Re: [DIYbio] Re: Can a plasmid contain antibiotic synthesis and resistance genes?

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