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Topic: Introduction to Systems Biology (Read 19620 times) previous topic - next topic

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  • Pingu
Re: Introduction to Systems Biology
Reply #2225
So then the answer to this...
In addition to Entropy's burning question that he keeps asking, I have my own burning question ... namely, was the gene duplication event that allowed aerobic citrate uptake in Lenski's bugs RANDOM?  Or was it "directed" by the cell in response to sensing the environment. 
...according to Shapiro, would pretty clearly be that the cell's response to the environment was to increase mutability, not to direct a specific mutation, right?
Yes but I don't think that means relax error correction during replication. I think it means something along the lines of churning out a bunch of tools like skill saws and power drills and jackhammers.

Nobody is claiming that error correction is relaxed during replication.

What Shapiro is claiming is that error-prone repair processes, for one, become more frequent when the cell is under stress. 

Possibly, also, normally high-fidelity repair processes may become more error-prone under conditions of stress.  If you ever bothered to find out HOW the mismatch repair system works, for instance, you would discover that there is a specific mechanism that enables the repair enzyme to recognise the template as the template. That can go wrong.

It is also possible that the systems that generally suppress reshuffling of genetic material become less efficient under stress, but you'd have to read Shapiro to find that out.  It's a while since I read the book.

I have a Darwin-debased mind.

Re: Introduction to Systems Biology
Reply #2226
"Nobody is claiming that error correction is relaxed during replication."

Well that's good to know. With your weird views about polymerase, I wasn't sure what you thought.

Re: Introduction to Systems Biology
Reply #2227
So then the answer to this...
In addition to Entropy's burning question that he keeps asking, I have my own burning question ... namely, was the gene duplication event that allowed aerobic citrate uptake in Lenski's bugs RANDOM?  Or was it "directed" by the cell in response to sensing the environment. 
...according to Shapiro, would pretty clearly be that the cell's response to the environment was to increase mutability, not to direct a specific mutation, right?
Yes but I don't think that means relax error correction during replication. I think it means something along the lines of churning out a bunch of tools like skill saws and power drills and jackhammers.
Which is a metaphor for what?

  • Pingu
Re: Introduction to Systems Biology
Reply #2228
"Nobody is claiming that error correction is relaxed during replication."

Well that's good to know. With your weird views about polymerase, I wasn't sure what you thought.

How many times do I have to say that what you thought my weird views are aren't my weird views before you dispel your weird view that that weird view is mine?

Dave, you are being transparently disingenuous here.  You are deliberately misunderstanding me, and thus misrepresenting me, despite repeated correction, apparently so that you have an excuse to disregard anything I say.  It's pathetic.
I have a Darwin-debased mind.

Re: Introduction to Systems Biology
Reply #2229
So then the answer to this...
In addition to Entropy's burning question that he keeps asking, I have my own burning question ... namely, was the gene duplication event that allowed aerobic citrate uptake in Lenski's bugs RANDOM?  Or was it "directed" by the cell in response to sensing the environment. 
...according to Shapiro, would pretty clearly be that the cell's response to the environment was to increase mutability, not to direct a specific mutation, right?
Yes but I don't think that means relax error correction during replication. I think it means something along the lines of churning out a bunch of tools like skill saws and power drills and jackhammers.

Nobody is claiming that error correction is relaxed during replication.

What Shapiro is claiming is that error-prone repair processes, for one, become more frequent when the cell is under stress. 

Possibly, also, normally high-fidelity repair processes may become more error-prone under conditions of stress.  If you ever bothered to find out HOW the mismatch repair system works, for instance, you would discover that there is a specific mechanism that enables the repair enzyme to recognise the template as the template. That can go wrong.

It is also possible that the systems that generally suppress reshuffling of genetic material become less efficient under stress, but you'd have to read Shapiro to find that out.  It's a while since I read the book.
I have read all that and so I do understand that more errors can be generated under the SOS regime than during normal times.

But the key thing about this I believe is that a higher error rate is bad for the cell, that is, it would decrease Fitness under most conditions. And I believe when were talking about this type of error, we're talking about an A for a T or a G for a C and so on, I don't think we're talking about "oops I made two copies of that Gene that's 1000 bases long."
  • Last Edit: March 13, 2018, 01:22:33 PM by Dave Hawkins

Re: Introduction to Systems Biology
Reply #2230
"Nobody is claiming that error correction is relaxed during replication."

Well that's good to know. With your weird views about polymerase, I wasn't sure what you thought.

How many times do I have to say that what you thought my weird views are aren't my weird views before you dispel your weird view that that weird view is mine?

Dave, you are being transparently disingenuous here.  You are deliberately misunderstanding me, and thus misrepresenting me, despite repeated correction, apparently so that you have an excuse to disregard anything I say.  It's pathetic.
When your argument is that you want to believe your assumptions, straw people are requirements.
Love is like a magic penny
 if you hold it tight you won't have any
if you give it away you'll have so many
they'll be rolling all over the floor

Re: Introduction to Systems Biology
Reply #2231
So then the answer to this...
In addition to Entropy's burning question that he keeps asking, I have my own burning question ... namely, was the gene duplication event that allowed aerobic citrate uptake in Lenski's bugs RANDOM?  Or was it "directed" by the cell in response to sensing the environment. 
...according to Shapiro, would pretty clearly be that the cell's response to the environment was to increase mutability, not to direct a specific mutation, right?
Yes but I don't think that means relax error correction during replication. I think it means something along the lines of churning out a bunch of tools like skill saws and power drills and jackhammers.

Nobody is claiming that error correction is relaxed during replication.

What Shapiro is claiming is that error-prone repair processes, for one, become more frequent when the cell is under stress. 

Possibly, also, normally high-fidelity repair processes may become more error-prone under conditions of stress.  If you ever bothered to find out HOW the mismatch repair system works, for instance, you would discover that there is a specific mechanism that enables the repair enzyme to recognise the template as the template. That can go wrong.

It is also possible that the systems that generally suppress reshuffling of genetic material become less efficient under stress, but you'd have to read Shapiro to find that out.  It's a while since I read the book.
I have read all that and so I do understand that more errors can be generated under the SOS regime than during normal times.

But the key thing about this I believe is that a higher error rate is bad for the cell, that is, it would decrease Fitness under most conditions. And I believe when were talking about this type of error, we're talking about an A for a T or a G for a C and so on, I don't think we're talking about "oops I made two copies of that Gene that's 1000 bases long."
It's the "under most conditions" part you aren't getting. And, what is clear to anyone reading, it's you that isn't getting it.
Love is like a magic penny
 if you hold it tight you won't have any
if you give it away you'll have so many
they'll be rolling all over the floor

  • Pingu
Re: Introduction to Systems Biology
Reply #2232
So then the answer to this...
In addition to Entropy's burning question that he keeps asking, I have my own burning question ... namely, was the gene duplication event that allowed aerobic citrate uptake in Lenski's bugs RANDOM?  Or was it "directed" by the cell in response to sensing the environment. 
...according to Shapiro, would pretty clearly be that the cell's response to the environment was to increase mutability, not to direct a specific mutation, right?
Yes but I don't think that means relax error correction during replication. I think it means something along the lines of churning out a bunch of tools like skill saws and power drills and jackhammers.

Nobody is claiming that error correction is relaxed during replication.

What Shapiro is claiming is that error-prone repair processes, for one, become more frequent when the cell is under stress. 

Possibly, also, normally high-fidelity repair processes may become more error-prone under conditions of stress.  If you ever bothered to find out HOW the mismatch repair system works, for instance, you would discover that there is a specific mechanism that enables the repair enzyme to recognise the template as the template. That can go wrong.

It is also possible that the systems that generally suppress reshuffling of genetic material become less efficient under stress, but you'd have to read Shapiro to find that out.  It's a while since I read the book.
I have read all that and so I do understand that more errors can be generated under the SOS regime than during normal times.

But the key thing about this I believe is that a higher error rate is bad for the cell, that is, it would decrease Fitness under most conditions.

You still haven't even grokked the difference between a cell and a population.  A cell doesn't have an "error rate".  The population does.  Just as a cell doesn't have "diversity".  A population does.

A mutation rate is bad for a well-adapted population, as most of the mutations will be worse than the status quo.  However, a high mutation rate is good for a population under streess, as it increases the chance that a novel variant will be better than the status quo.

Which is one of Shapiro's two big points: that cell mechanisms are such that stress induces a higher error rate in stressed populations, thus increasing diversity and thus opening possibilities for natural selection.

And I believe when were talking about this type of error, we're talking about an A for a T or a G for a C and so on, I don't think we're talking about "oops I made two copies of that Gene that's 1000 bases long."

And there you go again, carving Nature at different joints to those carved at by Shapiro.  Both small mutations and large can be useful.  If you read Blount you will see that the key mutation (the duplication) was weak in effect at first.  Then it was refined.

Small mutations are likely to have been involved in the refinement.  Blount et al mention a couple of SNPs IIRC.
I have a Darwin-debased mind.

  • JonF
Re: Introduction to Systems Biology
Reply #2233
So then the answer to this...
In addition to Entropy's burning question that he keeps asking, I have my own burning question ... namely, was the gene duplication event that allowed aerobic citrate uptake in Lenski's bugs RANDOM?  Or was it "directed" by the cell in response to sensing the environment. 
...according to Shapiro, would pretty clearly be that the cell's response to the environment was to increase mutability, not to direct a specific mutation, right?
Yes but I don't think that means relax error correction during replication. I think it means something along the lines of churning out a bunch of tools like skill saws and power drills and jackhammers.

Nobody is claiming that error correction is relaxed during replication.

What Shapiro is claiming is that error-prone repair processes, for one, become more frequent when the cell is under stress. 

Possibly, also, normally high-fidelity repair processes may become more error-prone under conditions of stress.  If you ever bothered to find out HOW the mismatch repair system works, for instance, you would discover that there is a specific mechanism that enables the repair enzyme to recognise the template as the template. That can go wrong.

It is also possible that the systems that generally suppress reshuffling of genetic material become less efficient under stress, but you'd have to read Shapiro to find that out.  It's a while since I read the book.
I have read all that and so I do understand that more errors can be generated under the SOS regime than during normal times.

But the key thing about this I believe is that a higher error rate is bad for the cell, that is, it would decrease Fitness under most conditions.

Probably true. Most cells in such a stressful situation die one way or another. But once in a while one cell may hit the jackpot.

Quote
And I believe when were talking about this type of error, we're talking about an A for a T or a G for a C and so on, I don't think we're talking about "oops I made two copies of that Gene that's 1000 bases long."
In Lenski's experiment that's exactly what we are talking about.
"I would never consider my evaluation of his work to be fair minded unless I had actually read his own words." - Dave Hawkins

Re: Introduction to Systems Biology
Reply #2234
So then the answer to this...
In addition to Entropy's burning question that he keeps asking, I have my own burning question ... namely, was the gene duplication event that allowed aerobic citrate uptake in Lenski's bugs RANDOM?  Or was it "directed" by the cell in response to sensing the environment. 
...according to Shapiro, would pretty clearly be that the cell's response to the environment was to increase mutability, not to direct a specific mutation, right?
Yes but I don't think that means relax error correction during replication. I think it means something along the lines of churning out a bunch of tools like skill saws and power drills and jackhammers.

Nobody is claiming that error correction is relaxed during replication.

What Shapiro is claiming is that error-prone repair processes, for one, become more frequent when the cell is under stress. 

Possibly, also, normally high-fidelity repair processes may become more error-prone under conditions of stress.  If you ever bothered to find out HOW the mismatch repair system works, for instance, you would discover that there is a specific mechanism that enables the repair enzyme to recognise the template as the template. That can go wrong.

It is also possible that the systems that generally suppress reshuffling of genetic material become less efficient under stress, but you'd have to read Shapiro to find that out.  It's a while since I read the book.
I have read all that and so I do understand that more errors can be generated under the SOS regime than during normal times.

But the key thing about this I believe is that a higher error rate is bad for the cell, that is, it would decrease Fitness under most conditions.

You still haven't even grokked the difference between a cell and a population.  A cell doesn't have an "error rate".  The population does.  Just as a cell doesn't have "diversity".  A population does.

A mutation rate is bad for a well-adapted population, as most of the mutations will be worse than the status quo.  However, a high mutation rate is good for a population under streess, as it increases the chance that a novel variant will be better than the status quo.

Which is one of Shapiro's two big points: that cell mechanisms are such that stress induces a higher error rate in stressed populations, thus increasing diversity and thus opening possibilities for natural selection.

And I believe when were talking about this type of error, we're talking about an A for a T or a G for a C and so on, I don't think we're talking about "oops I made two copies of that Gene that's 1000 bases long."

And there you go again, carving Nature at different joints to those carved at by Shapiro.  Both small mutations and large can be useful.  If you read Blount you will see that the key mutation (the duplication) was weak in effect at first.  Then it was refined.

Small mutations are likely to have been involved in the refinement.  Blount et al mention a couple of SNPs IIRC.
Okay I'm going to try and contain my shock and amazement this time that you would have such a bad grasp of basic genetics. Maybe if I'm nicer to you, you will listen to me with respect to these basic things. Deal?

Let's keep this real simple and talk only about your second sentence first. You say that a cell doesn't have an error rate, but a population does.

How can you say this? Do you not know that cells divide? Do you not know that when they divide they have to copy their DNA? Do you not know that when they copy their DNA the copying process will not be perfect and has to have proofreading and error correction?

Let's get on the same page here with this basic concept.

Re: Introduction to Systems Biology
Reply #2235
Please ... I beg you... don't go beyond this second sentence right now. Things get confusing enough already without tackling several ideas at once.

Re: Introduction to Systems Biology
Reply #2236
Dave, you just demonstrated how fucking stupid you really are.
A walk through the ocean of most mens souls would scarcely get your feet wet.

Re: Introduction to Systems Biology
Reply #2237
If a cell divides it's a population. If a single cell never divides how can there be an error rate?

You just own goaled yourself dumdum

  • Pingu
Re: Introduction to Systems Biology
Reply #2238
So then the answer to this...
In addition to Entropy's burning question that he keeps asking, I have my own burning question ... namely, was the gene duplication event that allowed aerobic citrate uptake in Lenski's bugs RANDOM?  Or was it "directed" by the cell in response to sensing the environment. 
...according to Shapiro, would pretty clearly be that the cell's response to the environment was to increase mutability, not to direct a specific mutation, right?
Yes but I don't think that means relax error correction during replication. I think it means something along the lines of churning out a bunch of tools like skill saws and power drills and jackhammers.

Nobody is claiming that error correction is relaxed during replication.

What Shapiro is claiming is that error-prone repair processes, for one, become more frequent when the cell is under stress. 

Possibly, also, normally high-fidelity repair processes may become more error-prone under conditions of stress.  If you ever bothered to find out HOW the mismatch repair system works, for instance, you would discover that there is a specific mechanism that enables the repair enzyme to recognise the template as the template. That can go wrong.

It is also possible that the systems that generally suppress reshuffling of genetic material become less efficient under stress, but you'd have to read Shapiro to find that out.  It's a while since I read the book.
I have read all that and so I do understand that more errors can be generated under the SOS regime than during normal times.

But the key thing about this I believe is that a higher error rate is bad for the cell, that is, it would decrease Fitness under most conditions.

You still haven't even grokked the difference between a cell and a population.  A cell doesn't have an "error rate".  The population does.  Just as a cell doesn't have "diversity".  A population does.

A mutation rate is bad for a well-adapted population, as most of the mutations will be worse than the status quo.  However, a high mutation rate is good for a population under streess, as it increases the chance that a novel variant will be better than the status quo.

Which is one of Shapiro's two big points: that cell mechanisms are such that stress induces a higher error rate in stressed populations, thus increasing diversity and thus opening possibilities for natural selection.

And I believe when were talking about this type of error, we're talking about an A for a T or a G for a C and so on, I don't think we're talking about "oops I made two copies of that Gene that's 1000 bases long."

And there you go again, carving Nature at different joints to those carved at by Shapiro.  Both small mutations and large can be useful.  If you read Blount you will see that the key mutation (the duplication) was weak in effect at first.  Then it was refined.

Small mutations are likely to have been involved in the refinement.  Blount et al mention a couple of SNPs IIRC.
Okay I'm going to try and contain my shock and amazement this time that you would have such a bad grasp of basic genetics. Maybe if I'm nicer to you, you will listen to me with respect to these basic things. Deal?

Why would I want to learn "basic genetics" from you, Dave?  Why would anyone want to?  You don't have a grasp of basic genetics yourself.

Let's keep this real simple and talk only about your second sentence first. You say that a cell doesn't have an error rate, but a population does.

Yes.

How can you say this? Do you not know that cells divide?

Yes.


Do you not know that when they divide they have to copy their DNA?

Yes.

Do you not know that when they copy their DNA the copying process will not be perfect and has to have proofreading and error correction?

Well, it doesn't HAVE to have it, but in fact bacteria DO have mechanisms that check for mismatches and loops and repair any that there are, yes.

Let's get on the same page here with this basic concept.

You are insufferable.
I have a Darwin-debased mind.

Re: Introduction to Systems Biology
Reply #2239
Wait.  How am I being insufferable?  Are you actually quibbling about the fact that after the cell divides, it's now a "population"?  Is that really what this is about?  Or what?  I'm genuinely not following you.

  • Pingu
Re: Introduction to Systems Biology
Reply #2240
Wait.  How am I being insufferable?  Are you actually quibbling about the fact that after the cell divides, it's now a "population"?  Is that really what this is about?  Or what?  I'm genuinely not following you.

No, I know you aren't.  You think you are running rings round the rest of us.  In fact, you are failing to follow just about anything.
I have a Darwin-debased mind.

  • uncool
Re: Introduction to Systems Biology
Reply #2241
Wait.  How am I being insufferable?  Are you actually quibbling about the fact that after the cell divides, it's now a "population"?  Is that really what this is about?  Or what?  I'm genuinely not following you.
That's what the word "rate" is about. It's about how often an event happens, as averaged over a series of times it happens. It's analogous to "variance" or "diversity".

You can torture it to make it make sense for an individual, but its natural expression is as something about a population; the torture effectively remakes an individual into a population.

Re: Introduction to Systems Biology
Reply #2242
So then the answer to this...
In addition to Entropy's burning question that he keeps asking, I have my own burning question ... namely, was the gene duplication event that allowed aerobic citrate uptake in Lenski's bugs RANDOM?  Or was it "directed" by the cell in response to sensing the environment. 
...according to Shapiro, would pretty clearly be that the cell's response to the environment was to increase mutability, not to direct a specific mutation, right?
Yes but I don't think that means relax error correction during replication. I think it means something along the lines of churning out a bunch of tools like skill saws and power drills and jackhammers.

Nobody is claiming that error correction is relaxed during replication.

What Shapiro is claiming is that error-prone repair processes, for one, become more frequent when the cell is under stress. 

Possibly, also, normally high-fidelity repair processes may become more error-prone under conditions of stress.  If you ever bothered to find out HOW the mismatch repair system works, for instance, you would discover that there is a specific mechanism that enables the repair enzyme to recognise the template as the template. That can go wrong.

It is also possible that the systems that generally suppress reshuffling of genetic material become less efficient under stress, but you'd have to read Shapiro to find that out.  It's a while since I read the book.
I have read all that and so I do understand that more errors can be generated under the SOS regime than during normal times.

But the key thing about this I believe is that a higher error rate is bad for the cell, that is, it would decrease Fitness under most conditions.

You still haven't even grokked the difference between a cell and a population.  A cell doesn't have an "error rate".  The population does.  Just as a cell doesn't have "diversity".  A population does.

A mutation rate is bad for a well-adapted population, as most of the mutations will be worse than the status quo.  However, a high mutation rate is good for a population under streess, as it increases the chance that a novel variant will be better than the status quo.

Which is one of Shapiro's two big points: that cell mechanisms are such that stress induces a higher error rate in stressed populations, thus increasing diversity and thus opening possibilities for natural selection.

And I believe when were talking about this type of error, we're talking about an A for a T or a G for a C and so on, I don't think we're talking about "oops I made two copies of that Gene that's 1000 bases long."

And there you go again, carving Nature at different joints to those carved at by Shapiro.  Both small mutations and large can be useful.  If you read Blount you will see that the key mutation (the duplication) was weak in effect at first.  Then it was refined.

Small mutations are likely to have been involved in the refinement.  Blount et al mention a couple of SNPs IIRC.
Okay I'm going to try and contain my shock and amazement this time that you would have such a bad grasp of basic genetics. Maybe if I'm nicer to you, you will listen to me with respect to these basic things. Deal?

Let's keep this real simple and talk only about your second sentence first. You say that a cell doesn't have an error rate, but a population does.

How can you say this? Do you not know that cells divide? Do you not know that when they divide they have to copy their DNA? Do you not know that when they copy their DNA the copying process will not be perfect and has to have proofreading and error correction?

Let's get on the same page here with this basic concept.
you couldn't be much stupider.

eta: lol ninja'd
Love is like a magic penny
 if you hold it tight you won't have any
if you give it away you'll have so many
they'll be rolling all over the floor

Re: Introduction to Systems Biology
Reply #2243
Well excuuuuse me ... for daring to talk about a DNA error rate for an individual bacterium dividing.

Why do you even care about this anyway?  What difference does it make?  The error rate is something like 1 in 10 billion for E coli is it not?  And I forget how many bases E coli has in it's genome but you're going to get quite a bit of dividing before you get your first error are you not?

Re: Introduction to Systems Biology
Reply #2244
Wait.  How am I being insufferable?  Are you actually quibbling about the fact that after the cell divides, it's now a "population"?  Is that really what this is about?  Or what?  I'm genuinely not following you.
we all know you are not following Pingu on this. It's the problem with your whole dumbass analogized way of understanding this exact argument, i.e. your obvious and clear to anyone reading mistake which has continued through this whole thread,  in a way to support your dumbass original religious stupidity.
Love is like a magic penny
 if you hold it tight you won't have any
if you give it away you'll have so many
they'll be rolling all over the floor

Re: Introduction to Systems Biology
Reply #2245
Well excuuuuse me ... for daring to talk about a DNA error rate for an individual bacterium dividing.

Why do you even care about this anyway?  What difference does it make?  The error rate is something like 1 in 10 billion for E coli is it not?  And I forget how many bases E coli has in it's genome but you're going to get quite a bit of dividing before you get your first error are you not?
good fuckity fuck but you are thick. You are a poster child for how religion mindfucks people.
Love is like a magic penny
 if you hold it tight you won't have any
if you give it away you'll have so many
they'll be rolling all over the floor

  • uncool
Re: Introduction to Systems Biology
Reply #2246
Well excuuuuse me ... for daring to talk about a DNA error rate for an individual bacterium dividing.

Why do you even care about this anyway?  What difference does it make?  The error rate is something like 1 in 10 billion for E coli is it not?  And I forget how many bases E coli has in it's genome but you're going to get quite a bit of dividing before you get your first error are you not?
The point is that the deleteriousness or beneficialness should be measured over the whole population, not individuals. It's a correction to your statement that it is deleterious for cells.

Re: Introduction to Systems Biology
Reply #2247
Anyway, let's move on ...

Next you say ...
Quote
A mutation rate is bad for a well-adapted population, as most of the mutations will be worse than the status quo.  However, a high mutation rate is good for a population under streess, as it increases the chance that a novel variant will be better than the status quo.

Which is one of Shapiro's two big points: that cell mechanisms are such that stress induces a higher error rate in stressed populations, thus increasing diversity and thus opening possibilities for natural selection.
Now here is where we need to get specific about what you mean when you say "a high mutation rate is good for a population under stress" ... which of the following do you mean?

1) An increased rate of single base errors is good? Like swapping A's for G's or T's?  Or ...
2) An increased rate of larger "errors" like a gene being duplicated?
3) Something else?

Re: Introduction to Systems Biology
Reply #2248
Well excuuuuse me ... for daring to talk about a DNA error rate for an individual bacterium dividing.

Why do you even care about this anyway?  What difference does it make?  The error rate is something like 1 in 10 billion for E coli is it not?  And I forget how many bases E coli has in it's genome but you're going to get quite a bit of dividing before you get your first error are you not?
4.6 million bp.   Something like 1 in 100 ends up with a base pair substitution from replication

For the most part neither Lenski's not Minnish's E. coli are going to be dividing.  But as I showed for Minnish's bugs they differ from the parental strain at about 3000 locations.   
  • Last Edit: March 13, 2018, 02:47:22 PM by entropy
While you were getting your PhD in virology, I got my PhD in truth detection. :wave:  Dave Hawkins

Re: Introduction to Systems Biology
Reply #2249
Well excuuuuse me ... for daring to talk about a DNA error rate for an individual bacterium dividing.

Why do you even care about this anyway?  What difference does it make?  The error rate is something like 1 in 10 billion for E coli is it not?  And I forget how many bases E coli has in it's genome but you're going to get quite a bit of dividing before you get your first error are you not?
The point is that the deleteriousness or beneficialness should be measured over the whole population, not individuals. It's a correction to your statement that it is deleterious for cells.
OK fine.  Doesn't matter as you will see.