Skip to comments.Killing with the flip of a switch
Posted on 07/12/2012 2:42:08 PM PDT by neverdem
One genetic transformation turns friendly bacteria into assassins
Glow-in-the-dark bacteria living in nematode worms flip a genetic switch to change from peaceful cohabitants into killers.
The M-form (M for mutualism) of Photorhabdus luminescens bacteria make friendly colonies inside nematodes. But the microbes switch to the deadly toxin-producing P-form (P for pathogenic) when their hosts are ready to eat an insect from the inside out. Worms vomit up the bacteria into insects, and the bacterial toxins kill and help digest the feast...
(Excerpt) Read more at sciencenews.org ...
Can you take one more evolution question? ;-]
How do you get a gradual mutation to do this?
What are these nuts creating? Science has become like a bad mix of Medusa’s Head and Pandora’s Box!
No one knows what the long term results will be!!!
What if a human somehow ingests one of these suckers from a plant or food or whatever?
Good Lord! Save us all from the “Smart”!!!!
They created nothing. They observed this inversion mutation in those nematode microbes.
Don’t think this isn’t going somewhere because the great and wonderful uses for this techno/bio application will be railroaded down our throats for the “good” of all!
Just like GMO foods and all of the wonderful drugs that have been advertised on TV for 25 years.
We now have sleazeball lawyers pursuing litigants for all of the unforseen side effects from these miracle drugs.
Move along, nothing to see here folks...
They will find a nefarious agricultural use for this biotech... I guarantee it.
I would suggest you bring up your complaint with Mother Nature. Humans only documented this mechanism--Mother Nature invented it.
BTW, Mother Nature is a lot more creative about ways to make deadly organisms than human beings could ever dream of being. She's a... rhymes with "witch"...
Disclaimer: I haven't read the papers describing the technical details of this specific process, so I'm making my best educated guess based on what I already know about bacterial molecular biology. I'm not going to go to the beginning and describe a scheme by which all of the separate genes evolved; I'll just start at the part where these two pathways became linked.
What it looks like to me is that the bacteria had two "expression cassettes" located close to each other on the chromosome.
An expression cassette is a set of genes and associated regulatory elements that are all involved in a common pathway, and are placed next to each other on the chromosome. A bacterium only has one chromosome. Expression cassettes are very common in bacteria (and, to my knowledge, are not used by eukaryotes [organisms with nucleated cells, which includes all multicellular organisms]).
All organisms have a method of moving pieces of DNA from one part of a chromosome to another. These pieces of DNA are called "transposons." Some transposons require an enzyme in order to move. Transposons typically have the same, or complementary, DNA sequence at each end, which is necessary for them to be able to move. I'll call these identical or complementary DNA sequences "sticky ends."
What I surmise happened in these bacteria is that the control elements--promoters--for each of the two expression cassettes became part of the same transposon. This could be from random mutations, or it could be because a transposon inserted itself there and left behind copies of its sticky ends when it left. In any case, once the promoters become a transposon by being between sticky ends, all they have to do is excise themselves, turn around, and reinsert themselves. It's kind of like splicing a film, if you want a visual with that--you can cut out a segment of film, turn the cut piece over, and reinsert it backwards, and it will still run through the projector because the little holes on the edges still line up. Once that promoter area becomes a transposon, the bacteria no longer needs two promoters, so if one is deleted (through a "glitch" in transposon activity), the cassettes will still work... just not both at the same time, because there is only one promoter now. At this point, bacteria that can control the switch--probably through a transposase (the enzyme that catalyzes some transposon movements) mutation--have an advantage over bacteria that can't control the switch.
Switching mechanisms such as that described here are not unknown. Pathogenic bacteria use similar switches to evade the host immune system.
I appreciate your acknowlegement. It’s what the Government has done with said knowledge, and will continue to do.
We are still Reaping/Weeping over the 40’s and 50’s cold war experiments,
all of these new pathogens..... nah!
It's illegal for any scientist to intentionally make a pathogen more virulent.
Thanks for the great reply. Will you indulge my curiosity again? How did the symbiotic relationship between the worm and the bacteria begin? What I am thinking is that at some point they can only get together when things are just perfect and both are fully formed. How did they exist apart and by what mechanism would they have evolved together? Please pardon my ignorance if I’m missing something.
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