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Single Cellular --> Multi Cellular?


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#21 deadlock

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Posted 10 April 2010 - 02:33 PM

The choanocytes in a sponge develop from specific amoebocytes called archaeocytes. In that sense, choanocytes can be thought of as part of a cellular lifecycle of sorts, with archaeocytes serving as a kind of larval state. At the most basic level, differentiation is really no different than a pre-existing developmental cycle and wouldn’t require any complex mutation.


Really ? Can you tell us what so simple mutation would be ?

Sponge evolution may have involved a group of colonial choanoflagellates, some of which never fully developed into their “adult” form and instead remained amoeboid.


Just so story : The evolution of Sponge
Story teller : Isabella

#22 Cata

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Posted 10 April 2010 - 03:23 PM

Well I thought I’d give you one anyways, because quite frankly your original post shows that you don’t understand many aspects of cellular biology. Questions like “...if two cells stick together, how would they reproduce in the same state?” have nothing to do with refuting evolution. It just shows me you haven’t really studied this in detail.


I went ahead and looked at an article about it on the internet. If two cells stick together, they cannot creature two more stuck together unless they make two new cells that stick together. That is not multicellular.

The choanocytes in a sponge develop from specific amoebocytes called archaeocytes. In that sense, choanocytes can be thought of as part of a cellular lifecycle of sorts, with archaeocytes serving as a kind of larval state. At the most basic level, differentiation is really no different than a pre-existing developmental cycle and wouldn’t require any complex mutation.


I'm not asking for an example. Because that is already here. I am saying that genetic differentiation requires:

-Different enhancer sequences
-Different activators for those sequences
-Different genes for those

All of those would have to come at the same time. Or at least the first two.

Let me ask you a simple yes-or-no question.

Would different enhancers and activators matching those enhancers have to come at the same time for them to work?

#23 Isabella

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Posted 10 April 2010 - 03:42 PM

Really ? Can you tell us what so simple mutation would be ?

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Neoteny, when an adult retains a juvenile trait. It’s not all that uncommon. Dogs with short snouts, like pugs, show how a neotenic trait can arise in the population and maintained by selective pressures (in this case, from humans who are breeding the dogs).

Just so story : The evolution of  Sponge
Story teller : Isabella

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You’re right, I’m clearly just making all of this up off the top of my head. There’s probably no such thing as choanoflagellates. Or sponges, for that matter. You caught me.

I went ahead and looked at an article about it on the internet. If two cells stick together, they cannot creature two more stuck together unless they make two new cells that stick together. That is not multicellular.

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And I used sponges as an example of how a multicellular organism doesn’t need to have cells that are “stuck together” or connected by any sort of tissue.

I'm not asking for an example. Because that is already here. I am saying that genetic differentiation requires:

-Different enhancer sequences
-Different activators for those sequences
-Different genes for those

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It does not necessarily require those things. It could be caused by a developmental block in a pre-existing genome. A portion of DNA could become silenced or a mutation could render a codon unreadable.

Would different enhancers and activators matching those enhancers have to come at the same time for them to work?

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Under the assumption that the only way for a cell to differentiate is through an entirely new enhancer sequence, then yes I suppose they would. But I would never make that assumption so this question is kind of silly.

#24 Cata

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Posted 10 April 2010 - 04:05 PM

And I used sponges as an example of how a multicellular organism doesn’t need to have cells that are “stuck together” or connected by any sort of tissue.


That as not my point.

It does not necessarily require those things. It could be caused by a developmental block in a pre-existing genome. 


Er...

Here's how it works, or how I've been taught in school.

A cell has activators, which are molecules that bond to the enhancer sequence on mRNA.
Certain cells in the body have different activators, which makes them produce different proteins, as different parts of DNA can have different enhancers.
These different proteins are differentiation. if the cells do not have different proteins, they are not differentiated.

So... for differentiation as I was taught in school to happen, New activators AND enhancers would have to evolve at the same time for them to happen.

A portion of DNA could become silenced or a mutation could render a codon unreadable.


I can't find anything on google on how gene silencing works exactly, and how it could be used for differentiation.

A mutation is out of the question for obvious reasons, as to cause cell differentiation.

Under the assumption that the only way for a cell to differentiate is through an entirely new enhancer sequence, then yes I suppose they would. But I would never make that assumption so this question is kind of silly.


Why would you have to assume that for it to work? Aren't enhancers useless without an activator to bind to them? And activators are just molecules floating around. If they have some other purpose that does not explain how it could mutate so that it bonds to the newly added enhancer at the same time.

#25 Isabella

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Posted 10 April 2010 - 04:43 PM

These different proteins are differentiation. if the cells do not have different proteins, they are not differentiated.

So... for differentiation as I was taught in school to happen, New activators AND enhancers would have to evolve at the same time for them to happen.

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There is a major flaw in your logic here. The advantage of differentiation is NOT the ability of a cell to take on a new function, although that may eventually happen. It’s the fact that a cell is no longer responsible for all of its pre-existing functions. In other words, when a cell differentiates it is making less of the proteins it formerly needed to make, not necessarily a bunch of new proteins.

I can't find anything on google on how gene silencing works exactly, and how it could be used for differentiation.

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Gene silencing is basically a change in the proteins which pack DNA. Silenced DNA is packed so tightly that their sequences cannot be transcribed, however the silenced genes are still present and intact within the cell.

Because choanocytes come from archaeocytes, we know that all the archaeocytes have the genes to make a feeding apparatus and collect food. Collecting food can be energetically expensive, so it’s more economical if the choanocytes take care of the food collecting, while the archaeocytes focus on reproduction. The alternative would be having one cell responsible for feeding and reproduction, two tasks that take time and energy.

Why would you have to assume that for it to work? Aren't enhancers useless without an activator to bind to them? And activators are just molecules floating around. If they have some other purpose that does not explain how it could mutate so that it bonds to the newly added enhancer at the same time.

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Yes, I agreed that enhancers and activators must be present. I just disagree that a new enhancer must be added in order for a cell to differentiate.

#26 Cata

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Posted 10 April 2010 - 04:54 PM

There is a major flaw in your logic here. The advantage of differentiation is NOT the ability of a cell to take on a new function, although that may eventually happen. It’s the fact that a cell is no longer responsible for all of its pre-existing functions. In other words, when a cell differentiates it is making less of the proteins it formerly needed to make, not necessarily a bunch of new proteins.


Where did I say new proteins? I said new activators and enhancers.

Gene silencing is basically a change in the proteins which pack DNA. Silenced DNA is packed so tightly that their sequences cannot be transcribed, however the silenced genes are still present and intact within the cell.


I know that. i know that there are different kinds of silencing as well from wikipedia. I am wondering how exactly does the DNA code for genes to be silenced? Because DNA codes for activators and enhancers.

EDIT: I did some research for another topic I am typing up, and I found that there is a section on the DNA called a silencer, and that a repressor, another molecule, can bond to it to stop the activator from bonding. This only reinforces my point that the sequence and the molecule have to evolve at the same time.

Because choanocytes come from archaeocytes, we know that all the archaeocytes have the genes to make a feeding apparatus and collect food. Collecting food can be energetically expensive, so it’s more economical if the choanocytes take care of the food collecting, while the archaeocytes focus on reproduction. The alternative would be having one cell responsible for feeding and reproduction, two tasks that take time and energy. 


http://en.wikipedia....erentiated_cell

Yes, I agreed that enhancers and activators must be present. I just disagree that a new enhancer must be added in order for a cell to differentiate.


What?

My question is, would activators and corresponding enhancers have to come at the same time to work?

#27 Isabella

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Posted 10 April 2010 - 05:13 PM

Where did I say new proteins? I said new activators and enhancers.

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Ok. But why new activators and enhancers? Why would an existing sequence have to change? From the wiki article that you linked:
“...cellular differentiation almost never involves a change in the DNA sequence itself”

I know that. i know that there are different kinds of silencing as well from wikipedia. I am wondering how exactly does the DNA code for genes to be silenced? Because DNA codes for activators and enhancers.

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The type of silencing I was talking about is not coded for by DNA, but rather inherited in the form of proteins (something called epigenetic inheritance, but don’t worry about the details of that for now).
The main point here is that genes can be “turned off” by silencing, repression, or any process which prevents them from getting translated into proteins.

My question is, would activators and corresponding enhancers have to come at the same time to work?

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Yes, they would. And no one is claiming such a mutation ever happened or needed to happen.

#28 Cata

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Posted 10 April 2010 - 05:21 PM

Ok. But why new activators and enhancers? Why would an existing sequence have to change? From the wiki article that you linked:
“...cellular differentiation almost never involves a change in the DNA sequence itself”


Because the enhancer is a part of the DNA, but it is not a gene. It is bonded to by the activator.
You're right, there wouldn't have to be new activators and enhancers as there would be some already. However...
I need to learn more about how they are used for differentiation...

Sorry, I don't know enough about how they are used for differentiation to continue this.

Ehhhh..... Ignore this topic for now. I need to do some research about how an organism's shape/structure is defined in the DNA.



Yes, they would. And no one is claiming such a mutation ever happened or needed to happen.


Then how did they evolve? (Don't respond to this question, I'm writing a topic about it right now.)

#29 Isabella

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Posted 10 April 2010 - 05:41 PM

Enhancer sequences are usually “upstream” of the gene, and they are basically a region of DNA that binds to certain transcription proteins and enzymes. An enhancer could be silenced in some way, which would prevent the gene from being transcribed and lead to cell differentiation. But this doesn’t mean the enhancer would need to change, or co-evolve with a transcription factor as you seem to imply.

Then how did they evolve? (Don't respond to this question, I'm writing a topic about it right now.)

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I probably won’t respond to that new topic, even though I’d have plenty of arguments to contribute. You need to stop playing this endless cat-and-mouse game with us, Cata. Every time I answer one of your questions you change the topic of the debate instead of just addressing my response head-on.

#30 Cata

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Posted 10 April 2010 - 05:50 PM

I probably won’t respond to that new topic, even though I’d have plenty of arguments to contribute. You need to stop playing this endless cat-and-mouse game with us, Cata. Every time I answer one of your questions you change the topic of the debate instead of just addressing my response head-on.


I address the topics, unless I make an error like here. I admitted that I made a mistake.

#31 deadlock

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Posted 10 April 2010 - 05:52 PM

Neoteny, when an adult retains a juvenile trait. It’s not all that uncommon. Dogs with short snouts, like pugs, show how a neotenic trait can arise in the population and maintained by selective pressures (in this case, from humans who are breeding the dogs).


That´s not the same as cell differentiation

You’re right, I’m clearly just making all of this up off the top of my head. There’s probably no such thing as choanoflagellates. Or sponges, for that matter. You caught me.


What does not exist is your speculation, story, whatever you name it..

#32 AFJ

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Posted 11 April 2010 - 05:56 AM

Just a comment, because I don't have much time this morning. Basic microbiology says that genes get turned off and on all the time. Some 'housekeeping genes'--genes that are constantly needed for homeostasis, are never repressed. Many are repressed and activated as needed.

A repressor turns off a gene by binding to the promotor and blocking RNA polymerase, so that it cannot start transcription.

Look up Lac1 repressor. When lactose is not present for the bacteria, Lac1 protein binds to the gene promotor which is responsible for the enzyme that helps digest lactose. Guess what? It has a binding site just for lactose molecules. As soon as they show up, Lac1 binds a lactose molecule, changes shape and unbinds from the promotor. What a coincidence again!

The question no one wants to answer: (I wonder if evos even read this kind of question, the answer is just too painful for them I think)

So how did DNA just happen to mutate the gene that encodes an enzyme to digest lactose perfectly, and at the same time encode a repressor which not only has binding sites for the promotor of the lactose digesting enzyme, BUT also JUST HAPPENS to fold in such a way that it produces a binding site for LACTOSE ITSELF, so it will stop repressing the gene?

#33 Isabella

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Posted 11 April 2010 - 04:21 PM

That´s not the same as cell differentiation

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I think you missed what I was trying to get at. My point is that neoteny can have several causes, but the ultimate result will be the suppression of an adult trait.

The reason I brought up neoteny was to show that a mutation which suppresses a mature characteristics is very possible and we have observed it in larger animals.

Sponges are not an example of neoteny, but their cell differentiation is based on a similar concept. Only some cells mature, while others do not.

What does not exist is your speculation, story, whatever you name it..

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What, that a sponge may have evolved from a colonial organism similar to a choanoflagellate? Well, let’s see: choanoflagellates do form colonies, that’s not a speculation. And choanocytes are nearly identical to choanoflagellates, that’s not a speculation either. And a sponge is really just a colonial organization of choanocytes, with some amoeboid cells and a gel matrix.

And there are plenty of articles that outline the same “speculation” that I just did, so it’s not something that I personally made up.

#34 AFJ

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Posted 11 April 2010 - 07:56 PM

What, that a sponge may have evolved from a colonial organism similar to a choanoflagellate? Well, let’s see: choanoflagellates do form colonies, that’s not a speculation. And choanocytes are nearly identical to choanoflagellates, that’s not a speculation either. And a sponge is really just a colonial organization of choanocytes, with some amoeboid cells and a gel matrix.

And there are plenty of articles that outline the same “speculation” that I just did, so it’s not something that I personally made up.

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Choanoflagellates are also similar to sperm cells minus the collar cells.

Amoebae are phagocytes and so are white blood cells.

Since there's not much connection between these things, only appearance. Coupled with the fact that the sponges appear suddenly in the Cambrian strata (which are wrongly interpreted catastrophically covered sea bottoms), along with more phylla than we now have alive. Coupled with the fact that there is no model of how a colony of independent unicells cooperated genetically and were selected together as one organism, while the unicells (or was it their mysterious undefined and unfound ancestor) continued to exist and were not selected as such-----I prefer a similar design explanation.

A brand new Mercededes Benz has an internal combustion engine, just like a Model T, but a Model T was not an ancestor of the Mercedes Benz. Pehaps this seems like an unfair comparison, but not if your looking at it from design perspective, instead of the evolutionary perspective. The the fundamental truth is the similarity arises out of an engineering need--namely the designed mechanism can work in two very different variations and vehicles.

The unicellular to multicellular jump is not happening today and never has happened. The evos say we ignore evidence, but they ignore the impossibility of their theory.

#35 Isabella

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Posted 12 April 2010 - 03:58 PM

Choanoflagellates are also similar to sperm cells minus the collar cells.

Amoebae are phagocytes and so are white blood cells.

Since there's not much connection between these things, only appearance.

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There’s really not an obvious connection between choanoflagellates and sperm, besides the flagellum. I never tried to convince you that there was. Choanoflagellates and choanocytes, however, are similar in more ways than just appearance, like feeding mechanism and genome. Furthermore, a specific type of choanoflagellate called Proterospongia already does form colonies where several stick together.

Coupled with the fact that there is no model of how a colony of independent unicells cooperated genetically and were selected together as one organism while the unicells (or was it their mysterious undefined and unfound ancestor) continued to exist and were not selected as such-----I prefer a similar design explanation.

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They probably “cooperated genetically” because they were genetically identical, originating from the asexual reproduction of one cell. A mature sponge reproduces s*xually, but a sponge grows by asexual cell division and can regenerate into a new sponge from only a few isolated cells.

#36 Cata

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Posted 12 April 2010 - 04:34 PM

Is it not a colony of unicellular organisms then?
It does not have any system of genetic differentiation, does it?

#37 Isabella

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Posted 12 April 2010 - 04:41 PM

Sponges or choanoflagellates? Sponges are considered multicellular, with differentiated cells.

#38 Cata

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Posted 12 April 2010 - 04:54 PM

Sponges or choanoflagellates? Sponges are considered multicellular, with differentiated cells.

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http://en.wikipedia....erentiated_cell

cellular differentiation is the process by which a less specialized cell becomes a more specialized cell type.


Does it become differentiated, or does it merely take up a different task?

#39 deadlock

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Posted 12 April 2010 - 07:24 PM

I think you missed what I was trying to get at. My point is that neoteny can have several causes, but the ultimate result will be the suppression of an adult trait.

The reason I brought up neoteny was to show that a mutation which suppresses a mature characteristics is very possible and we have observed it in larger animals.

Sponges are not an example of neoteny, but their cell differentiation is based on a similar concept. Only some cells mature, while others do not.


None of that explain how unicellular turns into multicellular.

What, that a sponge may have evolved from a colonial organism similar to a choanoflagellate? Well, let’s see: choanoflagellates do form colonies, that’s not a speculation. And choanocytes are nearly identical to choanoflagellates, that’s not a speculation either. And a sponge is really just a colonial organization of choanocytes, with some amoeboid cells and a gel matrix.


So, take a colony of choanoflagellate and turn them into sponge.Can you ?

And there are plenty of articles that outline the same “speculation” that I just did, so it’s not something that I personally made up.

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Ok you are not the only one with imagination in the World.

#40 Isabella

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Posted 12 April 2010 - 08:27 PM

Does it become differentiated, or does it merely take up a different task?

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The cells differentiate. There are a few different types of cells found in a sponge, choanocytes and amoebocytes/archaeocytes were just a couple of examples.

None of that explain how unicellular turns into multicellular.

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You have a colonial organization of cells and due to mutation/silencing, some are able to remain in one form while others take on a different role.

So, take a colony of choanoflagellate and turn them into sponge.Can you ?

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When did I ever suggest that was possible? Choanoflagellates are not choanocytes, and they cannot turn into sponges. But their morphology and behaviour suggest that sponges could have originated from a similar organism.




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