TEXAS A&M (US) — Bacteria are able to develop resistance to antibiotics by co-opting the DNA of their natural enemies—viruses.
The battle between bacteria and bacteria-eating viruses has been going on for millions of years, with viruses attempting to replicate themselves by—in one approach—invading bacteria cells and integrating themselves into the chromosomes of the bacteria.
When this happens a bacterium makes a copy of its chromosome, which includes the virus particle that can then at a later time replicate itself, killing the bacterium—similar to a ticking time bomb.
However, things can go radically wrong for the virus because of random but abundant mutations that occur within the chromosome of the bacterium.
Having already integrated itself into the bacterium’s chromosome, the virus is subject to mutation as well, and some of these mutations, render the virus unable to replicate and kill the bacterium.
With this new diverse blend of genetic material, a bacterium not only overcomes the virus’ lethal intentions but also flourishes at a greater rate than similar bacteria that have not incorporated viral DNA.
“Over millions of years, this virus becomes a normal part of the bacterium,” says Thomas Wood, professor of chemical engineering at Texas A&M University.
“It brings in new tricks, new genes, new proteins, new enzymes, new things that it can do. The bacterium learns how to do things from this.
“What we have found is that with this new viral DNA that has been trapped over millions of years in the chromosome, the cell has created a new immune system,” he says.
“It has developed new proteins that have enabled it to resists antibiotics and other harmful things that attempt to oxidize cells, such as hydrogen peroxide. These cells that have the new viral set of tricks don’t die or don’t die as rapidly.”
To understand the significance of viral DNA to bacteria, Wood deleted all of the viral DNA on the chromosome of a bacterium, in this case bacteria from a strain of E. coli.
The research is reported in the journal Nature Communications.
Wood’s team, led by postdoctoral researcher Xiaoxue Wang, used what in a sense could be described as “enzymatic scissors” to cut out the nine viral patches, which amounted to precisely removing 166,000 nucleotides.
Once the viral patches were successfully removed, the team examined how the bacterium cell changed. What they found was a dramatically increased sensitivity to antibiotics by the bacterium.
Similar processes have taken place on a massive, widespread scale—viral DNA can be found in nearly all bacteria, with some strains possessing as much as 20 percent viral DNA within their chromosome.
“To put this into perspective, for some bacteria, one-fifth of their chromosome came from their enemy, and until our study, people had largely neglected to study that 20 percent of the chromosome,” Wood says. “This viral DNA had been believed to be silent and unimportant, not having much impact on the cell.
“Our study is the first to show that we need to look at all bacteria and look at their old viral particles to see how they are affecting the bacteria’s current ability to withstand things like antibiotics.
“If we can figure out how the cells are more resistant to antibiotics because of this additional DNA, we can perhaps make new, effective antibiotics.”
More news from Texas A&M University: http://tamunews.tamu.edu