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Topic: Introduction to Systems Biology (Read 17103 times) previous topic - next topic

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Re: Introduction to Systems Biology
Reply #2325
You two should get a room.


Like you and your adopted daughter?

He did build a playfort just for that sort of thing.

Re: Introduction to Systems Biology
Reply #2326
Perverts

Re: Introduction to Systems Biology
Reply #2327
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?

All mutations. Any situation in which the DNA sequence changes.
Thanks for your answer ... anyone else?


I mean that a diverse population enables a population to adapt more readily.  But adaptation results in loss of diversity.

Therefore some rate of mutation is important to replace diversity lost to during adaptation. And as bacterial populations tend not to be very diverse (because they clone) then it makes sense that an increased mutation rate when diversity is needed to help a population adapt will help because it will increase diversity.

And this is what Shapiro is claiming happens - mutation rates increase when diversity is most needed.

Feel free to ask me if you find any of this ambiguous or unclear.
all I asked you to do was answer the following questions. I just want a 1 or 2 or 3.

I didn't ask for a long sermon.

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?


If you are referring to the Lenski experiment and subsequent investigation, 3.

1)  In the Lenski experiment (specifically the ability to metabolize citrate in an aerobic environment), many base pair changes were noted.  Most or these did not affect citrate transport.

2)  It was not a duplication of a single gene.  Learn some more and refine your question.
Is that so? Are you sure?

Re: Introduction to Systems Biology
Reply #2328
You two should get a room.


Like you and your adopted daughter?
can you please try to refrain from talking about penis size and dave's sexual habits? It is derailing even to a guy with pretty severe add
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 #2329
Dave, what on earth is the point of posting great screeds of Shapiro, when you don't even understand what he's saying? Remember YOU were the one that had to be "sold on" reading him (despite having pre-canonised him).  Many of the rest of us have already read lots of his papers, and his book.

You don't have to reprint them here.
I guess you are not following the conversation. I'm trying to find out what caused the gene duplication in lenski's lab. Was it random? Or was it under cellular control?. The latest Shapiro article that I posted talks about cell cognition which relates to this topic. Try to keep up. I know it's it's tough with all the idiots and perverts around here, but do try.

  • RickB
Re: Introduction to Systems Biology
Reply #2330
Note: if you can't be smart, then it's good to be witty.
Note: if you can't be smart, then it's good to be witty.


And you fail on both points.

But, oddly no-one is surprised.


  • RickB
Re: Introduction to Systems Biology
Reply #2331
Perverts

Commenting about what you know??


  • RickB
Re: Introduction to Systems Biology
Reply #2332
Dave, what on earth is the point of posting great screeds of Shapiro, when you don't even understand what he's saying? Remember YOU were the one that had to be "sold on" reading him (despite having pre-canonised him).  Many of the rest of us have already read lots of his papers, and his book.

You don't have to reprint them here.
I guess you are not following the conversation. I'm trying to find out what caused the gene duplication in lenski's lab. Was it random? Or was it under cellular control?. The latest Shapiro article that I posted talks about cell cognition which relates to this topic. Try to keep up. I know it's it's tough with all the idiots and perverts around here, but do try.

  • RickB
Re: Introduction to Systems Biology
Reply #2333
Dave, what on earth is the point of posting great screeds of Shapiro, when you don't even understand what he's saying? Remember YOU were the one that had to be "sold on" reading him (despite having pre-canonised him).  Many of the rest of us have already read lots of his papers, and his book.

You don't have to reprint them here.
I guess you are not following the conversation. I'm trying to find out what caused the gene duplication in lenski's lab. Was it random? Or was it under cellular control?. The latest Shapiro article that I posted talks about cell cognition which relates to this topic. Try to keep up. I know it's it's tough with all the idiots and perverts around here, but do try.


No you aren't.  You are pimping your idea that any non-SNP change was a reasoned , deliberate NGE change to the genone.

That is the 'NGE; consulted the 'Big Book Of Mutations'  and came to the realization that response 476B2 was the correct response.


Re: Introduction to Systems Biology
Reply #2334
You two should get a room.


Like you and your adopted daughter?
can you please try to refrain from talking about penis size and dave's sexual habits? It is derailing even to a guy with pretty severe add

Lol like it'll make any difference.

  • Faid
Re: Introduction to Systems Biology
Reply #2335
Who even made the rule that we cannot group ducks and fish together for the simple reason that they are both aquatic? If I want to group them that way and it serves my purpose then I can jolly well do it however I want to and it is still a nested hierarchy and you can't tell me that it's not.

  • Faid
Re: Introduction to Systems Biology
Reply #2336
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?

All mutations. Any situation in which the DNA sequence changes.
Thanks for your answer ... anyone else?


I mean that a diverse population enables a population to adapt more readily.  But adaptation results in loss of diversity.

Therefore some rate of mutation is important to replace diversity lost to during adaptation. And as bacterial populations tend not to be very diverse (because they clone) then it makes sense that an increased mutation rate when diversity is needed to help a population adapt will help because it will increase diversity.

And this is what Shapiro is claiming happens - mutation rates increase when diversity is most needed.

Feel free to ask me if you find any of this ambiguous or unclear.
all I asked you to do was answer the following questions. I just want a 1 or 2 or 3.

I didn't ask for a long sermon.

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?


If you are referring to the Lenski experiment and subsequent investigation, 3.

1)  In the Lenski experiment (specifically the ability to metabolize citrate in an aerobic environment), many base pair changes were noted.  Most or these did not affect citrate transport.

2)  It was not a duplication of a single gene.  Learn some more and refine your question.
Is that so? Are you sure?

Dave, you haven't even read the presentation yet.
Dave, what on earth is the point of posting great screeds of Shapiro, when you don't even understand what he's saying? Remember YOU were the one that had to be "sold on" reading him (despite having pre-canonised him).  Many of the rest of us have already read lots of his papers, and his book.

You don't have to reprint them here.
I guess you are not following the conversation. I'm trying to find out what caused the gene duplication in lenski's lab. Was it random? Or was it under cellular control?. The latest Shapiro article that I posted talks about cell cognition which relates to this topic. Try to keep up. I know it's it's tough with all the idiots and perverts around here, but do try.
Why did we suddenly become "perverts" as well? Do you think it's some kind of perversion to disagree with you?
Who even made the rule that we cannot group ducks and fish together for the simple reason that they are both aquatic? If I want to group them that way and it serves my purpose then I can jolly well do it however I want to and it is still a nested hierarchy and you can't tell me that it's not.

  • Faid
Re: Introduction to Systems Biology
Reply #2337
Anyway: Care to respond to this?
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?

All mutations. Any situation in which the DNA sequence changes.
Congratulations to JonF, the only one with enough balls to answer the question straight up. Pingu is just dispensing Squid Ink as usual.

All mutations, he says, which I assume includes copying errors and gene duplications and whatever else.

Now I would agree with you that things like gene duplications are a good thing ... because ... they fall under the heading of natural genetic engineering. Makes sense too if we compare with human technology. You can kind of see that one way that humans might adapt to a change from living on open land to living in woodland might be that they all go shopping at Northern Tool for all the things they might need for living in the woods. And of course if we wanted to make it a little closer to how the cell probably works, we could randomize it somewhat and just have a big Factory that churns out a bunch of Woodland tools at random and some of them are going to be useful and some not so useful. If I'm reading Shapiro correctly, this is the sort of thing that he is talking about when he talks about natural genetic engineering.  So a tool in our analogy would be comprable to a gene, the sequence of which I posted earlier for the CIT T Gene. What was that? Something like 1,000 bases or so? I didn't count. I guess more accurately it would be the code which runs the machine for building the tool, but it's just an analogy anyway so it doesn't need to be perfect.

What Shapiro is not categorizing under the heading of natural genetic engineering as far as I can tell, is copying errors which normally involve a single base substitution. In our analogy this seems to be equivalent to randomly throwing out three-letter mnemonic codes which control the software for making the tools we were talking about in the previous paragraph.
So you think gene duplications are not 'copying errors'? Or is it that only copying errors resulting in SNPs are excluded from 'NGE', and copying errors leading to gene duplications are part of it?

Always "as far as you can tell", of course.
Perhaps you don't want to respond, of course. I understand.
Who even made the rule that we cannot group ducks and fish together for the simple reason that they are both aquatic? If I want to group them that way and it serves my purpose then I can jolly well do it however I want to and it is still a nested hierarchy and you can't tell me that it's not.

Re: Introduction to Systems Biology
Reply #2338
You two should get a room.


Like you and your adopted daughter?

He did build a playfort just for that sort of thing.

Woohoo!

Re: Introduction to Systems Biology
Reply #2339

  • VoxRat
  • wtactualf
Re: Introduction to Systems Biology
Reply #2340
Dave now has it in for small mutations  Yet in the human genome, by far the most common alleles, and therefore the ones most viable, are distinguished by very small differences, typically single nucleotide substitutions or small repeats.

I wonder why?
About 90% of the DNA differences between any two individuals are SNPs.
Pretty much exactly what Ayala was talking about, all those years ago.
I'm not aware of any "NGE's" that produce SNPs.
"I understand Donald Trump better than many people because I really am a lot like him." - Dave Hawkins

  • VoxRat
  • wtactualf
Re: Introduction to Systems Biology
Reply #2341
Was it random? Or was it under cellular control?.
Have you considered the possibility that this is a false dichotomy?
"I understand Donald Trump better than many people because I really am a lot like him." - Dave Hawkins

Re: Introduction to Systems Biology
Reply #2342
It is common today for molecular, cell and developmental biologists to speak of cells "knowing" and "choosing" what to do under various conditions. While most scientists using these terms would insist they are just handy metaphors, I argue here that we should take these instinctive words more literally. --James Shapiro

EDIT: Link added
https://www.huffingtonpost.com/james-a-shapiro/cell-cognition_b_1354889.html
  • Last Edit: March 14, 2018, 03:29:05 AM by Dave Hawkins

Re: Introduction to Systems Biology
Reply #2343
what is his argument that he argues 'here' wherever 'here' is?
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 #2344
In E. coli, the signal that glucose is absent is an intracellular "second messenger" molecule that is purely symbolic; it has no structural connection to the glucose transport process. --James Shapiro

https://www.huffingtonpost.com/james-a-shapiro/cell-cognition_b_1354889.html

Re: Introduction to Systems Biology
Reply #2345
what does that mean, dave?
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 #2346
Quote
Front Microbiol. 2015; 6: 264.
Published online 2015 Apr 14. doi:  10.3389/fmicb.2015.00264
PMCID: PMC4396460

The cognitive cell: bacterial behavior reconsidered

Pamela Lyon*†
Author information ► Article notes ► Copyright and License information ►
This article has been cited by other articles in PMC.
Go to:
Abstract
Research on how bacteria adapt to changing environments underlies the contemporary biological understanding of signal transduction (ST), and ST provides the foundation of the information-processing approach that is the hallmark of the 'cognitive revolution,' which began in the mid-20th century. Yet cognitive scientists largely remain oblivious to research into microbial behavior that might provide insights into problems in their own domains, while microbiologists seem equally unaware of the potential importance of their work to understanding cognitive capacities in multicellular organisms, including vertebrates. Evidence in bacteria for capacities encompassed by the concept of cognition is reviewed. Parallels exist not only at the heuristic level of functional analogue, but also at the level of molecular mechanism, evolution and ecology, which is where fruitful cross-fertilization among disciplines might be found.

...

More recently, in view of tremendous advances in methods for studying individual cells as well as population-based microbial behavior, the bacterium has been compared explicitly to a parallel distributed processing (PDP) network (Bray, 2009) that displays 'minimal cognition' (Lengeler et al., 2000; van Duijn et al., 2006; Shapiro, 2007). Arguments concerning bacterial 'intelligence' (Jacob et al., 2004; Hellingwerf, 2005; Marijuán et al., 2010) and even cells 'thinking' (Ramanathan and Broach, 2007) are appearing in mainstream journals, including the special series in this one. British psychologist Richardson (2012), who has been researching human intelligence (sometimes despairingly) since the early 1970s, recently concluded in an extraordinary article in EMBO that the nascent study of unicellular intelligence might provide the key to understanding intelligence in complex vertebrates, including humans. Unknown to Richardson (2012), a microbiologist specializing in computational biology has introduced a plausible formula for establishing 'bacterial IQ,' based on genome size and proportion of DNA segments coding for signal transduction (ST) proteins, as well as a rough gage of 'introversion' or 'extroversion' based on the relative proportion of environment-contacting ST systems (Galperin, 2005). Finally, neuroscientists and neurobiologists tracing the evolution of complex human, brain-based behavior increasingly locate its origins in the microbial realm (Allman, 1999; Damasio, 1999; Greenspan, 2007).

...

To stay alive, bacteria also appear to possess a 'basic toolkit' (Godfrey-Smith, 1996), which in other forms of life--especially mammalian life - would be termed cognitive. In the case of well-studied bacterial species (e.g., E. coli, B. subtilis, M. xanthus, Pseudomonas aeruginosa), the basic toolkit includes at least eight capacities found in different but recognizable forms in complex metazoans (see Box 1).

BOX 1: The basic cognitive 'toolkit.'
  • Sensing/Perception   The capacity to sense and recognize (re-cognize) existentially salient features of the surrounding milieu.
    Valence   The capacity of an organism to assign a value to the summary of information about its surroundings at a given moment, relative to its own current state.
    Behavior   The capacity of an organism to adapt via changing its spatial, structural or functional relation to its external or internal milieu.
    Memory   The capacity to retain information about the immediate (and possibly distant) past, and to calibrate the sensorium to take account of this information, for example, via signal amplification.
    Learning   The capacity to adapt behavior according to past experience, enabling a faster response time.
    Anticipation   The capacity to predict what is likely to happen next based on an early stimulus.
    Signal integration (decision making)   The capacity to combine information from multiple sources, because all organisms appear to sense more than one thing, and some bacterial species are equipped to sense dozens of different states of affairs.
    Communication   The capacity to interact profitably with conspecifics, including initiating collective action, which may or may not include an explicit method of differentiating 'us' from 'them'.

...

Autoinduction: Indirect Sensing Via Proxies
Autoinduction is the process by which an organism synthesizes a class of molecules, called autoinducers (AIs), which stimulate a change in genetic expression in the organism itself when the molecules reach a threshold concentration (Miller and Bassler, 2001).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4396460/

Re: Introduction to Systems Biology
Reply #2347
what does that mean, dave?
Hell if I know ... but I'm trying to find out ... specifically, I'm trying to find out if gene duplications are random?  Or a controlled cellular response to external stimuli?

  • Photon
  • I interfere with myself
Re: Introduction to Systems Biology
Reply #2348
All the franoogling is a clear sign you don't understand what those sources are saying, Dave. Ctrl-F is no substitute for understanding.

Re: Introduction to Systems Biology
Reply #2349
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