Can self-assembling molecules show us how cells function?

[Diderot]

This has strayed WAY off topic. Please return to discussion of the OP.

My special thanks to Darwin123 for his patience and effort. I fully enjoyed our debate which ended so very abruptly.

 

[Evo]

My special thanks to Darwin123 for his patience and effort. I fully enjoyed our debate which ended so very abruptly.

Please be careful not to derail threads going forward.

 

[Darwin123]

Which mechanism is dominant in the cell 'diffusion' or 'transport'?

Physicists and biologists think of diffusion as one specific type of transport. Transport is any process that gets a scalar from one location to the other. Two types of transport studied by physicists and biologists are diffusion and advection.
Diffusion is the transport that is characterized by "random" motions of the molecules. Advection is the transport that is characterized by "coherent" motion of the molecules.
On large distance scales, advection is usually greater than diffusion. On distance scales comparable to the diameter of a prokaryote cell, diffusion is usually greater than advection.
Eukaryote cells are broken up into compartments called organelles. Each organelle has a size on the order of a prokaryote cell. Therefore, diffusion dominates within an organelle. However, the cytoskeleton provides a type of advection between organelles. Advection is at least as important as diffusion between organelles.
I think the OP was asking about chemical reactions that occur inside prokaryotes or inside organelles. On this distance scale, collisions are truly random. However, the probability per collision of a useful chemical reaction is relatively high. There are millions of collisions per second, so a useful reaction are quite probably in one second.
The correct answer to the OP's question may be this. The description of "random collisions" at a "rapid rate" is probably valid inside a prokaryote cell. However, eukaryote cells have a higher level of complexity. The description of "random collisions" at a "rapid rate" is probably valid inside individual organelles of the eukaryote cell, but not in the cytoplasm between organelles. Between organelles, one has to take into account the cytoskeleton.
One way to visualize this is to think of some of the organelles as being prokaryotes. Some prokaryotes evolved to live together as a eukaryote cell. The cytoskeleton is a "telephone network" to aid communication between prokaryote cells. A eukaryote cell is basically a colony of prokaryote cells.

 

[atyy]

The cytoskeleton is a "telephone network" to aid communication between prokaryote cells.

What are some examples of this?

 

[Pythagorean]

What are some examples of this?

http://www.ncbi.nlm.nih.gov/books/NBK9964/

 

[Diderot]

(...) the components of the cell work together so nicely simply because that combination of matter happened to work out so nicely. (...)

Is it fair to say that there is a very 'delicate balance' between all the chemical reactions in the cell? There must be an exact amount of everything? The smallest change (mutation) can destroy this balance, and shatter the coincidental cooperation of the parts?
And is it fair to say that this balance is unsupported? Nothing is 'interested' in keeping this delicate balance; not the parts of the cell, not the surroundings of the cell and not the cell itself?

 

[Ryan_m_b]

Is it fair to say that there is a very 'delicate balance' between all the chemical reactions in the cell? There must be an exact amount of everything? The smallest change (mutation) can destroy this balance, and shatter the coincidental cooperation of the parts?
And is it fair to say that this balance is unsupported? Nothing is 'interested' in keeping this delicate balance; not the parts of the cell, not the surroundings of the cell and not the cell itself?

No, homeostasis takes care of matters like these. Cells can respond to changes in the environment in ways that counter whatever negative condition has arisen. A good example is the hypoxia (low oxygen) response pathway.

In human cells the protein HIF1-a is constantly synthesised but immediately destroyed via an oxygen dependent reaction. In low oxygen this degredation reaction stops "stabilising" HIF1-a. These proteins then migrate into the nucleus to form the HIF1 transcriotion factor which causes the activation of a myriad of genes involved in pathways that will help the cell survive e.g. by upregulating glycolysis and releasing angiogenic factors to bring more oxygen.

 

[Diderot]

Is it fair to say that there is a very 'delicate balance' between all the chemical reactions in the cell? There must be an exact amount of everything? The smallest change (mutation) can destroy this balance, and shatter the coincidental cooperation of the parts?
And is it fair to say that this balance is unsupported? Nothing is 'interested' in keeping this delicate balance; not the parts of the cell, not the surroundings of the cell and not the cell itself?

No, homeostasis takes care of matters like these. Cells can respond to changes in the environment in ways that counter whatever negative condition has arisen. A good example is the hypoxia (low oxygen) response pathway. (…)

I do not think that this is an answer to my question. The parts of the cell that constitute homeostasis are obviously part of the chemicals that are in a ‘delicate balance’.
So the question ‘is there an unsupported delicate balance between all the chemical reactions in the cell?’ includes the chemicals in the cell that constitute homeostasis.

 

[Ryan_m_b]

I do not think that this is an answer to my question. The parts of the cell that constitute homeostasis are obviously part of the chemicals that are in a ‘delicate balance’.
So the question ‘is there an unsupported delicate balance between all the chemical reactions in the cell?’ includes the chemicals in the cell that constitute homeostasis.

Why isn't it an answer to your question? If something were to damage a cell or require a change in behaviour (including hypothetical spontanous breakdown of a pathway) this itself will cause changes that deal with the issue. Within reason of course, cells aren't immortal. Too much damage at once or over time will ensure that the cell dies no matter what it tries.

 

[Diderot]

Why isn't it an answer to your question? If something were to damage a cell or require a change in behaviour (including hypothetical spontanous breakdown of a pathway) this itself will cause changes that deal with the issue. Within reason of course, cells aren't immortal. Too much damage at once or over time will ensure that the cell dies no matter what it tries.

My question includes the parts which constitute homeostatic activities. If I understand you correctly your answer just seems to shift attention to these parts.
If it is of any help I can rephrase my question like this:
Is it fair to say that there is a very 'delicate balance' between all the chemical reactions of the ‘homeostatic system’ in the cell? There must be an exact amount of everything? The smallest change (mutation) can destroy this balance, and shatter the coincidental cooperation of the parts?
And is it fair to say that this balance is unsupported? Nothing is 'interested' in keeping this delicate balance; not the parts of the ‘homeostatic system’, not the surroundings of the ‘homeostatic system’ and not the ‘homeostatic system’ itself?

 

[Ryan_m_b]

My question includes the parts which constitute homeostatic activities. If I understand you correctly your answer just seems to shift attention to these parts.
If it is of any help I can rephrase my question like this:
Is it fair to say that there is a very 'delicate balance' between all the chemical reactions of the ‘homeostatic system’ in the cell? There must be an exact amount of everything? The smallest change (mutation) can destroy this balance, and shatter the coincidental cooperation of the parts?
And is it fair to say that this balance is unsupported? Nothing is 'interested' in keeping this delicate balance; not the parts of the ‘homeostatic system’, not the surroundings of the ‘homeostatic system’ and not the ‘homeostatic system’ itself?

Yes I understand but this is covered in what I have said previously. To reiterate though:

- No the phrase "delicate balance" is not applicable because in many cases it's not delicate and it isn't a balance.

- No it doesn't require an "exact amount" though many processes require an optimum amount which is regulated, usually by some form of negative feedback.

- That negative feedback is not any kind of top down oversight, it's built into the system (like the oxygen dependent reaction supressing hypoxia response).

- Cells are very redundant, they can take (relatively) a lot of damage before dying and have mechanisms to fix themselves; just look at how robust DNA repair systems are.

- If the damage is such that the cell cannot fix itself then it will die but this is an extensive amount of damage.

Forgive me for being blunt but are you trying to push intelligent design via irreducible complexity here?

 

[Diderot]

Yes I understand but this is covered in what I have said previously. (…)

I do not agree. Thank you for your patience and effort. There is a barrier between us.

Forgive me for being blunt but are you trying to push intelligent design via irreducible complexity here?

No.

 

[Ryan_m_b]

I do not agree. Thank you for your patience and effort. There is a barrier between us.

No worries, feel free to ask further questions. Either I'm missing something or not explaining it well enough and I'm interested in fixing that.

No.

Cool. I had to ask, we frequently get people joining to ask questions like this purely so that they can try to justify their belief (usually by ignoring any post that disagrees with them and taking any post that hints that it does as proof). I'd rather nip it in the bud than waste time.

 

[Diderot]

Cool. I had to ask, we frequently get people joining to ask questions like this purely so that they can try to justify their belief (usually by ignoring any post that disagrees with them and taking any post that hints that it does as proof). I'd rather nip it in the bud than waste time.

I can feel your outrage with these people. Why don’t they embrace the beauty and clarity of reductionism? ‘Homeostasis’ is still no answer to my question though.

 

[Simon Bridge]

What makes you think there is a "delicate balance" at all?

If we can understand the way you use these terms then perhaps the answers can more directly answer the question. As far as I can see, the "homeostasis" answer does answer the question as it is written - especially with the clarification in post #41.

A mechanical example of a delicate balance would be a pin balanced on it's point - it is unstable: the slightest nudge dramatically changes it's state. A pin on it's side is in a stable situation - even quite large nudges still leaves the pin on it's side.

And example of a running mechanical homeostasis would be a steam-engine with a governor - nobody would say the engine is in a "delicate balance" because a small nudge quickly restores it through negative feedback.

Ryan has told you that the processes in a cell are, and the cell itself is, very robust ... it takes quite a big nudge to break them. Therefore, the phrase "delicate balance", as it is usually understood by scientists and engineers, does not apply to the processes in a cell.

 

[Ryan_m_b]

I can feel your outrage with these people. Why don’t they embrace the beauty and clarity of reductionism?

That's not how I feel. In fact I haven't said anything about reductionism, why are you bringing it up and putting these words in my mouth? I feel frustrated when people are willfully ignorant, especially when they waste forum member's time.

‘Homeostasis’ is still no answer to my question though.

I'll try from the beginning. Within a cell there is a myriad of dynamic metabolic pathways active at once (see these images). These pathways interact with each other and the environment and can modify internal processes for different behaviours. When something happens to effect the cell in a negative way (i.e. something disrupts one of these pathways) negtive feedback mechanisms strive to correct this. If the damage is to great or something inhibits the homeostatic mechanisms the cell dies.

 

[Diderot]

If the damage is to great or something inhibits the homeostatic mechanisms the cell dies.

In posting #40 I rephrased my question like this:
Part 1: “Is it fair to say that there is a very 'delicate balance' between all the chemical reactions of the ‘homeostatic system’ in the cell? There must be an exact amount of everything? The smallest change (mutation) can destroy this balance, and shatter the coincidental cooperation of the parts?”
Now you say that if ‘something inhibits the homeostatic mechanisms the cell dies’. So why not answer ‘yes’ to my questions? There doesn’t seem to be a homeostatic system C for homeostatic system B of homeostatic system A, right?

I retract ‘part 2’ of my question in posting #40. This has philosophical implications (reductionism) which I feel no longer free to discuss. Maybe I'm mistaken but I do feel a lack of enthusiasm towards my efforts. Thank you for your time and sharing your thorough knowledge.

 

[Ryan_m_b]

In posting #40 I rephrased my question like this:
Part 1: “Is it fair to say that there is a very 'delicate balance' between all the chemical reactions of the ‘homeostatic system’ in the cell? There must be an exact amount of everything? The smallest change (mutation) can destroy this balance, and shatter the coincidental cooperation of the parts?”
Now you say that if ‘something inhibits the homeostatic mechanisms the cell dies’. So why not answer ‘yes’ to my questions? There doesn’t seem to be a homeostatic system C for homeostatic system B of homeostatic system A, right?

I didn't answer yes because your question was loaded. You're proposing that the system is finely balanced which as as Simon pointed out with his excellent pin analogy doesn't hold. Did you take a look at the images I linked? Metabolic pathways are rarely as simple as A --> B --> C. They are more of a web that generally avoids critical links.

In essence the answer to your question is no. Cells are not finely balanced and are inherently self regulating. To ask whether or not they would die if self regulation was inhibited seems to be a pointless question.

I retract ‘part 2’ of my question in posting #40. This has philosophical implications (reductionism) which I feel no longer free to discuss. Maybe I'm mistaken but I do feel a lack of enthusiasm towards my efforts. Thank you for your time and sharing your thorough knowledge.

What efforts? If you're sensing any negativity it's probably because you keep asking loaded questions, reject the answers you are given without clarifying what you don't understand and post with an undertone that you have an axe to grind wrt "reductionism", I've put that in quotes because you haven't outlined how reductionism comes into your question about cellular biology.

If you want to learn about cellular biology then feel free to continue asking (without the loaded questions), if you want to discuss reductionism then why not start a thread in the philosophy forum?

 

[Simon Bridge]

In posting #40 I rephrased my question like this:
Part 1: “Is it fair to say that there is a very 'delicate balance' between all the chemical reactions of the ‘homeostatic system’ in the cell? There must be an exact amount of everything? The smallest change (mutation) can destroy this balance, and shatter the coincidental cooperation of the parts?”

I don't think it is possible to answer these questions to your satisfaction without first knowing how your use of the words "delicate balance" differ from the usual meanings in engineering and science (particularly biology). If you won't answer questions, we cannot help you.

Now you say that if ‘something inhibits the homeostatic mechanisms the cell dies’. So why not answer ‘yes’ to my questions? There doesn’t seem to be a homeostatic system C for homeostatic system B of homeostatic system A, right?

In the example of a steam engine - I can "inhibit the homeostatic system" by ramming a wrench in the governor. The engine then dies down or explodes. The engine homeostasis is still not a delicate balance in the engineering sense because ramming foreign objects in the works is not a small nudge.

So a cell's homeostasis may be interrupted by injecting a strong acid into it, hitting it with a hammer, being invaded by a virus, stuff like that ... it can even interrupt it's own by apoptosis. Bad damage would trigger apoptosis. But you seem to be asserting that a small change on the scale of cellular processes could catastrophically affect the cell's performance? This is simply not the case and saying "it is" and "I disagree" does not make it so. Perhaps you can provide an example to back up your assertions?

Maybe I'm mistaken but I do feel a lack of enthusiasm towards my efforts. Thank you for your time and sharing your thorough knowledge.

You are mistaken - if there were a "lack of enthusiasm", the thread would be quickly abandoned.

However - if you won't answer direct questions, and reject the answers offered to you, then the enthusiasm will drain away very quickly.

 

[Darwin123]

What are some examples of this?

My speculation, from Margulis, is that many organelles were originally prokaryotes that evolved to be organelles. So I answer your question with two types of links. Articles about communication between organelles in eukaryotic cells, and articles about communication between prokaryotes using filamentary structures.
The first few articles present communication between organelles in the eukaryote cell.

http://www.landesbioscience.com/journals/BioArchitecture/article/20302/
“Crosslinking proteins maintain organelle structure and facilitate their function through the crosslinking of cytoskeletal elements. We recently found an interaction between the giant crosslinking protein dystonin-a2 and the microtubule-associated protein-1B (MAP1B), occurring in the centrosomal region of the cell. In addition, we showed that this interaction is necessary to maintain microtubule acetylation. Loss of dystonin-a2 disrupts MT stability, Golgi organization, and flux through the secretory pathway. This, coupled to our recent finding that dystonin-a2 is critical in maintaining endoplasmic reticulum (ER) structure and function, provides novel insight into the importance of dystonin in maintenance of organelle structure and in facilitating intracellular transport. These results highlight the importance of cytoskeletal dynamics in communicating signals between organelle membranes and the cytoskeleton. Importantly, they demonstrate how defects in cytoskeletal dynamics can translate into a failure of vesicular trafficking associated with neurodegenerative disease.”

http://netresearch.ics.uci.edu/mc/papers/NSTI06.pdf
“A molecular communication system using a network of cytoskeletal filaments.
…
Using molecular communication to control communication between nanomachines is inspired by the observation of biological systems which already commonly communicate through molecules.”

http://www.scielo.br/scielo.php?pid=S0074-02762012000300001&script=sci_arttext
“This review also examines recent data on the presence of nanotubes, which are structures that are well characterised in mammalian cells that allow direct contact and communication between cells.”

http://jcs.biologists.org/content/113/15/2747.full.pdf
“Trafficking and signaling through the cytoskeleton: a specific mechanism
We conclude that diffusion along cytoskeletal tracks is a reliable alternative to other established ways of intracellular trafficking and signaling, and therefore provides an additional level of cell function regulation.”

http://www.scielo.br/scielo.php?pid=S0074-02762012000300001&script=sci_arttext
“Prokaryotic cells: structural organisation of the cytoskeleton and organelles”

The articles below describe specific interactions between prokaryotes using pili, filamentary structures. Thus, filamentary structures are used for communication between free-living prokaryotes.

http://en.wikipedia.org/wiki/Pilus
“A pilus (Latin for 'hair'; plural : pili) is a hairlike appendage found on the surface of many bacteria.[1][2] The terms pilus and fimbria (Latin for 'thread' or 'fiber'; plural: fimbriae) can be used interchangeably, although some researchers reserve the term pilus for the appendage required for bacterial conjugation. All pili are primarily composed of oligomeric pilin proteins.
Conjugative pili allow the transfer of DNA between bacteria, in the process of bacterial conjugation. They are sometimes called "sex pili", in analogy to sexual reproduction, because they allow for the exchange of genes via the formation of "mating pairs". Perhaps the most well-studied is the F pilus of Escherichia coli, encoded by the F plasmid or fertility factor.”

http://faculty.ccbcmd.edu/courses/bio141/lecguide/unit1/prostruct/pili.html
“The short attachment pili or fimbriae are organelles of adhesion allowing bacteria to colonize environmental surfaces or cells and resist flushing. The pilus has a shaft composed of a protein called pilin. At the end of the shaft is the adhesive tip structure having a shape corresponding to that of specific glycoprotein or glycolipid receptors on a host cell (see Fig. 1).
Because both the bacteria and the host cells have a negative charge, pili may enable the bacteria to bind to host cells without initially having to get close enough to be pushed away by electrostatic repulsion. Once attached to the host cell, the pili can depolymerize and enable adhesions in the bacterial cell wall to make more intimate contact.”

I apologize for this fellows compounds sentences. The point is that filamentary structures like pili probably evolved for bacterial cells to bind to other cells.
http://grupos.unican.es/intergenomica/docencia/pdfs/seubert03.pdf
“The identification of transferred substrates would be a major step forward in the molecular understanding of how the B. tribocorum Trw system contributes to pathogenesis.Alternatively, but not mutually exclusively to substrate translocation, the Trw system may have evolved primarily to mediate binding to various host cell structures via surface-exposed pili.”

 

[Diderot]

"The essence of cellular life is regulation: The cell controls how much and what kinds of chemicals it makes; when it loses control, it dies."
In respect to the demand for fine-tuned regulation I'm still struggling with the concept of diffusion as a transport system.

Physicists and biologists think of diffusion as one specific type of transport. ... Diffusion is the transport that is characterized by "random" motions of the molecules. [D]iffusion dominates within an organelle.

Earlier in this thread I wrote:

I'm trying to incorporate these speeds in my understanding of the cell. According to Ken Shirrif these speeds explain a lot: “Watching the video, you might wonder how the different pieces just happen to move to the right place. In reality, they are covering so much ground in the cell so fast that they will be in the ‘right place’ very frequently just by chance.” This seems debatable to me. If in a workshop all the parts of a car are floating around it’s hard to imagine that a car will be assembled. ...

[T]hough everything is moving fast, the interactions are even faster. On top of that, the different bits have a range of ways they attract and repel other bits...

If the different bits have the possibility to form all sorts of chemical bonds the only result can be chaos. Random movement of Lego parts cannot explain a complex Lego car. So the different bits must all be highly specified and have just one possibility to fall into place.

To use your analogy of car assembly - it's like the situation where different workers and parts arrive at different times ... when someone sees the right part, they put it in the car. You can build a car that way - in fact, hobby auto-mechanics (restoring a car for eg) often works like that...

Another thing that is necessary is sequence of assembly. So highly specified part A must have just one possibility B at moment C and highly specified part A’ must have just one possibility B’ at moment C’ … etc.

What do you think? Am I getting closer to understanding?

 

[Ryan_m_b]

If the different bits have the possibility to form all sorts of chemical bonds the only result can be chaos. Random movement of Lego parts cannot explain a complex Lego car. So the different bits must all be highly specified and have just one possibility to fall into place.

A quick piece of advice; when learning about a topic it is best to not making conclusions that contradict what is already known. It doesn't give the impression of a good attitude for learning and in the case of something relevant to evolution may get you branded as a creationist with an agenda.

Whilst many molecules such as proteins have multiple roles they generally have very specific active sites. With regards to assembly look into chaperone proteins.

 

[Diderot]

A quick piece of advice; when learning about a topic it is best to not making conclusions that contradict what is already known. It doesn't give the impression of a good attitude for learning and in the case of something relevant to evolution may get you branded as a creationist with an agenda.
Whilst many molecules such as proteins have multiple roles they generally have very specific active sites. With regards to assembly look into chaperone proteins.

First of all, please excuse me for my bad English writing. It is not my intention to make a creationist point here. I'm trying to imagine how diffusion can contribute to order. All sorts of possibilities for chemical bonds seemed like an obvious threat to order to me, so I’m arguing for highly specified parts that can fall in their unique places in a specific sequence.
Unfortunately my knowledge of biology is also extremely poor so it’s no surprise that my statements contradict what is already known.
I would appreciate it very much if someone points out where I go wrong.

 

[Darwin123]

First of all, please excuse me for my bad English writing. It is not my intention to make a creationist point here. I'm trying to imagine how diffusion can contribute to order. All sorts of possibilities for chemical bonds seemed like an obvious threat to order to me, so I’m arguing for highly specified parts that can fall in their unique places in a specific sequence.
Unfortunately my knowledge of biology is also extremely poor so it’s no surprise that my statements contradict what is already known.
I would appreciate it very much if someone points out where I go wrong.

I am not sure what you are asking. The way you write English makes it appear as though you are pointing out something you think is wrong. I don't really know what issues to address.
One problem with the English is that you are excessively anthropomorphizing everything. For instance, you say that "all sorts of possibilities for chemical bonds seems like an obvious threat to order to me." Are the chemical bonds really threatening order? Is it obvious that the chemical bonds are threatening? Furthermore, you are "trying to imagine how diffusion can contribute to order." Did anyone say "diffusion is contributing to order"? You seem to think that diffusion is countering the threat of the possible chemical bonds.
Maybe you are asking what reduces the probability of most chemical bonds forming, and why some chemical bonds are likely to form anyway. With that:
In what are called living things, there are these large molecules with specific shapes. This simplified model is called "lock and key theory." The shape of the molecule makes certain chemical bonds unlikely to form after collision with other molecules. The shape of the molecule allows certain bonds to for after collision with other molecules.
The selectivity is 80% of the time determined just by the geometry (shape) of the molecule. There are also electrical and magnetic forces involved. Quantum mechanics is also involved. What is important is that some chemical reactions are more likely than others for certain molecules. I will dump all these different properties into the word "shape". The randomness of the collision is greatly reduced by the shape and properties of the molecules.
Now, maybe you want to know how the shape of the molecule got that way.
The shape of each molecule is copied with high fidelity from generation to generation. However, high fidelity doesn't mean infinite fidelity. Some cells in each generation have a molecule or two which is slightly different. These are called inherited variations. Most mutations increase the probability of the cell dying or not reproducing in a certain environment. Some inherited variations improve the probability of the cell dying out in that environment. The cells with the improvements eventually outnumber the ones that remained the same or decreased the chance of survival. This is natural selection.
Natural selection together with inherited variation supposedly determined the current shape of the molecules. Hypothetically, the molecules in the first generations of life did not have the specific shapes they had now. However, generation after generation of variation and selection has resulted in molecules of very specific shape.
Now, what in my description can't you imagine?
There was an article in the Washington Post on 20 September 2012 (Wedsday) in the Politics and Nation section. Some scientists kept a colony in a bacteria (E. coli) in bottle for 25 years. This corresponds to 50,000 generations of bacteria. The PI was Richard Lenski of Michigan State University. The full experiment is described in a recent issue of Nature. Alas, I don't have the original article in Nature.
Every 500 generations, a sample from the colony was frozen as a record of changes. Some challenge was given every day to the flask. Every day, part of the colony was transferred to a new sugar solution. However, there was no exotic manipulation of the bacteria.
The bacteria in the flask now have different molecules and different chemical reaction chains then their distant ancestors.
The current bacteria now can digest citrate, something their distant ancestors could not do. This took about 30,000 generations of bacteria. Some of these chemical reaction chains seem very specific and rather complex.
Yet at no time did any scientist "design" the molecules or reactions. The shape was not directly controlled except by providing that very general "challenge". There was no guidance to the shape. They just moved the bacteria into a new flask with fresh sugar every day. Yet, the new molecules have to have a really complex and specific shape to digest citrate. There are several other "unlikely" changes that have occurred over the 50,000 generations.
Now, what do you think happened in that flask over 25 years and 50,000 generations?
Please answer without anthropomorphizing anything. The E. coli may be insulted.

 

[atyy]

If the different bits have the possibility to form all sorts of chemical bonds the only result can be chaos. Random movement of Lego parts cannot explain a complex Lego car. So the different bits must all be highly specified and have just one possibility to fall into place.

Another thing that is necessary is sequence of assembly. So highly specified part A must have just one possibility B at moment C and highly specified part A’ must have just one possibility B’ at moment C’ … etc.

Yes, this is essentially correct. There are also various ways of preventing and undoing errors.
http://www.ncbi.nlm.nih.gov/books/NBK26850/
http://www.ncbi.nlm.nih.gov/books/NBK26829/
http://en.wikipedia.org/wiki/Kinetic_proofreading

 

[Pythagorean]

If the different bits have the possibility to form all sorts of chemical bonds the only result can be chaos. Random movement of Lego parts cannot explain a complex Lego car. So the different bits must all be highly specified and have just one possibility to fall into place.

This, I think, is the problem statement (especially in the context of your quotes). In the first place, Legos are a bad example because they have very limited degrees of freedom for coupling (there's very few ways you can put Legos together). The building blocks of life, on the other hand, are rather "sticky" (they stick together in all kinds of different ways).

But more importantly, your statement opposes the view that these sticky pieces can, indeed, through random motion, form functional structures. You have to remember the age of Earth and how many chances it's had to perform random trials. Even with legos, if you jumble them around in a box enough times, there is a chance they will eventually make some simple structures (even a car, though the chance is very very low). In none of these examples would you be able to commit enough trials in your lifetime... but life exceeds many lifetimes; billions of years of trials. It's not really surprising that all these sticky components had a chance to stick together in complicated ways.

And remember that they didn't start out quite as complicated, it's been a very long period of emergence. There's a point at which early Earth chemistry becomes "life" through these small, random changes. Self-organized complexity.

Here's a very simple example:

KPP-4-LEHXQ[/youtube] notice that ... heat vents, the lipid layer, and the ocean.)

 

[gravenewworld]

Have fun

http://www.sigmaaldrich.com/etc/medialib/docs/Sigma-Aldrich/General_Information/metabolicpathways_updated_02_07.Par.0001.File.tmp/metabolic_pathways_poster.pdf

 

[atyy]

This, I think, is the problem statement (especially in the context of your quotes). In the first place, Legos are a bad example because they have very limited degrees of freedom for coupling (there's very few ways you can put Legos together). The building blocks of life, on the other hand, are rather "sticky" (they stick together in all kinds of different ways).

But more importantly, your statement opposes the view that these sticky pieces can, indeed, through random motion, form functional structures. You have to remember the age of Earth and how many chances it's had to perform random trials. Even with legos, if you jumble them around in a box enough times, there is a chance they will eventually make some simple structures (even a car, though the chance is very very low). In none of these examples would you be able to commit enough trials in your lifetime... but life exceeds many lifetimes; billions of years of trials. It's not really surprising that all these sticky components had a chance to stick together in complicated ways.

And remember that they didn't start out quite as complicated, it's been a very long period of emergence. There's a point at which early Earth chemistry becomes "life" through these small, random changes. Self-organized complexity.

Here's a very simple example:

KPP-4-LEHXQ[/youtube] notice tha...gent laws that are essentially deterministic.

 

[Pythagorean]

Could you also address that "random" may mean essentially deterministic? For example, can the second law of thermodynamics be violated? Theoretically yes, practically no. So it would not be wrong to say that there are emergent laws that are essentially deterministic.

When I use random in this context, I mean in the noise sense. We can use a random distribution to model noise, but the noise could have easily come from several unrelated deterministic processes. The "random" terminology illustrates that aspect: that the sources are uncorrelated.

 

[atyy]

When I use random in this context, I mean in the noise sense. We can use a random distribution to model noise, but the noise could have easily come from several unrelated deterministic processes. The "random" terminology illustrates that aspect: that the sources are uncorrelated.

Hmmm, would "1/f noise" be noise then, since it would have correlations on all time scales?