Definition of created kind!

Hi, Im new and a creationist. I looked back at messages 46 to 60 where a creationist and an evolutionists discussed created kinds. I didnt have more energy to read much further.
But a good definition of microevolution and impossible macroevolution would be this:Every individuals in a created kind have the same protein transduction pathways, one spieces might have LOST a protein transduction pathway or the protein transduction pathways might be linked to each other by mutations. (Testosterone give rise to a mane in lions but not to other cats.)That is for example protein chains producing different cells that have even more different protein system.There might be arised dubble genes or one or a few extra proteins acting together with these ordinary vitally important systems. An extra protein change the regulation. That protein might cause a shortnosed dog like a pekingese, like a cat.But the cats have a more flexible spine. This might be due - (I dont know. But I would like to know) - to many different proteins acting together. If the cats have this protein system and the dogs doesnt, it shows 2 different kinds.

I think this thread more belongs in the Evolution forum, but if you disagree please explain. Otherwise I will move this thread in a day or two.--------------------EvC Forum Administrator

Do so! Ill start discussing from there!

Some clarification:1. Are you suggesting a possible starting point for a defintion of "kind", or are you arguing that "different protein transduction pathways" could NOT arise via evolution. Or both?2. You seem to allow that proteins can double (rather, the gene that codes a protein can have another copy in the genome), and that proteins can change due to mutation. If you allow these, what exactly is left for a new "protein transduction pathway"? Those two things can create two genes that code for two different proteins. What's missing?3. At the end, you also include the idea of multiple proteins being necessary for a different kind. Could you maybe clarify this? You seem to mean something more than just "different kinds have many different proteins", but I'm not 100% clear on what else you specifically mean.

I hope I can post in this thread even though my user name doesn't start with 'Z'.I definitely agree that the kind concept will become more clear as we get more genomes and that issues of 'loss' vs 'gain' are very improtant. In other recent threads I have shown refs that demonstrate that biochemical and cellular novelty is assocaited with the occurance of novel protein families.Creationists expect 'distinct' genomes diversified through microevolutionary processes.

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Originally posted by Zhimbo:

1. Are you suggesting a possible starting point for a defintion of "kind", or are you arguing that "different protein transduction pathways" could NOT arise via evolution. Or both?

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Both! The definition of created kind refers to both microevolution and macroevolution.

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Originally posted by Zhimbo:

2. You seem to allow that proteins can double (rather, the gene that codes a protein can have another copy in the genome), and that proteins can change due to mutation. If you allow these, what exactly is left for a new "protein transduction pathway"? Those two things can create two genes that code for two different proteins. What's missing?

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Those accumulating new proteins should start interact with one another or interact with already existing proteins. The question is how many new proteins can interact with eachother before they stop vitally important Signal Transduction Pathways (STP). So how big could a new STP be at maximum. 3-5 new proteins, I dont know. And every mutation doesnt produce new proteins.
So whats missing is a whole set of new proteins, sugars that interact without breaking a vitally important STP.

Ofcourse! Only A, T and Z are welcome here. Hehe!Can you show me those interesting refs?

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Originally posted by ZAURUZ:
Those accumulating new proteins should start interact with one another or interact with already existing proteins. The question is how many new proteins can interact with eachother before they stop vitally important Signal Transduction Pathways (STP). So how big could a new STP be at maximum. 3-5 new proteins, I dont know. And every mutation doesnt produce new proteins.
So whats missing is a whole set of new proteins, sugars that interact without breaking a vitally important STP.

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1. First, you've switched terms on me: you originally said "protein transduction pathway", and now you say "signal transduction pathway". The first would refer, I believe, to proteins being formed from a genetic code, which is what my orignal comments were based on. The second term refers to a pathway that moves a signal from outside a cell to inside a cell (e.g., neurotransmitters attach to a receptor on a nerve cell, the receptor causes changes internally). Did you mean one of these specific meanings?2. Second, I'm not sure why any new protein would necessarily "break" an exisiting transduction pathway (of either sort), or why 3-5 new proteins suddenly would, or whatever. As long as the original proteins were also being made, I don't see any necessary problem.Unfortunately, I don't think you're suceeding in creating a workable definition/standard for "created kind", although I'm still seeing where you're going. It seems more like you're just saying you don't see how systems of proteins could form. I don't see that you've created any barrier, though. You talk about new proteins breaking old pathways, but I don't see how this is inevitable.

I would like to say, I wish you well in your endeavor to define 'created kinds' but could you speculate for a moment?If this definition were established, and we see a 'cat kind' ( felines ) and we see a 'wolf-kind' ( canines ), is it possible we would also notice that humans and chimpanzees would be members of the same 'kind' ?regards,jeff------------------
"Freedom of Religion" equates to Freedom -FROM- those religions we find unbelievable.

ZAURUZ, in the thread below we talked about the assocaiton of novelty with protein fold families and I think we agreed that at least biochemical and cellular novelty is typically assocaited with new protein fold families: http://www.evcforum.net/cgi-bin/dm.cgi?action=page&f=5&t=35&p=6Here is one of the papers I came up with:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8706840&dopt=AbstractIn the pdf (if you have access to it) it says:

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"Using the presence of the protein families as taxonomic traits, and linking them to biochemical pathways . . ."

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and

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The mere presence or absence of a protein family can be indicative of the existence of an entire cellular process"

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I suspect that anatmical ovelty will typically be associated with new protein families too but that's just a guess.

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[This message has been edited by Tranquility Base, 06-24-2002]

I meant Signal Transduction Pathway (STP). Someone corrected me about this. So I use Signal and not protein.

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Originally posted by Zhimbo:

2. Second, I'm not sure why any new protein would necessarily "break" an exisiting transduction pathway (of either sort), or why 3-5 new proteins suddenly would, or whatever. As long as the original proteins were also being made, I don't see any necessary problem.

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Unfortunately, I don't think you're suceeding in creating a workable definition/standard for "created kind", although I'm still seeing where you're going. It seems more like you're just saying you don't see how systems of proteins could form. I don't see that you've created any barrier, though. You talk about new proteins breaking old pathways, but I don't see how this is inevitable.

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We should consider a typical STP+extracellular signals. Well, maybe I should use the word protein systems. Because STP only occurs within a cell. I focusing on the total intelligent signal from molecule to molecule.Ok, we have Protein System A: signal molecule A, receptor A, the transduction proteins within a cell, reprossors and inducers. The more molecules and bigger reaction sites the more complex it is.Protein System B: signal molecule B, receptor B, the transduction proteins within a cell, reprossors and inducers. The more molecules and bigger reaction sites the more complex it is.Protein System C: signal molecule C, receptor C, the transduction proteins within a cell, reprossors and inducers. The more molecules and bigger reaction sites the more complex it is.If a new protein in celltype A arise would it immediately cause
any trouble by acting with those transduction proteins. If it would be good it would maybe make the transduction more efficient. A protein is added to STP A. But what would next protein in celltype A do. If that also is good it would make the STP a little more even efficient. They dont produce any new protein system, they are just being added to the existing one. But soon enought bad mutations occur and destroy the whole package of accumulated proteins.And if celltype A produce a hormone that trigger signal molecule C its good. And then celltype B produce another hormone that also might help protein system C. The third hormone from celltype B produce a protein that destroy protein system C totally. The organism die.If a new protein system is going to be produced the new proteins must NEVER EVER disturb a vitally important system. So how the questions is: Will these new proteins react only themselves and how many new proteins until the organism die.

Dont worry Jeff.Maybe we havnt FOUND a protein systeme (PS)=(STP + Extracellular signals)=(STP + ES) yet that differ us from chimps.But the clear anatomical differences indicate that there are some particular different PS:s that differ us.

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Originally posted by ZAURUZ:
If a new protein system is going to be produced the new proteins must NEVER EVER disturb a vitally important system.

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Sickle cell anemia does just this, yet in malaria ridden regions it provides some survival value.------------------
www.hells-handmaiden.com

[QUOTE]Originally posted by ZAURUZ:
[b]Ok, we have Protein System A: signal molecule A, receptor A, the transduction proteins within a cell, reprossors and inducers. The more molecules and bigger reaction sites the more complex it is.Protein System B: signal molecule B, receptor B, the transduction proteins within a cell, reprossors and inducers. The more molecules and bigger reaction sites the more complex it is.Protein System C: signal molecule C, receptor C, the transduction proteins within a cell, reprossors and inducers. The more molecules and bigger reaction sites the more complex it is.If a new protein in celltype A arise would it immediately cause
any trouble by acting with those transduction proteins. If it would be good it would maybe make the transduction more efficient. A protein is added to STP A. But what would next protein in celltype A do. If that also is good it would make the STP a little more even efficient. They dont produce any new protein system, they are just being added to the existing one. [/QUOTE][/b]That's one possibility. Another possibility is that a new protein doesn't interact the original group at all. There are lots of possibilities. [QUOTE][b] But soon enought bad mutations occur and destroy the whole package of accumulated proteins.[/QUOTE][/b]Why? I mean it could happen, but why *MUST* it happen? [QUOTE][/B]
And if celltype A produce a hormone that trigger signal molecule C its good. And then celltype B produce another hormone that also might help protein system C. The third hormone from celltype B produce a protein that destroy protein system C totally. The organism die.If a new protein system is going to be produced the new proteins must NEVER EVER disturb a vitally important system. So how the questions is: Will these new proteins react only themselves and how many new proteins until the organism die.[/B][/QUOTE]New proteins can interact with any number of systems, or none. I can't figure out why you assume at some point the influence *must* be destructive. You ask "how many new proteins until the organism die." I say - not necessarily ever. There's no necessary limit to the number of protein changes. Sure, at some point some individual will have a bad mutation, but chances are it won't get passed on, assuming it's really bad. That's selection at work.

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Originally posted by ZAURUZ:
Dont worry Jeff.

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Maybe we havnt FOUND a protein systeme (PS)=(STP + Extracellular signals)=(STP + ES) yet that differ us from chimps.

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But the clear anatomical differences indicate that there are some particular different PS:s that differ us.

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There are clear anatomical differences between lions and pet cats, yet creationists generally consider them the same kind.