on Jan, 8 2015 @ 09:51 AM
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a reply to: PhotonEffect

I'm having trouble seeing your issue. Of course a mutation on one species can have a completely different affect on a another, even if it's the same gene. You can only modify what is already there, they aren't universal for all species. All you have to do is compare the human breast to a mouse breast to see they are vastly different. If one gene mutation had the exact same effect on all species we'd have a very different evolutionary picture than we actually see today. Genomes are HUGE. Just because it may be 98% or so similar to a chimp, doesn't mean that the 2% is nothing. When you have 3 billion base pairs, as humans do, 2% actually comes out to something like 120 million genes. The difference is big, but the genome is so much bigger since our history is written into it. It's kind of like the earth in comparison with the rest of the universe only on a smaller scale.
edit on 8-1-2015 by Barcs because: (no reason given)



posted on Jan, 8 2015 @ 08:57 PM
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a reply to: Noinden


What I feel you are missing here, is despite a high level of similarity the human genome is still very distinct from that of mice. Thus a single gene BRCA 1, will most likely be interacting with other genes in a different manner. Cell apoptosis (cell death) in the mouse, due to mucking about with BRCA genes is not that surprising. It just means that that gene holds a slightly different role in the mouse.

I'm not missing anything, of course they're distinct. What exactly did I say to make you think otherwise? I already made the reference to the effect of genetic backgrounds two posts up.


As for the LCT gene, you would be a IDer? Because its a natural mutation, and follows the path of migration of domestication quite nicely.

Am I an "IDer"? Absolutely not. Why are we being judgmental already? I'm confused by such a moronic question.

Are you adverse to the nature of non-random mutations ? Non-random mutations are naturally occurring, you know. That lactase persistence occurred specifically when humans began dairying is not a mere coincidence. And neither is the fact that dairying is found only in lactase persistent populations. But alas, under the current belief system i.e the evolutionary synthesis- this was all the work of random chance mutations. Forget the role behavior may have played. Makes sense.



posted on Jan, 8 2015 @ 09:24 PM
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a reply to: Barcs


Of course a mutation on one species can have a completely different affect on a another, even if it's the same gene.

That's it? Gimme more....


All you have to do is compare the human breast to a mouse breast to see they are vastly different.

You're comparing phenotypes. I'm talking about genotypes. That two relatively similar genotypes can give way to completely different phenotypes is the point being made. Or do you believe that phenotypes can be directly read from a genotype?


If one gene mutation had the exact same effect on all species we'd have a very different evolutionary picture than we actually see today.

You do realize that mice are the single species, due to their apparent genetic similarity to humans, used by biotech labs to test for all sorts of monogenic diseases, right? So they can see how it might affect humans. Why might that be? research.jax.org...

But monogenic diseases are rare. They represent only a small % of the full disease load. Of the 20000 or so protein encoding genes in the human genome roughly 10% of them are estimated to be associated with monogenic disease (i.e diseases that can be identified by a single gene mutation). BUT, the identities of the majority of these genes are unknown, largely because of their rarity.

Why do I bring this up? Because they segregate according to the traditional Mendelian principles of inheritance, which as we all know is the backbone of the modern synthesis, and natural selection. Hence this idea of genetic determinism that I don't agree with.

Most diseases are multifactorial which as you know means that multiple genes and/or other epigenetic factors contribute to their development. The environment, interactions between cells, and the organism etc all play a role. Quite simply - it's not only the genes. It's much more complex than that.

These interactions between cell>organism>environment which contribute to epigenetic factors governing evolution are largely left out of the synthesis though. Why?
edit on 8-1-2015 by PhotonEffect because: stat correction



posted on Jan, 11 2015 @ 11:58 AM
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originally posted by: PhotonEffect
You're comparing phenotypes. I'm talking about genotypes. That two relatively similar genotypes can give way to completely different phenotypes is the point being made. Or do you believe that phenotypes can be directly read from a genotype?


Genotype plus environment influences phenotype, so what you are saying doesn't go against my points in the least. Mutations on the genetic level affects phenotype. Genes are essentially like blueprints. You change the blueprint, you change the final product.


You do realize that mice are the single species, due to their apparent genetic similarity to humans, used by biotech labs to test for all sorts of monogenic diseases, right? So they can see how it might affect humans. Why might that be? research.jax.org...


That doesn't mean that every single genetic mutation affects mice in the same way it affects humans. That assumption is a nonsensical proposition. If they were strictly doing it because of similarities they'd use chimps instead of mice. But humans don't value a mouse's life in the same regard, plus it's cost efficient. I'm not a fan of animal testing, regardless, and mice aren't the be all end all of learning about human conditions. Yes, you can learn quite a bit, but that doesn't mean every single mutation is going to have the same affect as you pointed out.


Why do I bring this up? Because they segregate according to the traditional Mendelian principles of inheritance, which as we all know is the backbone of the modern synthesis, and natural selection. Hence this idea of genetic determinism that I don't agree with.


So you honestly do not believe that genes influence phenotype and that genetic mutations cannot influence an organism's morphology? I don't know what to say other than that is pretty much the way it is.


Most diseases are multifactorial which as you know means that multiple genes and/or other epigenetic factors contribute to their development. The environment, interactions between cells, and the organism etc all play a role. Quite simply - it's not only the genes. It's much more complex than that.


It doesn't matter whether it's multiple genes or a single gene. What matters is that the diseases (and risk factors thereof) are caused by the mutations along with environmental factors. It may not be strictly the genes, but without those specific mutations many of those diseases wouldn't happen.


These interactions between cell>organism>environment which contribute to epigenetic factors governing evolution are largely left out of the synthesis though. Why?


Please explain how they are left out? Last I checked the environment can cause genetic mutations, which can change morphology of an organism and influence it's adaptability to a certain environment. That is the cornerstone of modern synthesis. It isn't left out.

edit on 11-1-2015 by Barcs because: (no reason given)



posted on Jan, 11 2015 @ 05:24 PM
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a reply to: PhotonEffect

Not being judgemental, I am just trying to get a point of reference for what your disconnect with the subject is. You don't seem to be able to point out what exactly your problem with evolution is. Sure you can wave vague statements about linear and non linear around, and say you don't beleive that certain adaptions are natural, but thats not really helping here



posted on Jan, 13 2015 @ 08:28 AM
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a reply to: Barcs

Mutations on the genetic level affects phenotype.

While this is evident to an extent, despite what you may think, phenotypes are not always impacted by genetic mutations.


Genes are essentially like blueprints. You change the blueprint, you change the final product.

Ah yes, the good ole blueprint metaphor. Well sorry to say genes are no longer being looked at in that way, thanks to a better understanding of what is actually happening on the molecular level, and overall.

How can something be a blueprint if it gives only a partial picture? You would never be able to look at an anonymous genotype and predict the phenotype that would come from it.

You have to remember too, that two completely different genotypes can still produce very similar if not almost identical phenotypes. So no, in this vein, changing the "blueprint" as you say does not necessarily change the end product.


That doesn't mean that every single genetic mutation affects mice in the same way it affects humans. That assumption is a nonsensical proposition. If they were strictly doing it because of similarities they'd use chimps instead of mice.

They are doing it because of the similarity of genomes though. It's just easier to work with mice. This is the whole idea behind animal testing, which like you, I disagree with. To be clear though, I don't think that we can know what effect a particular gene will have on two different species of organisms. What I was trying to show, but may have failed, is that there are entire industries (biotech, big pharma) resting on the idea that certain genes when mutated will have the same affects across some species, of mammals anyway. This idea that we can cure cancer or obesity by identifying their genes and simply turning them on or off. Nope, it's not that simple, nor direct, I'm afraid.


So you honestly do not believe that genes influence phenotype and that genetic mutations cannot influence an organism's morphology? I don't know what to say other than that is pretty much the way it is.

Not saying that. I'm saying that less importance is being placed on those mechanisms because of other factors that are known to come into play. The whole picture needs to be taken into account.

The idea that genes are the blueprints containing all the instructions needed to create a complete organismal form with all its physical structures, physiological functions and behaviors is a fallacious one. As is the prevailing notion that evolution is driven by chance mutations. It's broader and more complex than that.


Please explain how they are left out? Last I checked the environment can cause genetic mutations, which can change morphology of an organism and influence it's adaptability to a certain environment. That is the cornerstone of modern synthesis. It isn't left out.

Epigenetics is the cornerstone of the evolutionary synthesis? When did this happen?
edit on 13-1-2015 by PhotonEffect because: (no reason given)



posted on Jan, 13 2015 @ 08:32 AM
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a reply to: Noinden

Sure you were. There was no need for you to bring up ID given my statement about non-random mutation.

And why are you making up these ideas that I don't believe lactose tolerance is a natural adaptation? When did non-random mutation become unnatural? If you're going to resort to ad homs, that's fine, but at least do it with some integrity.

edit to add:
I meant to mention that my problem is not with evolution, but more with the generally held view of how it operates. When folks such as yourself go on and on about their credentials and then proceed to try to school people by saying things like:


I am most likely more informed than most creationists on the science behind evolution, but part of my tertiary education is in Bioinformatics and Biochemistry (thus genomics and genetics). So please show me where youa re having issues with the part of evolution which is "change through mutation", because THAT is evolution in a simple statement.


Then I feel like I have a gripe. This isn't a helpful review of evolution in my opinion.
edit on 13-1-2015 by PhotonEffect because: (no reason given)



posted on Jan, 13 2015 @ 02:22 PM
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originally posted by: PhotonEffect
While this is evident to an extent, despite what you may think, phenotypes are not always impacted by genetic mutations.


I don't recall saying anything contrary to this. I'm well aware of neutral mutations.


Ah yes, the good ole blueprint metaphor. Well sorry to say genes are no longer being looked at in that way, thanks to a better understanding of what is actually happening on the molecular level, and overall.

By whom? What molecular changes are you referring to that suggest genes don't affect the phenotype?


How can something be a blueprint if it gives only a partial picture? You would never be able to look at an anonymous genotype and predict the phenotype that would come from it.


That statement reinforces my previous point that genetic mutations in different species affect the phenotype differently. Obviously, you can't study an anonymous genome and know exactly how a mutation will affect it. The problem is you say anonymous, but that is an unrealistic concept because they are not anonymous. Scientists know what genomes they are studying, and can reference other genomes of the same species, and can indeed predict mutations and changes to the phenotype. It happens in modern medicine quite a bit.


You have to remember too, that two completely different genotypes can still produce very similar if not almost identical phenotypes. So no, in this vein, changing the "blueprint" as you say does not necessarily change the end product.


Generally speaking, the bigger the difference in DNA, the bigger the difference in morphology. Do you have examples of "completely different" genotypes producing "almost identical" phenotypes? It's not coincidence that chimps share the most common DNA with humans and look more human like than any other animal on earth.

Roughly speaking, cats are around 90%, Cows are 80%, bananas are 50%, fruit fly is between around 40-50%, chicken is 60%, mouse is 75%, Platypus is 69%, Honey Bee is near 45%, roundworms are near 40%, Grapes are 24%, yeast is 18%. The pattern looks clear to me, but maybe you have some examples that go against this trend. I know those percentages aren't exact because we haven't mapped every single animal around, but they give a good rough idea of the genetic code we share with those creatures.

And yes, it does affect the end product. Just because the change is negligible does not mean the change isn't there. Quite often you have multiple neutral mutations that eventually combine together to affect the phenotype. Each one by themselves has no noticeable affect, but once they all combine in the right way, it does. Yes, the blueprint affects the final product, even if the change can't be detected. A genetic mutation could be like a building blueprint switching the type of bolts used in one place. By itself it doesn't affect the building in the least, but switch the bolts for most of a floor and you could have a more stable structure, depending.



They are doing it because of the similarity of genomes though. It's just easier to work with mice. This is the whole idea behind animal testing, which like you, I disagree with. To be clear though, I don't think that we can know what effect a particular gene will have on two different species of organisms. What I was trying to show, but may have failed, is that there are entire industries (biotech, big pharma) resting on the idea that certain genes when mutated will have the same affects across some species, of mammals anyway. This idea that we can cure cancer or obesity by identifying their genes and simply turning them on or off. Nope, it's not that simple, nor direct, I'm afraid.


I can't really disagree with anything you said here. Maybe we're actually even on the same page because one of my main points was that, even though they are similar genomes, they aren't the most similar and every mutation does not affect them the same way. 4% difference may seem small, but genomes are huge, so it's actually a large amount of genes that are different.


The idea that genes are the blueprints containing all the instructions needed to create a complete organismal form with all its physical structures, physiological functions and behaviors is a fallacious one. As is the prevailing notion that evolution is driven by chance mutations. It's broader and more complex than that.

Then why is it geneticists can create a living organism from just the DNA? Of course it contains all of the instructions needed. If not, we couldn't have cloned a sheep along with various other species. No logical fallacies involved. Yes the mutations of the DNA are random, but we're talking about genotype affecting phenotype and that's direct evidence.

You said the whole picture is not taken into account? Which parts are you referring to specifically?
edit on 13-1-2015 by Barcs because: (no reason given)



posted on Jan, 13 2015 @ 07:01 PM
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a reply to: PhotonEffect

Well one, until recently we as a species did not know how to force mutations. All positive mutations tend to be "non random" as they tend to allow members of the species to survive in a manner that benifits the species. However they are not induced, rather they are selected for. QED its still evolution.

You got very defensive over the IDer comment, which leads me to believe it hit home. You are welcome to your beliefs however be open about them. You came in here gunning at those who stood against 'the farce" part of the thread. WHy is that? Why not go in after the OP, or his fellow deniers? Because those of us who you have gone after are not the uneducated masses who rely on a sacred scripture, or the media. As I've pointed out, I've got a background in the sciences (PhD chemistry, Masters in bioinformatics), I understand this subject very well thanks.



posted on Jan, 14 2015 @ 08:31 AM
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a reply to: Barcs



What molecular changes are you referring to that suggest genes don't affect the phenotype?

I believe the actual words I used were "better understanding of what's happening at the molecular level", which was in reference to your blueprint metaphor. I don't think I said that genes don't affect phenotype. They do, but not to the extent we've all been lead to believe, especially thanks to the blueprint [deterministic] view. This idea that we can know ourselves from our genes is misleading, and quite incorrect in light of more recent discoveries.

Geneticists like now to refer to the genome as a landscape, or map, more so since the sequencing of the human genome. Here's an interesting paper on the subject that makes a good case www.academia.edu...


That statement reinforces my previous point that genetic mutations in different species affect the phenotype differently.

Yes, I made a similar point earlier referring to the role that genetic backgrounds play. The same gene across different species can have vastly differing outcomes. We can at least agree on that point. Where we differ apparently is where I think the blueprint metaphor, which is hard lined in its deterministic meaning, should be abandoned.


Obviously, you can't study an anonymous genome and know exactly how a mutation will affect it. The problem is you say anonymous, but that is an unrealistic concept because they are not anonymous.

I think you might be focusing on the wrong argument. It's a hypothetical to show that if you could take an anonymous genome you would not be able to tell what type of organism would come from it. It's to drive home the point that genes don't lead to specific outcomes, most of the time.


Do you have examples of "completely different" genotypes producing "almost identical" phenotypes?

It's called convergent evolution, and there are very many examples. I'll provide a couple here for you:

The one on the left is American while the one on the right is African. Both survive in arid climates with very similar shapes and features, presumably to reduce water loss and predation.
____

Keeping with American vs African varieties, of birds this time. Not only do they look the same but their behaviors are said to be very similar as well.
____

The Emerald tree boa is found in South America. His counterpart is found in Australia. Both live in rainforest type environments and can be found high up in the canopy, and both eat birds. Adults are green, blending with the colors of leaves. The juveniles of both species are bright yellow or orange.
____

Both of these eyes independently evolved complex camera-like eyes complete with an aperture, lens, and retina. Cephalopods are mollusks, like an octopus. They get the edge when it comes to the better eye though.
www.zo.utexas.edu...


Then why is it geneticists can create a living organism from just the DNA? Of course it contains all of the instructions needed. If not, we couldn't have cloned a sheep along with various other species. No logical fallacies involved. Yes the mutations of the DNA are random, but we're talking about genotype affecting phenotype and that's direct evidence.

I disagree.. It's information, yes, but raw information which has to be put into useful/meaningful patterns first. It's not all there written out nice and neat pointing us in the direction of the end product, kinda like a blue print would.

[Tin foil hat on] Genetic engineering I see as a speculative science. The general public has no clue what's really going on behind those closed doors. But rest assured big time funding is coming from governments and large corporations. There is pressure to show that the technology of genetically engineering things to our liking works like charm. Well I have my deep reservations about that. I wonder just how many trial and error rounds it took to get a glow in the dark cat, or a cloned sheep that survived past 24 hours. What's going to happen 3 or 10 generations down the road when the modified genes find a way to mutate themselves? How many organisms were sacrificed to show the world that we've cracked the code? This is far from being a sure thing. It's unsettling to me that we are developing completely synthetic and alien DNA without really knowing what could come from it.

But there are entire industries, from insurance to bio-tech to big pharma, all banking on the assurances that we can determine anything we want just by tweaking some genes here and there. That there's this idea we probably know the outcome better than 90% of the time with low margins of error. It's full proof. Well, that's a fantasy as I see it. And I'm fully aware of the motivation in keeping this idea as the status quo in the public eye. Too much money at stake now, turn up the PR machine. Who else is going to pay for those expensive gene therapy sessions, genetic testing or medications for genetic disorders? [tin foil hat off]
edit on 14-1-2015 by PhotonEffect because: (no reason given)



posted on Jan, 14 2015 @ 09:20 AM
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a reply to: Noinden


QED its still evolution.

My apologies as I don't know what "QED" means in this context


You got very defensive over the IDer comment, which leads me to believe it hit home. You are welcome to your beliefs however be open about them. You came in here gunning at those who stood against 'the farce" part of the thread. WHy is that?

I don't like being called something I'm not. Was my reaction unreasonable? How would you like to be referred to as an obnoxious neo-darwinist?

Your only reference came from a comment I made about a non-random adaptation, plus the fact that I'm not supporting you in your views. This leads you to believe, then, that I side with the ID crowd since I'm going after you and not them. No, I don't think so friend. Your deductive reasoning needs more work as it's lead you astray.

Why waste your time with IDers and creationists in the first place? No one can or will ever change their minds on how they see evolution. It's a pointless endeavor that leads both parties to no where. If you believe in god then you believe he/she created everything - including evolution. It's how Darwin reconciled it with himself. God was at the beginning.

I've been following along this thread and have waited for you to provide something of value given your self proclaimed credentials and all. Then you said something to the effect of evolution is simply change through mutation. This is misleading so I felt I should jump in and question you about it.

Be clear on something- I know there is evolution and I don't deny it. It's an amazing phenomenon. That people debate it's existence makes no sense. With that said, what I don't agree with is the current view of how it operates. I also don't agree with the OP, nor creationist thinking either. I'm on my own path to research the material and draw my own conclusions. In this regard I am an independent. This should be celebrated not mocked.

There is this pervasive problem with the mentality of folks who adhere to the current paradigm and shun those who oppose it, simply for opposing. Well it's counter productive only serving to stifle what could become progressive dialogue.


As I've pointed out, I've got a background in the sciences (PhD chemistry, Masters in bioinformatics), I understand this subject very well thanks.

Yes, if nothing else, you've managed to point this out more than is necessary in my estimation.

If you want to continue this discussion without the ad homs then I'm in. You want to point out where I'm wrong and correct me, you're free to do so. Ill only research it more deeply. If one or both of us can learn something new or see something differently at the end of the day then this discussion would have been more rewarding then most in this forum.



posted on Jan, 14 2015 @ 01:28 PM
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a reply to: PhotonEffect

Well neighbour, I point it out, as people continually question how I am qualified to speak on these subjects. I've actually worked in the area, hence I know.

As for "God" being involved, which one? No need to be vague.



posted on Jan, 14 2015 @ 01:53 PM
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a reply to: PhotonEffect

Blue print is a metaphor. I never said that was exactly how it worked, but it's true in the sense that it does indeed contain all the information. Just because it isn't written out in modern English, doesn't make it untrue. Maybe map is a better metaphor? They are both almost the same in the sense that it contains all of the information needs to make the organism as my cloning example shows.


Do you have examples of "completely different" genotypes producing "almost identical" phenotypes?



originally posted by: PhotonEffect
It's called convergent evolution, and there are very many examples. I'll provide a couple here for you:

The one on the left is American while the one on the right is African. Both survive in arid climates with very similar shapes and features, presumably to reduce water loss and predation.


I'm well aware of convergent evolution, but we're talking about genotype similarity and you you didn't even mention the difference between these organisms. What is the percentage of DNA that these 2 and your other examples share in common? You said "completely different", which suggests they would share a very small percent of DNA. Just saying one is American and one is African means nothing and they still share a common ancestor, so please drop the numbers for me. You also forget that natural selection plays a bigger role than genetics when it comes to what types of creatures survive, so if they are in similar environments, it makes sense that they would have similar traits. The 2 snakes you posted are in the same sub order, but different families and genus. Something tells me their genetics are not that much different, but you made the claim, so please post those numbers for me. If they share less than 75% of their genes I will be very surprised.

Thanks

edit on 14-1-2015 by Barcs because: (no reason given)



posted on Jan, 15 2015 @ 11:34 AM
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a reply to: Noinden

Well, friend, I never once asked for your qualifications. DOnly that you cease with the ad homs.

Vague about what? Which god?? I dont believe in god so what does it matter in this discussion.



posted on Jan, 15 2015 @ 12:05 PM
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originally posted by: PhotonEffect
a reply to: Noinden
DOnly that you cease with the ad homs.


I don't think you know what an ad hominem attack actually is. Getting butthurt isn't an ad hominem. Even insulting someone isn't an ad hominem. An ad hominem is ONLY when "a claim or argument is dismissed on the basis of some irrelevant fact or supposition about the author or the person being criticized". Eg: "your argument is invalid because you are an idiot". And no, actually countering an argument with logic and then also attacking someone's character is not an ad hominem (neither of which have happened so I have no idea why you're throwing around the term "ad hom").
edit on 15-1-2015 by GetHyped because: (no reason given)



posted on Jan, 15 2015 @ 12:32 PM
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a reply to: Barcs

Blue print is a metaphor.

Yes, that's been well established by now. I see it as misleading because we don't always know by looking at a gene what the end product will be. It depends on the environment and how it interacts within the genome. We agreed on this point I thought.

If an architect has a blue print to build a 2 story house and the builders follow it to a tee, then theres 0 chance they wind up with a sky scraper as the end product. Regardless of the location of the build site or who the builders are, it's a certainty there will be a 2 story house at the end of construction. The same can not be said with genes. Which is why I think the metaphor breaks down.


I'm well aware of convergent evolution, but we're talking about genotype similarity and you you didn't even mention the difference between these organisms. What is the percentage of DNA that these 2 and your other examples share in common?


Okay then you'd know these examples show two distinct and independent lineages evolving in the same way, in other words - homoplasies. You asked to see examples of different genotypes producing similar phenotypes. Now you want % differences- I will have to do some more digging but:

How about streamlined body morphology (aquatic life such as fish, ichthyosaurs, whales, seals and diving birds - e.g. penguins)? How about powered flight ( birds, bats, insects, pterodactyls)? How about Echolocation (dolphins, bats, whales, and some birds)? And you seemed to skip right over the camera eyes example (independently evolved in cnidarians (certain jellyfish), cephalopods (such as squid and octopus) and vertebrates (birds, mammals)?

How different would you wager these genotypes to be?

As a reminder, it was you who said that even a 4% difference in genomes is a lot given all the base pairs we're talking about. But suddenly that doesn't apply here. Interesting. If you really thought that I was going to show how a grape and a flying squirrel have similar phenotypes then Im sorry to have disappointed you. But then it seems you might have missed the point I was trying to make.

Despite what you make think I am trying to find some common ground here, and not necessarily debate and nit pick everything. You seem like a reasonable person so I think you can understand the points being made.




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