Jump to content
Science Forums

Punctuated Equilibria theories


bumab

Recommended Posts

TeleMad: Species are "built" to OPTIMIZE mutations, not avoid them. Both too many and too few mutations can be detrimental to a species.

 

Biochemist: Pure conjecture, but a nice idea.

 

Which of these do you reject, and why?

 

1) Too many mutations can be bad for a species. Natural selection may not be able to keep pace with too rapid a pace and the species could go extinct. For example, if we humans averaged one million mutations per gamete, how long do you think we'd be around?

 

2) Too few mutations can be bad for a species. A species is fit only in regard to the current environment. If the environment changes, the species needs to have built up enough genetic diversity in order to survive under the new conditions.

 

TeleMad: We can trigger rapid speciation in the lab. I gave an example involving plants.

 

Biochemist: But you might have noticed that the topic of the thread is PE, and this is a discussion about animals. The plant examples (as have been noted at least twice in this thread) are not applicable to animals due to significant variances in the handling of foreign proteins.

 

Make up your mind. If the thread is about PE, then "handling foregin proteins" is not relevant.

 

And did you see that quote I provided that stated genome duplications have occurred in animals too?

 

 

 

TeleMad: We can also see organisms adapting to new niches in the lab: look at the example I posted last night about a chain of beneficial mutations leading to a new regulated metabolic pathway. The "eat xylitol" niche was vacant and and bacteria evolved the ability to metabolize it efficiently.

 

Biochemist: And this one is directly refuted above.

 

Only to a hardcore Creationist, like yourself. To us rational and scientific types, it's you who was refuted.

 

Biochemist: It is nice that a damaged enzyme still works at all ...

 

It wasn't damaged: it was IMPROVED. Its ability to catalyze a useful metabolic reaction was increased.

Link to comment
Share on other sites

TeleMad: Note that the protein synthesizing machinery itself has no idea what it is making (i.e., foreign or self proteins). That's why viruses can function: they inject their genetic material into the host cell and the host cell blindly goes about synthesizing proteins from it.

 

Biochemist: This is another example of pure conjecture.

 

No its not. It's recognized fact ... oh, that is, to those who accept science. Maybe to Creationists like yourself, who reject accepted science, this might be pure conjucture, but then, everything is to you guys (except the religious mumbo jumbo that clouds your minds and biases your view of the world).

Link to comment
Share on other sites

1. The fossil record shows rapid speciation events following large scale extinctions.

2. Traditionally, this is ascribed to niche availability.

3. Niche availability is a nice, logical thought, but fails to answer all the questions

- Species are built to AVOID mutations (spellchecking during transcription, for example). Why the rapid speciation after an extinction event, and why can't we trigger that in a lab?

- Mutations are often "against the odds," so why are so many beneficial ones conserved, when new protiens introduced into creatures induce an autoimmune response? How do they recognize their own new mutations? Etc...

 

Let's stay on topic.

This is a huge thread, but to answer point 3:

 

Yes, the transcription is very, very good, with built-in checks and repair systems. However, errors still arise. I think it is two or three per million base pairs? Not sure.

 

However, we know that stress increases the likelihood of mistake, even right down at the cellular level. I would suggest that at times of mass extinction, the entire organism is stressed, and so mutation rates go up, ensuring more rapid differentiation, and thus filling the new niches more rapidly than otherwise. This, combined with the natural selection pressures, would cause rapid speciation.

Link to comment
Share on other sites

TM- thanks for the reasoned and civil response.

 

Species are "built" to OPTIMIZE mutations, not avoid them. Both too many and too few mutations can be detrimental to a species.

 

True- I apologize. However there is no mechanism known FOR mutation, so we are seeing a balance where none in fact may have been intended. Mutations occur, but not through a cells intent (there are no protiens that induce mutation, to my knowledge). Thus, one can't say cells are built to optimize them, rather you can only say cells seem to have about the right amount because of mistakes made by the protiens that spellcheck (and various other things). May sound like a small diffence, but it's really a large one. Perhaps the spellchecking genes that made msitakes were conserved intentonally, perhaps there's something else at work that creates the mutations.

 

Tow reasons are the opening up of new niches and the reduction in selective pressures due to decreased competition.

 

Tradionaly answers, how come they only happen on a global scale? This is not a question that has been answered.

 

We can trigger rapid speciation in the lab. I gave an example involving plants.

 

Plants are easily mutated, I'm talking about animals, say protazoa. I understand about the time problem. But that only goes to show that animals are more difficult to get to radiate then plants- it took 4 generations for a plant. MUCH more so for even simple, rapid generation animals. That alone indicates something different is going on.

 

We can also see organisms adapting to new niches in the lab: look at the example I posted last night about a chain of beneficial mutations leading to a new regulated metabolic pathway. The "eat xylitol" niche was vacant and and bacteria evolved the ability to metabolize it efficiently.

 

It was a great example. 1 example won't win the war, but it was a great thing for your case. Thanks!

 

One reason we can't do these experiments with humans (or other organism that have similar generation times) is simply time. If an experiment involves 10,000 generations of bacteria, that could come to only about 7 months (many bacteria have generation times of 20 to 30 minutes). For a human the same number of generations would take about 150,000 years (considering a generation time of 15 years). That's not feasible. Heck, evolutionary theory is only about 150 years old, nowhere near 150,000.

 

Obviously. Do you know of any computer simulations that take spellchecking and anti-mutation protiens in the organisms into account? I've only seen mutation models that assume extremly rapid mutation rates, unseen in the real world.

 

Uhm, because they are beneficial.

 

Yeah, I worded that wrong. Sorry. :turtle:

 

 

I am not aware of the goats engineered to produce spider silk having autoimmune responses, especially not any that killed them.......foreign proteins are not automatically rejected by the cells; in fact, we know this because we can insert protein-coding genes into many organisms and they will happily produce that protein.

 

Good point. Perhaps that hurdle is not very high.

 

The main determinant of whether or not a synthesized protein is given the thumbs up or thumbs down may be related to folding. In euks, the RER (rough endoplasmic reticulum) has proteins that check for unfolded proteins, and prevent them from entering the Golgi apparatus; in fact, the unfolded proteins (if they can't be folded properly by a chaperone) are taking backwards and ejected from the RER. So in general if a protein is folded - whether it's a self protein or a foreign protein - it's allowed to continue into the Goldi; if a protein - self or foreign - is not folded, it's rejected.

 

May be related? I've heard this before, but all protiens (of a large enough size) fold- some fold into functional units, some not. How does the ER tell the difference? I was under the impression the Golgi packaged anything with amino acids at all. My questions about internal protien degredation were mre related to ubiquitin and it's conservation over the millenia, as protiens changed.

Link to comment
Share on other sites

TeleMad: Species are "built" to OPTIMIZE mutations, not avoid them. Both too many and too few mutations can be detrimental to a species.

 

bumab: However there is no mechanism known FOR mutation, so we are seeing a balance where none in fact may have been intended. Mutations occur, but not through a cells intent (there are no protiens that induce mutation, to my knowledge). Thus, one can't say cells are built to optimize them, rather you can only say cells seem to have about the right amount because of mistakes made by the protiens that spellcheck (and various other things). May sound like a small diffence, but it's really a large one.

 

Nature "built" the not-too-many, not-too-few nature of mutations into organisms because it is only those organisms that have survived - by not having too many and not too few mutations - that exist. In other words, in general, natural selection has weeded out those species/organisms that fell outside of an appropriate range for mutation rate, leaving behind only those that mutate somewhere between a excessively low rate and an excessively high rate.

 

Of course, the "proper" rate is depends on many things: for example, humans and bacteria don't have to have the same "ideal" mutation rates.

 

 

TeleMad: Tow reasons are the opening up of new niches and the reduction in selective pressures due to decreased competition.

 

bumab: Tradionaly answers, how come they only happen on a global scale? This is not a question that has been answered.

 

Occupying an open niche has been observed in the lab: for example, bacteria that evolve a new pathway to metabolize a new food source. Niches fill up, so "strategies" to efficiently share niches exist, such as resource partitioning. Why partition the resources? Because no two species can occupy the same niche indefinitely because one will eventually outcompete the other and lead to its extinction (competive exclusion). I know of no evidence that indicates organisms cannot occupr a niche that open up. Now, since that new niche will not be identical to the previous niche, the organism will be under different selective pressures and adaptation will lead to genetic and phenotypic differences between it and the original organisms. Again, I know of no evidence that indicates this cannot happen.

 

First, what logic indicates that a reduction in selective pressure - which we know would be associated with a reduction in competition - could not allow for changes that would normally not be maintained in population, followed by one or more of these additional differences leading to change that would not have otherwise occurred? I know of none. That's logic: I could probably find some info in my texts about reduction in selective pressures (I believe there's some in relatino to the founder effect/founder-flush process), aybe I'll look tomorrow, but right now, I've been on the net for 5 continuous hours and I'm too lazy! I'm gonna zip through the rest of this and then calli t a night.

 

TeleMad: We can trigger rapid speciation in the lab. I gave an example involving plants.

 

bumab: Plants are easily mutated, I'm talking about animals ...

 

Okay, and remember the quote that stated genomic duplications occur in animals too? Like the plants, that would make the offspring with the duplication virtually unable to successfully mate with others, and could lead to speciation (which seems to be the case since we do see the duplication: if a new species never arose - if those with the duplication died off without mating, we wouldn't see the duplication).

 

TeleMad: We can also see organisms adapting to new niches in the lab: look at the example I posted last night about a chain of beneficial mutations leading to a new regulated metabolic pathway. The "eat xylitol" niche was vacant and and bacteria evolved the ability to metabolize it efficiently.

 

bumad: It was a great example. 1 example won't win the war, but it was a great thing for your case. Thanks!

 

It's not the only case in bacteria: I could find others.

Link to comment
Share on other sites

The 'mutant' enzyme INCREASED its efficiency in processing xylitol. Thats an improvement in function - those were beneficial mutations. ...And at the end, some bacteria could efficiently metabolize BOTH xylitol AND the original sugar: that's a gain of a new function and a new source of food - those were beneficial mutations.
I do understand you have difficulty with biochemistry, so I will try this again. The enzyme was damaged by mutation, and lost specificity. Therefore the specific activity on ribulose was decreased and the processing of other similar sugars was increased. All this proves is that some damage is not fatal.

 

This is like taking the performance chip out of your BMW and throwing it away. The performance decays, but the mileage improves. Look! A positive mutation! But it was just minimal damage with residual functionality.

 

Any other interpretation is the "spin".

Link to comment
Share on other sites

The enzyme was damaged by mutation, and lost specificity. Therefore the specific activity on ribulose was decreased and the processing of other similar sugars was increased. All this proves is that some damage is not fatal.

 

This is like taking the performance chip out of your BMW and throwing it away. The performance decays, but the mileage improves. Look! A positive mutation! But it was just minimal damage with residual functionality.

 

Take out damage, insert change and you have a beneficial mutation. To a bacteria who's environment changes it's food supply about the same time, it's a very beneficial change. Mutations cannot be considered out of context- they are almost always bad unless the enivronment has changed as well.

 

And nice anology, but consider if the gas prices sky rocketed to $20 a gallon. Then it's beneficial, and you'd see a lot more BMW's without performance chips. It's pretty simple.

 

But I do see your point- it is damage. It's not a new gene, it's an old one that was slightly changed. On the long term, presumably those could change into entirely new coding regions, un-connectable with the origional sequence. This is where the PE phenomenon starts to show the model might not be correct. It's one thing to modify a gene, it's another to come up with entirely new ones on a short time scale.

 

TM's example of a mutation-caused beneficial change in the species was accurate. It doesn't alleviate the problem of PE, however, but it does show mutations can be beneficial.

Link to comment
Share on other sites

Nature "built" the not-too-many, not-too-few nature of mutations into organisms because it is only those organisms that have survived - by not having too many and not too few mutations - that exist.
So you are saying that the only animals that survied are the ones that exist? How about mentioning that things are more like they are now than they have ever been before?

 

That certainly proves the mutative speciation model. You are saying that species exist because they mutated, and that positive mutations exist because we have species.

 

Sheesh.

Link to comment
Share on other sites

No its not. It's recognized fact ...
I, of course, can't help but note that you seem to think that reiterating unsubstantiated claims somehow improves their credibility.

 

1) There is absolutely no evidence that the damage to the ribulose enzyme increased information content. There is evidence that it lost specificty. I believe you are aware of this. I think it would be more than fair to call this an intentional misrepresentation.

 

2) There is absolutely no evidence that species "need" mutation to survive. In fact, we have substantial evidence in the opposite direction.

 

Your tendency to select your facts, misrepresent others, and ignore the remainder is quite troubling.

Link to comment
Share on other sites

Nature "built" the not-too-many, not-too-few nature of mutations into organisms because it is only those organisms that have survived - by not having too many and not too few mutations - that exist. In other words, in general, natural selection has weeded out those species/organisms that fell outside of an appropriate range for mutation rate, leaving behind only those that mutate somewhere between a excessively low rate and an excessively high rate.

 

I already know the traditional view...

 

First, what logic indicates that a reduction in selective pressure - which we know would be associated with a reduction in competition - could not allow for changes that would normally not be maintained in population, followed by one or more of these additional differences leading to change that would not have otherwise occurred? I know of none. That's logic: I could probably find some info in my texts about reduction in selective pressures (I believe there's some in relatino to the founder effect/founder-flush process)...

 

There is, but that lack in selective pressure RARELY creates new phyla and orders. Species do radiate, but usually amongst themselves. You get new beak sizes in finches, new insects, new sizes of lizards. Large animals tend to shrink (due to lack of resources- see the elephants in Oceania), small animals tend to get larger, etc etc. Their basic body types remain the same, overall, however speciation is not the issue. PE deals with species producing new higher taxonomic levels.

 

Okay, and remember the quote that stated genomic duplications occur in animals too? Like the plants, that would make the offspring with the duplication virtually unable to successfully mate with others, and could lead to speciation (which seems to be the case since we do see the duplication: if a new species never arose - if those with the duplication died off without mating, we wouldn't see the duplication).

 

That would lead to speciation. But new body plans? Dramatically? The issue is time- PE events seem to take less then 10 million years, at most. For bacteria- not a problem. For higher animals (mammals, for example, but really anything big), any randiation event is more problematic.

 

Speciation can occur through mutation, I'm not arguing that at all. It's basically a time problem and a level of mutation problem.

Link to comment
Share on other sites

Take out damage, insert change and you have a beneficial mutation. To a bacteria who's environment changes it's food supply about the same time, it's a very beneficial change. Mutations cannot be considered out of context- they are almost always bad unless the enivronment has changed as well...T M's example of a mutation-caused beneficial change in the species was accurate. It doesn't alleviate the problem of PE, however, but it does show mutations can be beneficial.
Sure, we can characterize this change as beneficial, as long as you treat the context narrowly. But it certainly did nothing to advance the case of serial change showing serial improvement. What would the next mutation do to this enzyme? What is the next part to throw off of the BMW to improve it?

 

All we demonstratred is that some damage is not lethal. Doesn't it bother you a little that this is the best example that exists?

Link to comment
Share on other sites

All we demonstratred is that some damage is not lethal. Doesn't it bother you a little that this is the best example that exists?

 

Sure, I addressed that concern in my reply to TM.

 

Slowly changing genes will turn into novel genes given enough time. It's really the time-frame problem with PE: how do you get so many novel genes so fast? I'll bet there's a mechanism beyond randomness and natural selection. We're on the same page there. I was just trying to remain explict for the benefit of others....

Link to comment
Share on other sites

1) There is absolutely no evidence that the damage to the ribulose enzyme increased information content. There is evidence that it lost specificty. I believe you are aware of this. I think it would be more than fair to call this an intentional misrepresentation.

 

It didn't. It just changed it around.

 

2) There is absolutely no evidence that species "need" mutation to survive. In fact, we have substantial evidence in the opposite direction.

 

The only evidence you need is this: Environmental change makes some organisms obsolete. Change with the times or die with 'em. During periods of environmental stability, change is bad. Most species are equistely adapted to their niche, and change is bad. Sometimes they need to change fast. THAT'S the dichotomy that is being addressed.

Link to comment
Share on other sites

The only evidence you need is this: Environmental change makes some organisms obsolete. Change with the times or die with 'em. During periods of environmental stability, change is bad. Most species are equistely adapted to their niche, and change is bad. Sometimes they need to change fast. THAT'S the dichotomy that is being addressed.
Now this I completely agree with. Well said.
Link to comment
Share on other sites

Bumab: The only evidence you need is this: Environmental change makes some organisms obsolete. Change with the times or die with 'em. During periods of environmental stability, change is bad. Most species are equistely adapted to their niche, and change is bad. Sometimes they need to change fast. THAT'S the dichotomy that is being addressed
I agree too. So, what is it that happens at these times? Massive stress across a species. Starvation, extreme temperature changes possibly, radiation maybe, poisons and probably more.

The result of stress would be pain, a subject I am revolted by. However, that would be one common denominator. Could it be a causative agent for change in the sense of a feedback mechanism?

Link to comment
Share on other sites

Guest
This topic is now closed to further replies.
×
×
  • Create New...