WEDNESDAY, SEPTEMBER 28, 2016

Researchers find certain genes key to antibiotic-resistance bacteria

Scripps Research Institute Professor Floyd Romesberg and Research Associate Arryn Craney were among the authors of the new study. | The Scripps Research Institute

Researchers from The Scripps Research Institute (TSRI) recently discovered that antibiotic-resistant bacteria use a specific set of genes, previously uncharacterized, to develop resistance.

Each year, more bacteria strains develop antibiotic resistance. The growing number of antibiotic-resistant bacteria has many health professionals concerned about the future of modern medicine.

The TSRI researchers have been developing new forms of antibiotics, including arylomycin, but tests have shown that bacteria can develop resistance against arylomycin as well.

During their studies, the TSRI scientists found that Staphylococcus aureus, an important human pathogen, created its own resistance to arylomycin by turning on a specific set of genes.

“This explains why antibiotic resistance rates in some bacteria are higher than in others,” Floyd Romesberg, TSRI professor and senior author of the new study, said. “Resistance depends on this little set of genes that no one knew could contribute to tolerating the arylomycins.”

Arylomycin antibiotics are able to stop the growth of bacteria by interrupting a specific protein, known as Type I signal peptidase (SPase). This protein has been considered “essential,” meaning that researchers thought bacteria could not live without it. SPase stops peptide sequences as proteins transit from the cell’s inside to its outside. Without SPase, proteins are stuck inside of the cell, where they gradually accumulate, killing the bacterium.

“We took it for granted that we knew all the steps of protein secretion,” Arryn Craney, a TSRI research associate and first author of the new study, said. “Now we’ve found a way to bypass SPase.”

Further details are available in this week's mBio journal.

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