Researchers from the University of Wisconsin-Madison and their colleagues from the University of California in San Francisco applied the tool to edit the genes to study which genes affect specific antibiotics. They plan to better understand existing antibiotics and develop new ones. Resistance of disease-causing pathogens to existing antibiotics is a growing problem which, according to estimates, could endanger millions of lives.
The problem of antibiotic resistance
“We need to figure out a new weakness of these bacteria,” says Jason Peters, who developed the system. A technique called the Mobile-CRISPRi allows scientists to carry out the screening functions of antibiotics have a wide spectrum of pathogenic bacteria.
In the process of a form of bacterial sex, scientists gave Mobile-CRISPRi from ordinary laboratory strains of various bacteria, including even the little-studied microbes that live on cheese crust. This simplicity of transfer makes the technique just a boon for scientists who study bacteria, causing diseases or, on the contrary, health-promoting.
Peters worked with Carol gross, Oren Rosenberg and other colleagues, developing Mobile-CRISPRi. This system reduces the production of protein from target genes, allowing scientists to determine how antibiotics inhibit the growth of pathogenic microorganisms. This knowledge can help direct investigations of antibiotic resistance.
The work of scientists was published January 7 in the journal Nature Microbiology. They took advantage of the increasingly popular molecular tool CRISPR, but in a unique way.
“Most people when they think of NASA, think about editing genes,” says Peters. “But that’s not what I do”.
Typically, the CRISPR system targets the gene, which cuts DNA in half. The gene can be edited, while cell regenerates damage.
But Peters and his team worked with a modified form of the CRISPR — CRISPRi. CRISPRi was designed to not allow DNA. Instead, he just sits down on DNA, blocking access of other proteins to a specific gene. The result was a reduced gene expression and reduced number of proteins that they encoded.
Scientists have shown that if you reduce the amount of protein, which aim antibiotic, bacteria become much more sensitive to lower levels of drug which indicates the relationship between gene and drug. Thus, thousands of genes can be simultaneously screened as potential targets for antibiotics, helping scientists to learn how antibiotics work and how to improve them.
To make CRISPRi cell, scientists have developed a method of system migration from conventional laboratory models of E. coli pathogenic types, which are often more difficult to study. Team Peters took advantage of one of the natural ways of exchanging DNA between bacteria, kind of bacterial sex, conjugation.
“You just mix the bacteria together and all turns out,” says Peters. “The easiest thing”.
Using conjugation, a team of Peters handed the Mobile-CRISPRi pathogens Pseudomonas, Salmonella, Staphylococcus and Listeria, among others.
“This means that now you can learn how antibiotics act directly on these pathogens,” says Peters. “We’d better find out how these drugs affect different organisms, and perhaps make them better.”
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