Nylon Oligomerase
Beowulf
http://www.talkorigins.org/faqs/mutations.html
We read about the evolution of enzymes to digest nylon oligomers
in the bacteria, Pseudomonas. Specifically, there is this quote:
"This adaptation has been experimentally duplicated. In the
experiments, non-nylon-metabolizing strains of Pseudomonas
were grown in media with nylon oligomers available as the
primary food source. Within a relatively small number of
generations, they developed these enzyme activities. This would
appear to be an example of documented occurrence of beneficial
mutations in the lab."
I'm currently in a debate with a
creationist here:
http://www.augustachronicle.com/ubb/Forum2/HTML/000036-4.html
And he is claiming that since these mutations have been duplicated
in a lab setting that they could not have been random mutations, but
must actually be the expression of some hidden trait that was already
in the genome before the introduction of nylon oligomers. I pointed
out that these were the result of a frame-shift mutation (probably
the most "random" of mutations), but he still contends:
"But mutations are chance changes in the genetic makeup of
an organism, however this so-called mutations is duplicated
many times (maybe every time) and easily in the laboratory,
therefore it can not be by chance that this is happening. It
is more likely that this ability was always in the bacterium
as an recessive gene, and by placing the bacterium in an
environment that favors this gene, the other genes that was
dominate and is hiding this gene are breed out of the bacterium."
Does anyone have more information on the evolution of nylon
oligomerase among Pseudomonas, specifically with a view to pointing
out how "random" mutations can be replicated in a lab?
My thoughts on it are that frame-shift mutations occur fairly
often and given that the Pseudomonas in the experiment were
in an environment that had nylon oligomers in it that the frame-shift
was advantageous for them. If they had been grown in a medium w/o
any nylon oligomers then the frame-shifted strains would not have
proliferated. However, I'm no biologist and would appreciate some
input from someone more knowledgable.
Thanks.
--
EAC Eater of Meatpies
Atheist #1942
Remove the ape to reply.
tos...@aol.com ab...@aol.com ab...@yahoo.com ab...@hotmail.com
ab...@msn.com ab...@sprint.com ab...@earthlink.com u...@ftc.gov
postm...@attglobal.net ab...@pacbell.net live...@icrmedia.org
Nathan McKaskle
> "But mutations are chance changes in the genetic makeup of
> an organism, however this so-called mutations is duplicated
> many times (maybe every time) and easily in the laboratory,
> therefore it can not be by chance that this is happening. It
> is more likely that this ability was always in the bacterium
> as an recessive gene, and by placing the bacterium in an
> environment that favors this gene, the other genes that was
> dominate and is hiding this gene are breed out of the bacterium."
So regardless if he is right or wrong, if it isn't a mutation, and is a
pre-existing recessive gene, wouldn't this still show evolution at work?
Seems he's arguing against mutation while acknowleging what creationists
normally deny as far as I know.
Beowulf
The thing is, since creationism is neither a scientific theory
nor a monolithic dogma, that you cannot generalize what a specific
creationist will take as "evolution".
For instance, are the numerous fossil hominids extinct apes or
small-brained humans? You can't get a consistent answer from
creationists. Their basic position is not a positive one, but
rather "Nuh uh."
Thanks for the input.
Ronald Okimoto
Beowulf wrote:
Bacteria are haploid. They only have one copy of most genes in their
genome. There usually are no recessive genes hanging around. You can
sequence the only gene that the bacteria has that you are interested in
and it does not have the mutation. You grow up clones of this gene
(asexual reproduction in bacteria), from a single bacteria with the non
mutant gene. You place the descendents of this bacteria under selection
and select for mutations that allow the bacteria to metabolize nylon.
This is fairly simple because you starve the bacteria on a poor food
source, but supply lots of nylon oligomers and just select for the
bacteria that can grow faster. Since all the bacteria are derived from
the original non mutant bacteria any changes in the genes are new
mutations that occurred randomly in the genome.
He can argue that the mutation was nonrandom and he could be correct.
We know that certain mutations will occur more often than others in a
given sequence, but we have no evidence that the mutations are directed,
just that there is something about the sequence or chemistry of the
nucleotides that make certain mutations more likely. For example we
know that frameshift mutations are more likely to occur in
mononucleotide repeats (AAAAAAA to AAAAAA). This is probably due to the
fact that slipage (replication errors) or abberant recombination or
repair can occur.
There is a mutation that causes the vast majority of spontaneous cases
of dwarfism in humans and in nearly all new cases the mutation is at the
same position and is a C to T transistion. This mutation occurs once in
around every 10,000 live births. We don't know why it occurs so often
at this postion, but it is a CpG sequence and we know that CpGs tend to
mutate at a higher rate than other sequences, but this would be an
anomoly even for CpGs. It is possible that something else about the
surrounding DNA sequence makes this mutation occur more often than
usual, or that the designer likes achondroplastic dwarfs.;-)
Ron Okimoto
Beowulf
Thanks for the further detail.
So the experimenters are actively selected for bacteria that
can generate nylon oligomerase, by providing a poor food source
meaning there is a selective pressure to develop the enzyme and
frame shift mutations are known to occur fairly commonly at
certain types of sites in the genome.
Thanks, I'll pass this along...not that it'll be worth my time.
The guy's best effort at supporting creationism is to make the
"evolve a watch" and the 2LOT arguments. Besides, since we
don't *know* why frameshifts occur it means "goddidit".
--
EAC Eater of Meatpies
Atheist #1942
Remove the ape to reply.
Wade Hines
> In the t.o FAQ found here:
> http://www.talkorigins.org/faqs/mutations.html
>
> We read about the evolution of enzymes to digest nylon oligomers
> in the bacteria, Pseudomonas. Specifically, there is this quote:
>
> "This adaptation has been experimentally duplicated. In the
> experiments, non-nylon-metabolizing strains of Pseudomonas
> were grown in media with nylon oligomers available as the
> primary food source. Within a relatively small number of
> generations, they developed these enzyme activities. This would
> appear to be an example of documented occurrence of beneficial
> mutations in the lab."
>
>
> I'm currently in a debate with a
> creationist here:
> http://www.augustachronicle.com/ubb/Forum2/HTML/000036-4.html
>
> And he is claiming that since these mutations have been duplicated
> in a lab setting that they could not have been random mutations, but
> must actually be the expression of some hidden trait that was already
> in the genome before the introduction of nylon oligomers. I pointed
> out that these were the result of a frame-shift mutation (probably
> the most "random" of mutations), but he still contends:
As a matter of basic genetics, the rates of spontaneous mutation
can, and has been determined. If the error is a point mutation,
the rate is approximately 1 in 10^9th chance which means if you
grow up 10^10 cells you expect to have 10 instances of this mutation.
Work that defines this used to be very common with bacteria.
Similar results occur for frameshift mutations. Just becuase
you get an high expectation value that the mutation occur in
some cell doesn't mean it isn't a random mutation. Please
consider that within those 10 trillion cells, hundreds of
billions had lethal mutations occur and they died!
> "But mutations are chance changes in the genetic makeup of
> an organism, however this so-called mutations is duplicated
> many times (maybe every time) and easily in the laboratory,
> therefore it can not be by chance that this is happening. It
> is more likely that this ability was always in the bacterium
> as an recessive gene, and by placing the bacterium in an
> environment that favors this gene, the other genes that was
> dominate and is hiding this gene are breed out of the bacterium."
This has been answered but need to be reinforced. Bacteria are
haploid and haploid organisms don't have recessive genes, except
in rare cases with plasmids. Excuses that document that one
doesn't understand genetics are a strange way to argue.
> Does anyone have more information on the evolution of nylon
> oligomerase among Pseudomonas, specifically with a view to pointing
> out how "random" mutations can be replicated in a lab?
Lots of random events can be duplicated. Rolling two sixes
with a pair of dice is only a 1/36 chance but roll the dice
360 times and you expect to get about 10 such rolls. Mutations
occur with a given frequency based on the nature of DNA,
how it is replicated and repaired.
Also, the nylonase activity involves more than a single
gene. Did you see actual references? Here's a review.
Biodegradation of nylon oligomers.
Negoro S.
Appl Microbiol Biotechnol 2000 Oct;54(4):461-
and an online article
http://aem.asm.org/cgi/reprint/61/5/2020.pdf
> My thoughts on it are that frame-shift mutations occur fairly
> often and given that the Pseudomonas in the experiment were
> in an environment that had nylon oligomers in it that the frame-shift
> was advantageous for them. If they had been grown in a medium w/o
> any nylon oligomers then the frame-shifted strains would not have
> proliferated. However, I'm no biologist and would appreciate some
> input from someone more knowledgable.
They wouldn't have proliferated faster than the rest, out growing
them.
Dunk
<skr...@homosapiens.attglobal.net> wrote:
>So the experimenters are actively selected for bacteria that
>can generate nylon oligomerase, by providing a poor food source
>meaning there is a selective pressure to develop the enzyme and
>frame shift mutations are known to occur fairly commonly at
>certain types of sites in the genome.
Umm, maybe this could be rewritten as three or four sentences,
carefully.
For instance, "selective pressure to develop the enzyme" is not an
ideal expression. IF the mutation(s) occurred, it/they would spread
because the lucky bacteria could eat more, faster, and hence multiply.
(assuming that the mutation is not at the same time having a harmful
effect)
See also the FAQ "Are Mutations Harmful?"
Dunk
Beowulf
>
> <snip>
Thanks for the further comments. This fills in very nicely
where Ronald Okimoto left off. I'm about to the end of this
debate, I think, given that I have dropped easily a dozen
URLs only 1 of which I can be certain was read.
Why should he bothered, anyway, there's no evidence for
evolution. Right?
I also referred to an older (1994?) edition of the Biodegradation
journal with an article by Negoro discussion nylon oligomerase, but
will update my post with this newer review.
Thanks again.
Ian Musgrave & Peta O'Donohue
Address altered to avoid spam, delete RemoveInsert
On 1 Nov 2001 11:29:31 -0500, Beowulf
<skr...@homosapiens.attglobal.net> wrote:
>In the t.o FAQ found here:
>http://www.talkorigins.org/faqs/mutations.html
>
>We read about the evolution of enzymes to digest nylon oligomers
>in the bacteria, Pseudomonas. Specifically, there is this quote:
>
>"This adaptation has been experimentally duplicated. In the
>experiments, non-nylon-metabolizing strains of Pseudomonas
>were grown in media with nylon oligomers available as the
>primary food source. Within a relatively small number of
>generations, they developed these enzyme activities. This would
>appear to be an example of documented occurrence of beneficial
>mutations in the lab."
>
>
>I'm currently in a debate with a
>creationist here:
>http://www.augustachronicle.com/ubb/Forum2/HTML/000036-4.html
>
>And he is claiming that since these mutations have been duplicated
>in a lab setting that they could not have been random mutations, but
>must actually be the expression of some hidden trait that was already
>in the genome before the introduction of nylon oligomers. I pointed
>out that these were the result of a frame-shift mutation (probably
>the most "random" of mutations), but he still contends:
Okay, a lot of people have given you good advice. I'll add my bit. The
experimental system evolved new nylonase activity, but it WASN'T the
same enzymes that were generated. Standard nylonase activity is due to
two enzymes nylA(EI) and nylB(EII). In these experiments a nylonase
activity was developed that did NOT utilize either the nylA or nylB
reaction path. It was a different enzyme. In another set of
experiments, yet another enzyme activity was evolved (Negoro S, Kakudo
S, Urabe I, and Okada H J Bacteriol 174 7948-53, 1992) that was
neither nylA, nylB or the nylonase activity above. This has been
characterized and is a mutation in a gene with no sequence similarity
to either nylA or nylB.
You opponent has made the mistake that because the same overall
pathway has re-evolved (nylon hydrolysis), the same mutation on the
same gene must of happened. It didn't, a different mutation has
produced nylon hydrolysis by a entirely different reaction path. As
with many other reactions, there is more than one way to get the job
done.
>"But mutations are chance changes in the genetic makeup of
>an organism, however this so-called mutations is duplicated
>many times (maybe every time) and easily in the laboratory,
Different mutations in different genes. The _only_ two experimental
demonstrations of nylonase evolution, and these produced two different
mutations, which are different again from the wild-type mutations.
>therefore it can not be by chance that this is happening.
Not so. For example, the commonest form streptomycin resistance is due
to a mutation of codon42, AAA -> ACA followed by AAA->AAC and
AAA->AGA. Random mutagenesis can produced this mutation again and
again (along with many others, but those that don't result in
resistance to streptomycin die out). Frame shift mutations occur with
a relatively low frequency, but there is no reason why _a_ frameshift
mutation to generate nylB could not be picked up with a large enough
population and strong selection (getting the _exactly_ the same
frame-shift mutation would be _very_ unlikely unless there was a "hot
spot" of some sort in the gene).
But, as it happens, the mutations generated were not nylB mutants.
>It
>is more likely that this ability was always in the bacterium
>as an recessive gene, and by placing the bacterium in an
>environment that favors this gene, the other genes that was
>dominate and is hiding this gene are breed out of the bacterium."
Bacteria are haploid, they _don't_ have recessive genes. And, as nylon
was not present in the environment until 50 years ago, any dormant
gene would have been mutated to uselessness or deleted from the genome
millennia before (as bacterial genomes are very slimmed down and don't
carry much non-working DNA).
>Does anyone have more information on the evolution of nylon
>oligomerase among Pseudomonas, specifically with a view to pointing
>out how "random" mutations can be replicated in a lab?
>
>My thoughts on it are that frame-shift mutations occur fairly
>often and given that the Pseudomonas in the experiment were
>in an environment that had nylon oligomers in it that the frame-shift
>was advantageous for them. If they had been grown in a medium w/o
>any nylon oligomers then the frame-shifted strains would not have
>proliferated. However, I'm no biologist and would appreciate some
>input from someone more knowledgable.
There is no reason why the frame shift mutation that generated
nylB(EII) could not re-occur at low frequency. The trap is thinking
that generating nylB is the ONLY way to generate nylonase, there is
obviously more than one way, nylA for one, the P arugenosa PO5052
mutants Ahx pathway and Flavobacter KI725R mutants that generate nylC.
Now, considering the "evolution of a watch" your opponet wants to
argue, try this
WHile this may not be exactly what you want, here is a repost of an
argument I made along these lines:
==============begin repost============================
[Consider the period gene of _Drosophila_] it's a watch. Or strictly
speaking, its the entrainment mechanism of a watch. The "watch" is the
circadian rythem generator in Drosophila, it consists of _Period_
_Timeless_ _Clock_ _Cycle_ and _Crypotchrome_, similar systems occur
in mammals.
CLK and CYC form a dimer which binds to DNA and starts the
transcription of PER and TIM, which then form a dimer and bind to
other genes (clock controlled genes, CCG), causing their
transcription. After a certain concentration of PER/TIM is reached, it
inhibits its own transcription, the levels of PER/TIM fall and the CCG
transcription is turned off. When PER/TIM falls low enough,
transcription is de-repressed, and the cycle starts all over again.
The system is a cyclic oscillator which acts as a "watch".
CRY is the light sensor, it entrains the PER/TIM cycle to the
day/night cycle.
Unlike Paleys watch, where we know
a) That watches are manufactured
b) That watches (or their components) can't reproduce
c) That small changes in any one component are unlikely to produce an
improvement in the watch
The Drosophila "Watch" can be fairly easily shown to evolved. PER,
TIM, CYC, AND CLK show significant homology to the receptors that
dimerise and translocate to the nucleus. These "watch" components are
also quite similar to the simpler (blue light sensitive) watch (WC-1
and WC-2) that is present in the fungus _Neurospora_crassa_, and they
are also related to the bacterial photoreactive yellow protein
(sensitive to blue light). Overall, the "watch" looks like it arose
fairly simply from proteins originally dedicated to blue light
photoreception and transduction.
You can also show mutation within the watch components, eg mutations
in PER can affect its function, a couple of amino acids difference
between the PER gene in D. melanogaster and D simulans, completely
changes the timing of the song cycle. Mutations in other parts of the
gene change the thermostability of the cycle, and clines of these
mutations can be found with increasing latitude.
Overall, while Paley's watch implies design, the Drosophila "watch"
implies evolution.
================end repost==============================
Cheers! Ian
=====================================================
Ian Musgrave Peta O'Donohue,Jack Francis and Michael James Musgrave
reyn...@werple.mira.net.au http://werple.mira.net.au/~reynella/
Southern Sky Watch http://www.abc.net.au/science/space/default.htm
mel turner
[Nathan McKaskle] wrote...
>> "But mutations are chance changes in the genetic makeup of
>> an organism, however this so-called mutations is duplicated
>> many times (maybe every time) and easily in the laboratory,
>> therefore it can not be by chance that this is happening.
Yes, it can, with lab culture populations of many millions or
billions of bacteria. Rare mutations are likely to recur often
on that scale.
It
>> is more likely that this ability was always in the bacterium
>> as an recessive gene,
Bacteria don't have recessive alleles. Nor do other haploid
organisms.
and by placing the bacterium in an
>> environment that favors this gene, the other genes that was
>> dominate and is hiding this gene are breed out of the bacterium."
Just shows he doesn't understand bacterial genetics.
No recessives or dominants. The "new genes" really are new.
>So regardless if he is right or wrong, if it isn't a mutation, and is a
>pre-existing recessive gene, wouldn't this still show evolution at work?
Sure, any change in the frequency of alleles in a population
over generations is evolution. Natural selection can and does
cause it [think peppered moths].
>Seems he's arguing against mutation while acknowleging what creationists
>normally deny as far as I know.
Which is odd, since where do new variations in alleles
come from if not mutation?
cheers
Nathan McKaskle
> >> an organism, however this so-called mutations is duplicated
> >> many times (maybe every time) and easily in the laboratory,
> >> therefore it can not be by chance that this is happening.
>
> Yes, it can, with lab culture populations of many millions or
> billions of bacteria. Rare mutations are likely to recur often
> on that scale.
>
> It
> >> is more likely that this ability was always in the bacterium
> >> as an recessive gene,
>
> Bacteria don't have recessive alleles. Nor do other haploid
> organisms.
Never knew that, interesting.
>
> and by placing the bacterium in an
> >> environment that favors this gene, the other genes that was
> >> dominate and is hiding this gene are breed out of the bacterium."
>
> Just shows he doesn't understand bacterial genetics.
> No recessives or dominants. The "new genes" really are new.
Good point if the above is true.
>
> >So regardless if he is right or wrong, if it isn't a mutation, and is a
> >pre-existing recessive gene, wouldn't this still show evolution at work?
>
> Sure, any change in the frequency of alleles in a population
> over generations is evolution. Natural selection can and does
> cause it [think peppered moths].
>
> >Seems he's arguing against mutation while acknowleging what creationists
> >normally deny as far as I know.
>
> Which is odd, since where do new variations in alleles
> come from if not mutation?
Heheh, goddidit...yeah..thats the ticket.
pz
"Nathan McKaskle" <zil...@zillien.com> wrote:
> > >> "But mutations are chance changes in the genetic makeup of
> > >> an organism, however this so-called mutations is duplicated
> > >> many times (maybe every time) and easily in the laboratory,
> > >> therefore it can not be by chance that this is happening.
> >
> > Yes, it can, with lab culture populations of many millions or
> > billions of bacteria. Rare mutations are likely to recur often
> > on that scale.
> >
> > It
> > >> is more likely that this ability was always in the bacterium
> > >> as an recessive gene,
> >
> > Bacteria don't have recessive alleles. Nor do other haploid
> > organisms.
>
> Never knew that, interesting.
>
> >
> > and by placing the bacterium in an
> > >> environment that favors this gene, the other genes that was
> > >> dominate and is hiding this gene are breed out of the bacterium."
> >
> > Just shows he doesn't understand bacterial genetics.
> > No recessives or dominants. The "new genes" really are new.
>
> Good point if the above is true.
Trust us, it's true (except for some not-so-uncommon special cases).
The other evidence that these are new mutations is that the bacteria are
grown from single cell stocks, so the colony you are looking at is a
clone -- most lack the ability, and a few acquire it. You can take any
single bacterium from a colony, culture it until you've got billions of
cells from it, and then select for the property you want. What you find
is that any cell from the original colony, if given time to produce
sufficient numbers of progeny, will have a few descendants with that
property. The argument that the trait is lurking in the population in a
haploid state is false both because they aren't haploid, and because if
the argument were correct, *all* of the members of the colony would have
to be carrying it.
>
> >
> > >So regardless if he is right or wrong, if it isn't a mutation, and is a
> > >pre-existing recessive gene, wouldn't this still show evolution at work?
> >
> > Sure, any change in the frequency of alleles in a population
> > over generations is evolution. Natural selection can and does
> > cause it [think peppered moths].
> >
> > >Seems he's arguing against mutation while acknowleging what creationists
> > >normally deny as far as I know.
> >
> > Which is odd, since where do new variations in alleles
> > come from if not mutation?
>
> Heheh, goddidit...yeah..thats the ticket.
>
>
>
--
pz
Nathan McKaskle
"pz" <my...@mac.com> wrote in message
news:myers-99C6AE....@laurel.tc.umn.edu...
I see, so am I right saying that since haploid cells only contain the
gametic or half the number of chromosomes of a normal somatic cell, the fact
that it doesn't combine to make a diploid cell makes it so that there is no
real recessive or dominate alleles, since there is no new set of chromosomes
to compare it to? Err to put it in a metaphorical sense, if there were only
one brand and size of styrofoam cups, there would be nothing to compare it
to in order to show a dominate average size of cup? Or maybe that was a bad
analogy lol.
Beowulf
>
> Okay, a lot of people have given you good advice. I'll add
> my bit.
Thanks so much for the late entry! You've given me some very
good info that hasn't been discussed until now.
> The experimental system evolved new nylonase
> activity, but it WASN'T the same enzymes that were generated.
> <snip>
> You opponent has made the mistake that because the same overall
> pathway has re-evolved (nylon hydrolysis), the same mutation on
> the same gene must of happened. It didn't, a different mutation
> has produced nylon hydrolysis by a entirely different reaction
> path. As with many other reactions, there is more than one way
> to get the job done.
I suspected this might be so, but wasn't familiar enough with
molecular biology nor had easy access to the original references
to confirm it.
> <snip>
>
> Now, considering the "evolution of a watch" your opponet wants
> to argue, try this WHile this may not be exactly what you want,
> here is a repost of an argument I made along these lines:
>
> <snip discussion of genetic timers>
This is a great rebuttal to the watch argument. I'm going to
recommend this entire thread to my opponent since it covers
issues he raised that I wasn't knowledgable enough to deal
with well.