Evolution My ToE

[ecco]

Your attempt at waving away Scripture history for no reason whatsoever, and arbitrarily declaring whatever involves the spiritual aspect of life is noted, and dismissed.

Actually, you are the one waving away scriptural history. Scriptural history, as supported by the majority of biblical scholars has ascertained:

• No one knows who authored the Gospels
• No one knows how the sayings attributed to Jesus were, or could have been recorded.
• OT stories, like the Exodus, have been found to be fiction.

You ignore these findings. You think you know better than biblical scholars who are out there every day doing actual research while you sit in front of a computer posting your unsubstantiated beliefs.

• As much as it is tempting to slay the dragons of false canards, old wives tales, shallow bible opinions, and etc...what has this little doubt fest have to do with the theory that man and all other life is here because of evolving?

There ya go again, losing track of the conversation. Forgetting what you posted and what I responded to. Don't you remember posting...

Your attempt at waving away Scripture history for no reason whatsoever, and arbitrarily declaring whatever involves the spiritual aspect of life is noted, and dismissed.​

Here's a suggestion, before posting, go back and try to get a grasp on the previous comments that you made. That should save you some further embarrassment.

On the other hand, it may be an actual strategy on your part - just another way of ducking and dodging.

The bottom line is...

• No one knows who authored the Gospels
• No one knows how the sayings attributed to Jesus were, or could have been recorded.
• OT stories, like the Exodus, have been found to be fiction.

Again, you ignore these findings. You think you know better than biblical scholars who are out there every day doing actual research while you sit in front of a computer posting your unsubstantiated beliefs.

 

[ecco]

I believe real spirits exist now and then also. Do you believe in any spirits at all?

I sure do.

 

[ecco]

Your stance is one that opposes all but one man-made mythological creation story. I know that all of them are the creations of man's imaginings. I have outgrown any childish need for magic men in the sky.

God, gods are the creations of man's imaginings. There is no difference between Atlas and Jupiter and Athena and Thor and your god and Shiva and Allah.

You seem to believe that spiritual things like gods and angels are real. Do you still believe in Santa and the Easter Bunny as well?

The fact that you put quotes around the word 'Christians' shows your utter disdain for science and all things scientific. You cannot even accept that many Christians do not share your silly fundamentalist concepts.

Why are you showing my comments as your own? Is this another sign that you are having problems mastering the art of forum posting?

 

[ecco]

What time in the far universe is like now is not known. What time was like on earth long ago is ot an issue. (unless you want to talk about how a year used to be 360 days rather than the current 365)

If this was intended as a joke OK.

But, given your past comments, I tend to believe that you really do not know why "a year used to be 360 days rather than the current 365". It's just one more indication of your abject lack of knowledge of science and history.

 

[ecco]

443 PP23 Dad

Almost wish that was true, as they are in a better position to get info out to a wide audience. But alas I must take the credit for the concept.​

So, yes. You admitted you made up the stories about the speed of light changing and about nature in the past being different.

False.

False?!? Are you still denying what you posted (Post # 443 PP23) even after I went back and found the post? That's really lame.

Even if all we want to discuss is how time may not be the same in far space as it is in the area of the solar system, the speed of light is not really an issue. Light would simply take whatever time exists for it to take wherever it moved!

Incoherent.

 

[dad]

The bottom line is...

• No one knows who authored the Gospels

Speak for yourself...I do.

• No one knows how the sayings attributed to Jesus were, or could have been recorded.

Speak for yourself, believers know. God sent His spirit to me to bring it exactly to their remembrance.

• 
  
  

  [*]
  
  [*]OT stories, like the Exodus, have been found to be fiction.

The basis upon which you claim this is found to be fiction.

 

[dad]

I sure do.

So, no then, you do not believe in spirits. Fine. The denial is noted.

 

[dad]

If this was intended as a joke OK.

But, given your past comments, I tend to believe that you really do not know why "a year used to be 360 days rather than the current 365". It's just one more indication of your abject lack of knowledge of science and history.

A year both in the future and in pre flood times in the bible was/will be 360 days. This is news?

 

[dad]

443 PP23 Dad

Almost wish that was true, as they are in a better position to get info out to a wide audience. But alas I must take the credit for the concept.​

So, yes. You admitted you made up the stories about the speed of light changing and about nature in the past being different.

Light speed changing? No idea what you are talking about. Where...when...why??

False?!? Are you still denying what you posted (Post # 443 PP23) even after I went back and found the post? That's really lame.

Here is post 443...no idea what you you thinking is wrong here...

ecco said: ↑
On the other hand, we do have evidence for why you believe that nature was different in the past.

Then it is exactly as I have said, science doesn't know either way.
That leaves the historical and Scriptural accounts that you deny for no reason.


Of course, I don't really believe that you made up that story. I don't think you are that creative. More likely some of the bright folks over at Answers in Genesis came up with it.

Almost wish that was true, as they are in a better position to get info out to a wide audience. But alas I must take the credit for the concept.

 

[Jose Fly]

You have given me papers.
However, the first two, don't clearly demonstrate resistance arising via mutation.

I'm not sure what you mean by "demonstrate". If you're referring to an actual lab experiment, as I noted earlier the paper includes many citations to papers that do exactly that (CLICK HERE). Also, I gave you a link to search results at the Proceedings of the National Academy of Sciences, which contained many different papers regarding resistance to insecticides arising via mutations.

Plus, I described an experiment I conducted myself where the entire point was to demonstrate how antibiotic resistance arises via mutation. So I'm not really sure what else I can do. That such resistance arises via mutation is simply common knowledge and isn't disputed by anyone that I know of.

I see the biofilm ndvB doing it's work in that regard.
Perhaps I missed what you saw.

Bacteria that form biofilms can be more resistant to antibiotics, but I don't see how that negates or counters what we've been discussing up to this point.

The other papers you pointed to, were to me, what scientists claim. I can't argue, as I am not a scientist, but I believe there can be other explanations. I will have to research further, before I can say, I agree.
So allow me time to do so, thanks.

Sure.

I think the reason you and I can talk is because we have a certain understanding, and respect. You also are willing to be challenged, or have your data, opinion, views, challenged. I'll stick around as long as we can reach a reasonable conclusion with clarity - that is, we both understand each other... even if we disagree.
Also I think there are some positive things about you... Ahem... recently , where I think we can get along in conversing at length.
Overall, you don't display the prime negative traits so common among some opponents.
I gotta watch my back though, if you know what I mean.

I understand. It's all good.

A question... Do you believe that mutations are random, or do you believe they are directed?

They're random, since they don't show any signs of occurring relative to an organism's specific need. If that were the case, then we'd have a heck of a time fighting pathogens and pests, since whatever measure we used against them, they'd just immediately mutate a counter-measure (and every individual in the population would do so instantaneously). Plus, the idea that some entity is secretly directing mutations would mean that entity is pretty evil, given how so many mutations are the bane of our existence. I mean, is this entity trying to mess with us by giving bacteria and pests the ability to resist our treatments? Is it deliberately giving people cancer?

 

[nPeace]

I'm not sure what you mean by "demonstrate". If you're referring to an actual lab experiment, as I noted earlier the paper includes many citations to papers that do exactly that (CLICK HERE). Also, I gave you a link to search results at the Proceedings of the National Academy of Sciences, which contained many different papers regarding resistance to insecticides arising via mutations.

Plus, I described an experiment I conducted myself where the entire point was to demonstrate how antibiotic resistance arises via mutation. So I'm not really sure what else I can do. That such resistance arises via mutation is simply common knowledge and isn't disputed by anyone that I know of.


Bacteria that form biofilms can be more resistant to antibiotics, but I don't see how that negates or counters what we've been discussing up to this point.

Since we know this to be true... genes do play a significant role in resistance and suppression of "foreigners"...
I'm only saying that it's the biofilm genes that are formed, which are providing the resistance. A mutation does not totally knock out a gene's function. Mutations can be repaired.
So technically, that would mean, the mutation is not providing the resistance... and we know that there are genes which communicate to get the job done.

What I mean by not demonstrated, is that finding a gene with a mutation, does not tell us when it got there, what state it was in, when it got there, and if it is in the same state or not. Was it sufficiently repaired as to be of no significant hindrance to the genes and their function?
What effect has natural selection had on the gene's abilities to adapt?

What if scientists said later that their conclusions needed to be adjusted, because there was more involved than they thought... and the resistance really was not the result of copying errors? Would you accept that?

Sure.


I understand. It's all good.


They're random, since they don't show any signs of occurring relative to an organism's specific need. If that were the case, then we'd have a heck of a time fighting pathogens and pests, since whatever measure we used against them, they'd just immediately mutate a counter-measure (and every individual in the population would do so instantaneously). Plus, the idea that some entity is secretly directing mutations would mean that entity is pretty evil, given how so many mutations are the bane of our existence. I mean, is this entity trying to mess with us by giving bacteria and pests the ability to resist our treatments? Is it deliberately giving people cancer?

That makes a lot of sense.
Just wanted to know which side you were on.
Mutations are random
Scientists generally think that the first explanation is the right one and that directed mutations, the second possible explanation, is not correct.

Researchers have performed many experiments in this area. Though results can be interpreted in several ways, none unambiguously support directed mutation. Nevertheless, scientists are still doing research that provides evidence relevant to this issue.

Spoiler: Situation & Explanations

In the U.S., where people use shampoos with particular chemicals in order to kill lice, we have a lot of lice that are resistant to the chemicals in those shampoos. There are two possible explanations for this:
Hypothesis A:
Resistant strains of lice were always there — and are just more frequent now because all the non-resistant lice died a sudsy death.

Hypothesis B:
Exposure to lice shampoo actually caused mutations for resistance to the shampoo.

Please note... these are scientists, with different opinions. Or maybe you think the small few who differ are Creationists?

However, this brings me back to your scenario - with the wolves.
So you are saying the mutations were there already (not that they popped up when needed). Right?
So all the individual deer had the same mutation. Correct?
So here is the thing... if the mutation was genetically passed down - not horizontally, how did all the deer have the same mutation? Are they all descendants of grand papa and grand mama, who carried the mutation?

What accounted for the different levels of immunity?
If it was heredity mixing, then we are looking at... how many fawn does a papa and mama deer have? One or two? That's not much for a deteriorating, or evolving mutation.
So the wolves aren't looking too successful here. Nor does the percentage of deer with high level of immunity.
Are you seeing the picture?

Remember, you are the one who created the scenario, so you need to make sure it works, by applying all the features you use. Otherwise, it no good.

 

[Jose Fly]

Since we know this to be true... genes do play a significant role in resistance and suppression of "foreigners"...
I'm only saying that it's the biofilm genes that are formed, which are providing the resistance.
A mutation does not totally knock out a gene's function. Mutations can be repaired.
So technically, that would mean, the mutation is not providing the resistance... and we know that there are genes which communicate to get the job done.

First, biofilm formation is not at all what went on with many of the resistance studies and such that I've provided you papers on. It's definitely not what happened in the experiment I conducted. Also, biofilm formation obviously doesn't explain insect resistance to pesticides either.

Second, it seems like we need to discuss what mutations are and what they do. So let's do that below.

What I mean by not demonstrated, is that finding a gene with a mutation, does not tell us when it got there, what state it was in, when it got there, and if it is in the same state or not.

That was the entire point of the experiment I conducted. That's why we used a single-clone strain and why we compared the genetics of the parental population (that didn't have resistance) with that of the evolved strain (that did have resistance). Through those simple methods, we were able to establish that the mutation conferring resistance occurred several generations after the initial culture.

Was it sufficiently repaired as to be of no significant hindrance to the genes and their function?

I think what may be confusing you with this is how you seem to be thinking that all mutations basically "break" something, and therefore some sort of "repair" needs to take place at a later point in time. If that's the case, then we should probably clear that up first. It's important to keep in mind that a "mutation" is merely a change in an organism's DNA. Some are bad for the organism, some are good for it, and most are neutral (don't affect it either way).

In a lot of the cases I've been giving you citations for, antibiotic resistance (and some of the insecticide resistance cases) occurs via the accumulation of a small number of amino acid substitutions in the organisms DNA (IOW, mutations). As noted in the Nature page I linked to earlier, microorganisms replicate and mutate at a pretty high rate...

Even if only a single S. aureus cell were to make its way into your wound, it would take only 10 generations for that single cell to grow into a colony of more than 1,000 (2^10 = 1,024), and just 10 more generations for it to erupt into a colony of more than 1 million (2^20 = 1,048,576). For a bacterium that divides about every half hour (which is how quickly S. aureus can grow in optimal conditions), that is a lot of bacteria in less than 12 hours. S. aureus has about 2.8 million nucleotide base pairs in its genome. At a rate of, say, 10^-10 mutations per nucleotide base, that amounts to nearly 300 mutations in that population of bacteria within 10 hours!

To better understand the impact of this situation, think of it this way: With a genome size of 2.8 × 10^6 and a mutation rate of 1 mutation per 10^10 base pairs, it would take a single bacterium 30 hours to grow into a population in which every single base pair in the genome will have mutated not once, but 30 times! Thus, any individual mutation that could theoretically occur in the bacteria will have occurred somewhere in that population—in just over a day.​

So these populations are constantly replicating and mutating. Obviously if every one of those mutations constituted "breaking" something, the population would die very quickly. Also, given the sheer number of replication events plus the mutation rate, it's not at all surprising to see them acquire a mutation (or set of mutations) that confer resistance to an antibiotic. In fact, it's pretty much inevitable. And then once that mutation occurs, that brings us to.....

What effect has natural selection had on the gene's abilities to adapt?

Once an organism acquires the mutation that confers resistance, it is more fit in the environment with the antibiotic or pesticide than the individuals without resistance, which means it's more likely to survive and reproduce, which means it's DNA (complete with the new mutation) will become more common in future generations.

It's like with our deer/wolf scenario, where the proportion of deer with parasite immunity increased after the wolves started picking off the deer without that trait/mutation.

What if scientists said later that their conclusions needed to be adjusted, because there was more involved than they thought... and the resistance really was not the result of copying errors? Would you accept that?

That would be rather weird, since it's something that's very well known and is trivially easy to demonstrate via experiment (as we did), but sure....if they had good evidence-based reasons for it.

That makes a lot of sense.
Just wanted to know which side you were on.
Mutations are random
Scientists generally think that the first explanation is the right one and that directed mutations, the second possible explanation, is not correct.

Researchers have performed many experiments in this area. Though results can be interpreted in several ways, none unambiguously support directed mutation. Nevertheless, scientists are still doing research that provides evidence relevant to this issue.

Spoiler: Situation & Explanations

In the U.S., where people use shampoos with particular chemicals in order to kill lice, we have a lot of lice that are resistant to the chemicals in those shampoos. There are two possible explanations for this:
Hypothesis A:
Resistant strains of lice were always there — and are just more frequent now because all the non-resistant lice died a sudsy death.

Hypothesis B:
Exposure to lice shampoo actually caused mutations for resistance to the shampoo.

Glad we cleared that up.

Please note... these are scientists, with different opinions. Or maybe you think the small few who differ are Creationists?

I'm not sure who you're referring to.

However, this brings me back to your scenario - with the wolves.
So you are saying the mutations were there already (not that they popped up when needed). Right?

Right. There were already deer in the population that had the immunity mutation before the wolves showed up.

So all the individual deer had the same mutation. Correct?

No. Remember, there were some deer that were not immune to the parasite, which means they didn't have the mutation. That was the "variability in the population" that the selective pressures (wolf predation) acted on.

So here is the thing... if the mutation was genetically passed down - not horizontally, how did all the deer have the same mutation? Are they all descendants of grand papa and grand mama, who carried the mutation?

See above.

What accounted for the different levels of immunity?

Some deer had the mutation, some didn't....."variability in the population".

If it was heredity mixing, then we are looking at... how many fawn does a papa and mama deer have? One or two? That's not much for a deteriorating, or evolving mutation.
So the wolves aren't looking too successful here. Nor does the percentage of deer with high level of immunity.
Are you seeing the picture?

Remember, you are the one who created the scenario, so you need to make sure it works, by applying all the features you use. Otherwise, it no good.

It works.

 

[ecco]

Speak for yourself...I do.

The basis upon which you claim this is found to be fiction.

It's well established that your ingrained religious beliefs prevent you from accepting the sciences like astro-physics and evolutionary biology. Now we see that your ingrained religious beliefs also prevent you from accepting the findings of Biblical Scholars.

How you can believe that you know so much more than so many well-educated people is truly amazing. You sound like Donald Trump when he says he knows more about ISIS than the generals do. You sound like Donald Trump when he says he will deliver the best health care plan ever. At least Donald admitted his lack of knowledge (once) when he said, regarding healthcare, "Who knew it could be so complicated?"

You, on the other hand, will continue to believe that you are smarter and more knowledgeable than all people with training and education far beyond your grasp. How pathetic.

 

[nPeace]

First, biofilm formation is not at all what went on with many of the resistance studies and such that I've provided you papers on. It's definitely not what happened in the experiment I conducted. Also, biofilm formation obviously doesn't explain insect resistance to pesticides either.

The paper you gave me did not discuss insect resistance.
Really Fly? You gave me two papers, each a mile and a half long, discussing antibiotic resistance, only to tell me what I read is not relevant to insect resistance?
After I read through them...
Okay then.
So, to be sure, what are we really discussing?

Second, it seems like we need to discuss what mutations are and what they do. So let's do that below.

There goes Evolution 101.
Let's head to the classroom nPeace.

That was the entire point of the experiment I conducted. That's why we used a single-clone strain and why we compared the genetics of the parental population (that didn't have resistance) with that of the evolved strain (that did have resistance). Through those simple methods, we were able to establish that the mutation conferring resistance occurred several generations after the initial culture.

I'm confused. We need a restart. I'm not following your argument now.

I think what may be confusing you with this is how you seem to be thinking that all mutations basically "break" something, and therefore some sort of "repair" needs to take place at a later point in time. If that's the case, then we should probably clear that up first. It's important to keep in mind that a "mutation" is merely a change in an organism's DNA. Some are bad for the organism, some are good for it, and most are neutral (don't affect it either way).

I think I am confused, because I don't know what you are talking about.
What is an error? If a mechanism does not make an accurate copy - that is, it does not carry out its intent, is something not broken?
Why are repairs done on anything... Is it not to mend what has been broken?
If we rip the seam in the crotch of our pants, was something not "broken"? The pants is not ruined by any means. We can still wear it, with the hole. We can do a terrible job of stitching it.
Whatever the case, it is not as it originally was, or was intended to be.

Changes in DNA are still the result of errors, or other unwanted factors. There are changes that were not welcomed, nor intended.
Whoever came up with the idea that mutations are good, did so with particular intent... imo.
I think they are good, because people want them to be.

A change in DNA does not mean the end of life, but neither does it mean a miracle just happened, and things are better than they used to be, or ever were.
A repaired mutations is still a mutation, even if one wants to add "beneficial" in front of it.
...when the cell repairs the DNA, it might not do a perfect job of the repair. So the cell would end up with DNA slightly different than the original DNA and hence, a mutation.

In a lot of the cases I've been giving you citations for, antibiotic resistance (and some of the insecticide resistance cases) occurs via the accumulation of a small number of amino acid substitutions in the organisms DNA (IOW, mutations). As noted in the Nature page I linked to earlier, microorganisms replicate and mutate at a pretty high rate...

Even if only a single S. aureus cell were to make its way into your wound, it would take only 10 generations for that single cell to grow into a colony of more than 1,000 (2^10 = 1,024), and just 10 more generations for it to erupt into a colony of more than 1 million (2^20 = 1,048,576). For a bacterium that divides about every half hour (which is how quickly S. aureus can grow in optimal conditions), that is a lot of bacteria in less than 12 hours. S. aureus has about 2.8 million nucleotide base pairs in its genome. At a rate of, say, 10^-10 mutations per nucleotide base, that amounts to nearly 300 mutations in that population of bacteria within 10 hours!

To better understand the impact of this situation, think of it this way: With a genome size of 2.8 × 10^6 and a mutation rate of 1 mutation per 10^10 base pairs, it would take a single bacterium 30 hours to grow into a population in which every single base pair in the genome will have mutated not once, but 30 times! Thus, any individual mutation that could theoretically occur in the bacteria will have occurred somewhere in that population—in just over a day.​

So these populations are constantly replicating and mutating. Obviously if every one of those mutations constituted "breaking" something, the population would die very quickly. Also, given the sheer number of replication events plus the mutation rate, it's not at all surprising to see them acquire a mutation (or set of mutations) that confer resistance to an antibiotic. In fact, it's pretty much inevitable. And then once that mutation occurs, that brings us to.....

Okay, so now you are back to antibiotic resistance.
Types of mutations
Substitution
A substitution is a mutation that exchanges one base for another (i.e., a change in a single "chemical letter" such as switching an A to a G). Such a substitution could:

1. change a codon to one that encodes a different amino acid and cause a small change in the protein produced. For example, sickle cell anemia is caused by a substitution in the beta-hemoglobin gene, which alters a single amino acid in the protein produced.
2. change a codon to one that encodes the same amino acid and causes no change in the protein produced. These are called silent mutations.
3. change an amino-acid-coding codon to a single "stop" codon and cause an incomplete protein. This can have serious effects since the incomplete protein probably won't function.

First. Based on the hypothetical you gave here, which type of mutation are you talking about?
Somehow, I suspect the other three types are ruled out.

Once an organism acquires the mutation that confers resistance, it is more fit in the environment with the antibiotic or pesticide than the individuals without resistance, which means it's more likely to survive and reproduce, which means it's DNA (complete with the new mutation) will become more common in future generations.

It's like with our deer/wolf scenario, where the proportion of deer with parasite immunity increased after the wolves started picking off the deer without that trait/mutation.

I'm really confused at this point, as to what you are saying. Really.
Can we stick to the question I am really interested in.
So rather than give me paper after paper, can we discuss what you have already given me, or stick to one.

That would be rather weird, since it's something that's very well known and is trivially easy to demonstrate via experiment (as we did), but sure....if they had good evidence-based reasons for it.

Good.

Glad we cleared that up.


I'm not sure who you're referring to.

The two hypotheses, and the issue related to them.

Right. There were already deer in the population that had the immunity mutation before the wolves showed up.


No. Remember, there were some deer that were not immune to the parasite, which means they didn't have the mutation. That was the "variability in the population" that the selective pressures (wolf predation) acted on.


See above.


Some deer had the mutation, some didn't....."variability in the population".


It works.

I'm not sure. What about those in between? How is it they were not fully immune, or had no immunity?

 

[ecco]

A year both in the future and in pre flood times in the bible was/will be 360 days. This is news?

Yes, it is news. It is just more of your nonsensical views. Have you really gone off the deep end completely?

 

[Jose Fly]

The paper you gave me did not discuss insect resistance.
Really Fly? You gave me two papers, each a mile and a half long, discussing antibiotic resistance, only to tell me what I read is not relevant to insect resistance?
After I read through them...
Okay then.
So, to be sure, what are we really discussing?

I provided you resources on insecticide resistance in THIS POST after you'd asked me to do so. I know there's a lot going on here and I've given you a lot to read, but as I said earlier....this is a fairly technical subject so it's going to take some work.

There goes Evolution 101.
Let's head to the classroom nPeace.

LOL....

I'm confused. We need a restart. I'm not following your argument now.

I think I am confused, because I don't know what you are talking about.
What is an error? If a mechanism does not make an accurate copy - that is, it does not carry out its intent, is something not broken?
Why are repairs done on anything... Is it not to mend what has been broken?
If we rip the seam in the crotch of our pants, was something not "broken"? The pants is not ruined by any means. We can still wear it, with the hole. We can do a terrible job of stitching it.
Whatever the case, it is not as it originally was, or was intended to be.

Changes in DNA are still the result of errors, or other unwanted factors. There are changes that were not welcomed, nor intended.
Whoever came up with the idea that mutations are good, did so with particular intent... imo.
I think they are good, because people want them to be.

A change in DNA does not mean the end of life, but neither does it mean a miracle just happened, and things are better than they used to be, or ever were.
A repaired mutations is still a mutation, even if one wants to add "beneficial" in front of it.
...when the cell repairs the DNA, it might not do a perfect job of the repair. So the cell would end up with DNA slightly different than the original DNA and hence, a mutation.

So far, we know that some organisms have resistance to things like antibiotics or insecticides, while other organisms don't (even some in the same populations as those with resistance). So the question at hand is, how did those organisms acquire that resistance?

To answer that we first have to figure out the cause of the resistance. As the papers and such I've provided you demonstrate, it's primarily genetic....and more specifically, it's that some organisms have genetic sequences that allow them to resist the antibiotic/insecticide, whereas other lack those genetic sequences. So then the question becomes, where did those genetic sequences for resistance come from?

That's where the lab studies and experiments (including the one I did) come in. Through those studies we have established that the genetic sequences that provide resistance to antibiotics/insecticides arise via mutations. Going back to the experiment I conducted, that's why we compared the genetics of the bacteria we started with, with the bacteria at the end. When we started the bacteria didn't have the necessary genetic sequences, but by the end a bunch of them did. As the Nature article noted, given the replication rate and mutation rate for bacteria, it was inevitable that at some point, one of the bacteria would get the mutation(s) that provided the resistance sequence, and once it did, that sequence would spread through subsequent generations (because it's a beneficial trait, and therefore is favored by natural selection).

And finally, yes mutations are copying "errors", which merely refers to the fact that they are not exact replicas of the original genome. But, and this is important, whether those copying errors are "good", "bad", or "neutral" depends on the effect they have on the organism. And as we've seen with all the studies and experiments, mutations that allow an organism to resist antibiotics or pesticides most definitely is "good" for that organism (otherwise it would succumb to the antibiotic/pesticide and die).

Okay, so now you are back to antibiotic resistance.

To be clear here, whether it's microbial resistance to antibiotics or insect resistance to insecticides, it's the same process (mutation and natural selection).

Types of mutations

Substitution
A substitution is a mutation that exchanges one base for another (i.e., a change in a single "chemical letter" such as switching an A to a G). Such a substitution could:

1. change a codon to one that encodes a different amino acid and cause a small change in the protein produced. For example, sickle cell anemia is caused by a substitution in the beta-hemoglobin gene, which alters a single amino acid in the protein produced.
2. change a codon to one that encodes the same amino acid and causes no change in the protein produced. These are called silent mutations.
3. change an amino-acid-coding codon to a single "stop" codon and cause an incomplete protein. This can have serious effects since the incomplete protein probably won't function.

First. Based on the hypothetical you gave here, which type of mutation are you talking about?
Somehow, I suspect the other three types are ruled out.

I'm not sure which hypothetical you're referring to, but there's no need to rely on that to illustrate the point. In THIS (edited to add link) paper I provided you earlier, in the "MUTATION AS THE PRIMARY EFFECTOR OF RESISTANCE: ANTIBIOTIC CLASSES" section, it cites a specific example...

Fluoroquinolones are bactericidal and target two homologous enzymes, namely DNA topoisomerases II (also known as DNA gyrase) and IV [8], which are essential for the supercoiling of bacterial DNA. Both enzymes are composed of subunits, encoded by gyrA and gyrB (for DNA gyrase) or parC and parE (for topoisomerase IV). Development of resistance to fluoroquinolones is a stepwise process, resulting from the accumulation of amino-acid substitutions in these subunits, and with increasing numbers of mutations generally correlating with increasing MICs [8, 9]. Most, but not all, of the mutations map into defined regions of the subunits, designated the quinolone resistance-determining regions [10].​

So that means in the case of resistance to flouroquinolnes, the answer to your question is #1.

I'm really confused at this point, as to what you are saying. Really.
Can we stick to the question I am really interested in.
So rather than give me paper after paper, can we discuss what you have already given me, or stick to one.

I can do that, but I do plan on referring back to papers or sources I've already provided if that's okay.

The two hypotheses, and the issue related to them.

Right, I understand the issue you're referring to (directed vs. undirected mutations). I'm just not clear on who you were referring to as advocates of the notion that mutations are directed.

I'm not sure. What about those in between? How is it they were not fully immune, or had no immunity?

With some types of immunity/resistance, there is "partial immunity/resistance", usually due to how full immunity/resistance is the result of a set of mutations, so if an organism only has a subset of those mutations they have partial immunity/resistance.

 

[nPeace]

I provided you resources on insecticide resistance in THIS POST after you'd asked me to do so. I know there's a lot going on here and I've given you a lot to read, but as I said earlier....this is a fairly technical subject so it's going to take some work.


LOL....


So far, we know that some organisms have resistance to things like antibiotics or insecticides, while other organisms don't (even some in the same populations as those with resistance). So the question at hand is, how did those organisms acquire that resistance?

To answer that we first have to figure out the cause of the resistance. As the papers and such I've provided you demonstrate, it's primarily genetic....and more specifically, it's that some organisms have genetic sequences that allow them to resist the antibiotic/insecticide, whereas other lack those genetic sequences. So then the question becomes, where did those genetic sequences for resistance come from?

Okay, so at this point, could you back this up with data.
As the papers and such I've provided you demonstrate, it's primarily genetic....and more specifically, it's that some organisms have genetic sequences that allow them to resist the antibiotic/insecticide, whereas other lack those genetic sequences.
Don't link me to papers, please. Just select a paper, and extract that part, but provide the link. Thanks.

That's where the lab studies and experiments (including the one I did) come in. Through those studies we have established that the genetic sequences that provide resistance to antibiotics/insecticides arise via mutations. Going back to the experiment I conducted, that's why we compared the genetics of the bacteria we started with, with the bacteria at the end. When we started the bacteria didn't have the necessary genetic sequences, but by the end a bunch of them did. As the Nature article noted, given the replication rate and mutation rate for bacteria, it was inevitable that at some point, one of the bacteria would get the mutation(s) that provided the resistance sequence, and once it did, that sequence would spread through subsequent generations (because it's a beneficial trait, and therefore is favored by natural selection).

You say... Through those studies we have established that the genetic sequences that provide resistance to antibiotics/insecticides arise via mutations.
Yet, is it not the case that you hypothesized this?
Can you link the specific paper of this experiment, and if it is loooooooooong, point out which paragraph the experiment begins. Thanks.

And finally, yes mutations are copying "errors", which merely refers to the fact that they are not exact replicas of the original genome. But, and this is important, whether those copying errors are "good", "bad", or "neutral" depends on the effect they have on the organism. And as we've seen with all the studies and experiments, mutations that allow an organism to resist antibiotics or pesticides most definitely is "good" for that organism (otherwise it would succumb to the antibiotic/pesticide and die).

Okay, so in other words, you would determine that a mutation is beneficial, simply by the fact that the gene where the mutation is located, is doing something positive. Is that correct?
If the gene doesn't appear to be doing anything, one way or other, then the mutation in that location is neutral. ...

Hmmmmm.

To be clear here, whether it's microbial resistance to antibiotics or insect resistance to insecticides, it's the same process (mutation and natural selection).


I'm not sure which hypothetical you're referring to, but there's no need to rely on that to illustrate the point. In THIS (edited to add link) paper I provided you earlier, in the "MUTATION AS THE PRIMARY EFFECTOR OF RESISTANCE: ANTIBIOTIC CLASSES" section, it cites a specific example...

Fluoroquinolones are bactericidal and target two homologous enzymes, namely DNA topoisomerases II (also known as DNA gyrase) and IV [8], which are essential for the supercoiling of bacterial DNA. Both enzymes are composed of subunits, encoded by gyrA and gyrB (for DNA gyrase) or parC and parE (for topoisomerase IV). Development of resistance to fluoroquinolones is a stepwise process, resulting from the accumulation of amino-acid substitutions in these subunits, and with increasing numbers of mutations generally correlating with increasing MICs [8, 9]. Most, but not all, of the mutations map into defined regions of the subunits, designated the quinolone resistance-determining regions [10].​

So that means in the case of resistance to flouroquinolnes, the answer to your question is #1.

I'll come back to this.

I can do that, but I do plan on referring back to papers or sources I've already provided if that's okay.

Cool.

Right, I understand the issue you're referring to (directed vs. undirected mutations). I'm just not clear on who you were referring to as advocates of the notion that mutations are directed.

Who else Fly? Who else could it possibly be, but scientists?

With some types of immunity/resistance, there is "partial immunity/resistance", usually due to how full immunity/resistance is the result of a set of mutations, so if an organism only has a subset of those mutations they have partial immunity/resistance.

Could you elaborate.

 

[Jose Fly]

Okay, so at this point, could you back this up with data.
As the papers and such I've provided you demonstrate, it's primarily genetic....and more specifically, it's that some organisms have genetic sequences that allow them to resist the antibiotic/insecticide, whereas other lack those genetic sequences.
Don't link me to papers, please. Just select a paper, and extract that part, but provide the link. Thanks.

Okay. We can start with THIS ONE and this specific part...

Recently, mosquitoes resistant to all available insecticides have been found in Tiassalé, West Africa, which could be problematic for resistance management, particularly if common genetic mechanisms are responsible (‘cross-resistance’). Tiassalé mosquitoes also exhibit extreme levels of resistance to the two most important classes, pyrethroids and carbamates. We investigated the genetic basis of extreme carbamate resistance and cross-resistance in Tiassalé, and the applicability of results in an additional population from Togo. We find that specific P450 enzymes are involved in both extreme and cross-resistance, including one, CYP6M2, which can cause resistance to three insecticide classes. However, amplification of a mutated version of the gene which codes for acetycholinesterase, the target site of both the carbamate and organophosphate insecticides, also plays an important role.​

You say... Through those studies we have established that the genetic sequences that provide resistance to antibiotics/insecticides arise via mutations.
Yet, is it not the case that you hypothesized this?
Can you link the specific paper of this experiment, and if it is loooooooooong, point out which paragraph the experiment begins. Thanks.

I can, but I don't see why I need to since I've already repeatedly described an experiment I conducted myself that established exactly that. I also described the specific protocols (single-clone strain, comparing genetics of parental and evolved populations) we followed that allowed us to reach that conclusion.

I'm curious about a couple of things. First, is there a specific reason you're so skeptical that at least some instances of antibiotic and insecticide resistance is genetically based? Also, if the Tissale mosquito's resistance to insecticides (described in the paper above) isn't genetically based, what exactly do you think is the cause?

Because honestly, at this point it kinda feels like you're asking me to prove to you that water is wet. That at least some types of resistance (to both antibiotics and insecticides) is genetically-based has been known for decades now. This isn't in dispute.

Okay, so in other words, you would determine that a mutation is beneficial, simply by the fact that the gene where the mutation is located, is doing something positive. Is that correct?

Sorta. When it comes to whether a mutation is beneficial or otherwise, it's simply a matter of the effect it has on the organism. That's it.

If the gene doesn't appear to be doing anything, one way or other, then the mutation in that location is neutral. ...

Hmmmmm.

If the mutation doesn't change the organism one way or the other, the mutation is neutral (it had no effect). FYI, with some amino acids you can substitute one for another and it won't affect the function of the protein one bit. It's called "redundancy in the genetic code" and I can provide you more info on that if you'd like.

Who else Fly? Who else could it possibly be, but scientists?

Which ones?

Could you elaborate.

I'll keep it brief as we've already covered quite a bit of material. But basically, if one type of resistance is due to the production of an enzyme, then if an organism has a version of the genetic sequences where the enzyme is only produced in small amounts, it may have only partial resistance (e.g., it reduces the function of the organism but doesn't kill it outright).

 

[nPeace]

Okay. We can start with THIS ONE and this specific part...

Recently, mosquitoes resistant to all available insecticides have been found in Tiassalé, West Africa, which could be problematic for resistance management, particularly if common genetic mechanisms are responsible (‘cross-resistance’). Tiassalé mosquitoes also exhibit extreme levels of resistance to the two most important classes, pyrethroids and carbamates. We investigated the genetic basis of extreme carbamate resistance and cross-resistance in Tiassalé, and the applicability of results in an additional population from Togo. We find that specific P450 enzymes are involved in both extreme and cross-resistance, including one, CYP6M2, which can cause resistance to three insecticide classes. However, amplification of a mutated version of the gene which codes for acetycholinesterase, the target site of both the carbamate and organophosphate insecticides, also plays an important role.​

I can, but I don't see why I need to since I've already repeatedly described an experiment I conducted myself that established exactly that. I also described the specific protocols (single-clone strain, comparing genetics of parental and evolved populations) we followed that allowed us to reach that conclusion.

I'm curious about a couple of things. First, is there a specific reason you're so skeptical that at least some instances of antibiotic and insecticide resistance is genetically based? Also, if the Tissale mosquito's resistance to insecticides (described in the paper above) isn't genetically based, what exactly do you think is the cause?

Because honestly, at this point it kinda feels like you're asking me to prove to you that water is wet. That at least some types of resistance (to both antibiotics and insecticides) is genetically-based has been known for decades now. This isn't in dispute.

Interesting.

Sorta. When it comes to whether a mutation is beneficial or otherwise, it's simply a matter of the effect it has on the organism. That's it.

Interesting.

If the mutation doesn't change the organism one way or the other, the mutation is neutral (it had no effect). FYI, with some amino acids you can substitute one for another and it won't affect the function of the protein one bit. It's called "redundancy in the genetic code" and I can provide you more info on that if you'd like.

Interesting.

Which ones?

Interesting.

I'll keep it brief as we've already covered quite a bit of material. But basically, if one type of resistance is due to the production of an enzyme, then if an organism has a version of the genetic sequences where the enzyme is only produced in small amounts, it may have only partial resistance (e.g., it reduces the function of the organism but doesn't kill it outright).

Interesting.

 

[dad]

It's well established that your ingrained religious beliefs prevent you from accepting the sciences like astro-physics and evolutionary biology. Now we see that your ingrained religious beliefs also prevent you from accepting the findings of Biblical Scholars.

How you can believe that you know so much more than so many well-educated people is truly amazing. You sound like Donald Trump when he says he knows more about ISIS than the generals do. You sound like Donald Trump when he says he will deliver the best health care plan ever. At least Donald admitted his lack of knowledge (once) when he said, regarding healthcare, "Who knew it could be so complicated?"

You, on the other hand, will continue to believe that you are smarter and more knowledgeable than all people with training and education far beyond your grasp. How pathetic.

Nothing to say on topic then. OK. Just admit you were defeated a long time ago, save your breath.