Researchers from Lawrence Berkeley National Laboratory, or Berkeley Lab, developed a technique that advanced the study of how phages, viruses that infect bacteria, kill their target bacteria using small proteins.

Vivek Mutalik, a co-senior author of the study from Berkeley Lab’s biosciences division, noted the importance of understanding how viruses infect and kill their bacterial host.

A Berkeley Lab press release said the team used a previously invented technology called Dual-Barcoded Shotgun Expression Library Sequencing and applied it to the study of the smallest viruses. This advanced researchers’ understanding of how viruses kill bacteria, information that can be applied in the development of new tools to fight antibiotic-resistant bacteria.

“Phages are extraordinary innovators when it comes to destroying bacteria. We’re really excited to uncover novel bacterial pathogen-targeting mechanisms that could be leveraged into therapies,” said first author Benjamin Adler in the press release.

Mutalik noted that his interest in the microbial environment stems from the fact that viruses are present everywhere from the human body to the ocean.

For this study, the researchers isolated the genes for the viral proteins involved in killing the bacteria to study them. He also noted the benefits of studying the gene functions in the microbes to learn about antibiotic resistance.

“Once we understand how (viruses) hijack and kill the bacteria host, we can use those tricks in eliminating pathogen bacteria especially, for treating antibiotic resistant bacterial infections,” Mutalik said in an email. “We are surrounded by thousands and thousands of these bacterial viruses and we don’t know exactly who they infect and how they lyse the target cell, so (this new technique) enables us to gain (more) insights about phage encoded single gene lysis systems at a scale which was not possible before.”

Funded in part by the Innovative Genomics Institute and the U.S. Department of Energy, this study was a collaboration between scientists from Berkeley Lab and Texas A&M University. Mutalik expressed his gratitude for connecting with these researchers, whom he called the “leaders in cell lysis mechanism,” describing the benefits of other researchers validating results produced in Berkeley.

With the abundance of the smallest viruses that encode genes to kill their host, Mutalik noted potential areas of study for the future of research on antibiotic resistance.

He explained that the tools developed in this study will aid efforts to investigate toxic genes that are within bacterial genes. This technology can enable researchers to understand what these genes target and how they target, providing greater insight into gene-function relationships.

The technique developed in this study will benefit the field of genomics, as it enables researchers to conduct these experimental validations at a much larger scale, according to Mutalik.

“With the rising incidents of antibiotic resistance infections, and no new antibiotics on the horizon, we are really in an uncharted territory,” Mutalik said in the email. “We urgently need scalable solutions and standardized approaches to address this problem.”

Correction: A previous version of this article incorrectly said that Berkeley Lab researchers developed techniques to study antibiotic resistant microbes. In fact, researchers developed a technique that advanced the study of how phages, viruses that infect bacteria, kill their target bacteria using small proteins.