The toxin has a half-life of 30 minutes while the antitoxin is much shorter. Was it half a minute or 5 minutes?
So, toxin/antitoxin will increase the stability of a plasmid
dramatically, but AFAIK they won't have any effect on surrounding cells;
if they did, they'd be reclassified as bacteriocins or antibiotics.
Well, if I add e.g. a chloroplast export signal peptide (are there any? There must be?!), it escapes the chloroplasts. The signal peptide is cleaved off, and it enters another chloroplast without resistance. And destroys it.
--
On Thu, Jan 31, 2013 at 5:53 PM, Cathal Garvey <cathalgarvey@cathalgarvey.me> wrote:
quickly by extracellular proteases?
Toxin/antitoxin systems more often appear to be selfish plasmid
strategies to force individual cells to keep the plasmid. Antibiotics,
on the other hand, are usually a cellular strategy (which might or might
not be plasmid-encoded) to kill off the competition.
Some antibiotics of course serve both purposes; bacteriocins are often
encoded with their own resistance gene, and so they will act as a
toxin/antitoxin and an antibiotic system. By contrast, most
"traditional" antibiotics don't actually have a "resistance" or
"immunity" gene, because they are made by a species that isn't affected
by them.
For example, penicillium fungi don't suffer any harm from penicillins,
so they don't have or need a gene to make them resistant; therefore, the
only natural resistance genes for penicillins that I know of are
beta-lactamases, which destroy the antibiotic rather than just making
the cell immune.
So, toxin/antitoxin will increase the stability of a plasmid
dramatically, but AFAIK they won't have any effect on surrounding cells;
if they did, they'd be reclassified as bacteriocins or antibiotics.
On 31/01/13 16:42, Mega wrote:
> But if the toxon is secreted, then it's self-selecting, I assume.
>
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Toxin/antitoxin systems more often appear to be selfish plasmid
strategies to force individual cells to keep the plasmid. Antibiotics,
on the other hand, are usually a cellular strategy (which might or might
not be plasmid-encoded) to kill off the competition.
Some antibiotics of course serve both purposes; bacteriocins are often
encoded with their own resistance gene, and so they will act as a
toxin/antitoxin and an antibiotic system. By contrast, most
"traditional" antibiotics don't actually have a "resistance" or
"immunity" gene, because they are made by a species that isn't affected
by them.
For example, penicillium fungi don't suffer any harm from penicillins,
so they don't have or need a gene to make them resistant; therefore, the
only natural resistance genes for penicillins that I know of are
beta-lactamases, which destroy the antibiotic rather than just making
the cell immune.
So, toxin/antitoxin will increase the stability of a plasmid
dramatically, but AFAIK they won't have any effect on surrounding cells;
if they did, they'd be reclassified as bacteriocins or antibiotics.
On 31/01/13 16:42, Mega wrote:
> But if the toxon is secreted, then it's self-selecting, I assume.
>
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Some antibiotics of course serve both purposes; bacteriocins are often
encoded with their own resistance gene, and so they will act as a
toxin/antitoxin and an antibiotic system. By contrast, most
"traditional" antibiotics don't actually have a "resistance" or
"immunity" gene, because they are made by a species that isn't affected
by them.
For example, penicillium fungi don't suffer any harm from penicillins,
so they don't have or need a gene to make them resistant; therefore, the
only natural resistance genes for penicillins that I know of are
beta-lactamases, which destroy the antibiotic rather than just making
the cell immune.
So, toxin/antitoxin will increase the stability of a plasmid
dramatically, but AFAIK they won't have any effect on surrounding cells;
if they did, they'd be reclassified as bacteriocins or antibiotics.
On 31/01/13 16:42, Mega wrote:
> But if the toxon is secreted, then it's self-selecting, I assume.
>
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For example, penicillium fungi don't suffer any harm from penicillins,
so they don't have or need a gene to make them resistant; therefore, the
only natural resistance genes for penicillins that I know of are
beta-lactamases, which destroy the antibiotic rather than just making
the cell immune.
So, toxin/antitoxin will increase the stability of a plasmid
dramatically, but AFAIK they won't have any effect on surrounding cells;
if they did, they'd be reclassified as bacteriocins or antibiotics.
On 31/01/13 16:42, Mega wrote:
> But if the toxon is secreted, then it's self-selecting, I assume.
>
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So, toxin/antitoxin will increase the stability of a plasmid
dramatically, but AFAIK they won't have any effect on surrounding cells;
if they did, they'd be reclassified as bacteriocins or antibiotics.
On 31/01/13 16:42, Mega wrote:
> But if the toxon is secreted, then it's self-selecting, I assume.
>
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Not necessarily; does the toxin enter other cells? Does it get degraded
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