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New research shows that bacteria get 'hangry' too

New research shows that bacteria get 'hangry' too
Microfluidic probe-based scRNA-seq method and validation. a, Cells were fixed and permeabilized to allow the penetration of thousands of unique, genome-specific oligonucleotide probes. Hybridized probes retrofitted transcripts with a poly-A tail and UMI, whereas unhybridized probes were washed away. b, Permeabilized cells with hybridized probes were flowed through a commercial microfluidic device that encapsulates single cells into droplets containing barcoded primers with poly-A capture sequence conjugated to a hydrogel microsphere and PCR reagents. c, Final droplets contain one or fewer cells and one hydrogel with a unique cell barcode. Barcoded cDNA was generated from the mRNA:probe hybridized complex via in-droplet PCR. Droplets were then broken and the pooled cDNA amplified further before sequencing. Single-cell transcriptomes were resolved, clustered and visualized. d, Transcriptome quantification by hybridization of a probe library followed by PCR correlates (Pearson’s correlation coefficient, r = 0.73) to traditional, bulk RNA-seq method (SMART-seq stranded kit, Takara) involving random priming of hexamers followed by reverse transcription (RT) and incorporation of template switching oligo. e, Species mixture (‘barnyard’) plot demonstrates that single cells of different bacterial species can be resolved by barcode after microfluidic encapsulation. f, Aggregated probe-based signal from thousands of single cells is well correlated (Pearson’s correlation coefficient, r = 0.94) to the average probe-based signal obtained from the bulk population (pre-encapsulation). RPKM, reads per kilobase of exon per million reads mapped. Credit: Nature Microbiology (2023). DOI: 10.1038/s41564-023-01348-4

Have you ever been so hungry that you become angry, otherwise known as "hangry?" New research by Adam Rosenthal, Ph.D., assistant professor in the Department of Microbiology and Immunology, has found that some bacteria cells get hangry too, releasing harmful toxins into our bodies and making us sick.

Rosenthal and his colleagues from Harvard, Princeton and Danisco Animal Nutrition discovered, using a recently developed technology, that genetically within a have different functions, with some members behaving more docile and others producing the very toxins that make us feel ill.

"Bacteria behave much more different than we traditionally thought," said Rosenthal. "Even when we study a community of bacteria that are all genetically identical, they don't all act the same way. We wanted to find out why."

The findings, published in Nature Microbiology, are particularly important in understanding how and why bacterial communities defer duties to certain cells—and could lead to new ways to tackle antibiotic tolerance further down the line.

New research shows that bacteria get “hangry," too
A fluorescent microscope image shows that in a population of genetically identical. The cell in green is expressing a green-fluorescent protein that is expressed by cells that are able to take up DNA from the environment. Credit: Adam Rosenthal et al.

Rosenthal decided to take a closer look into why some cells act as "well-behaved citizens" and others as "bad actors" that are tasked with releasing toxins into the environment. He selected Clostridium perfringens—a rod-shaped bacterium that can be found in the intestinal tract of humans and other vertebrates, insects, and soil—as his microbe of study.

With the help of a device called a microfluidic droplet generator, they were able to separate, or partition, single bacterial cells into droplets to decode every .

They found that the C. perfringens cells that were not producing toxins were well-fed with nutrients. On the other hand, -producing C. perfringens cells appear to be lacking those crucial nutrients.

"If we give more of these nutrients," postulated Rosenthal, "maybe we can get the toxin-producing cells to behave a little bit better."

Researchers then exposed the bad actor cells to a substance called acetate. Their hypothesis rang true. Not only did toxin levels drop across the community, but the number of bad actors reduced as well. But in the aftermath of such astounding results, even more questions are popping up.

Now that they know that nutrients play a significant role in toxicity, Rosenthal wonders if there are particular factors found in the environment that may be 'turning on' toxin production in other types of infections, or if this new finding is only true for C. perfringens.

Perhaps most importantly, Rosenthal theorizes that introducing nutrients to bacteria could provide a new alternative treatment for animals and humans, alike.

For example, the model organism Clostridium perfringens is a powerful foe in the hen house. As the is shifting away from the use of antibiotics, poultry are left defenseless from the rapidly spreading, fatal disease. The recent findings from Rosenthal et al. may give farmers a new tool to reduce without the use of antibiotics.

As for us humans, there is more work to be done. Rosenthal is in the process of partnering with colleagues across UNC to apply his recent findings to tackle antibiotic tolerance. Antibiotic tolerance occurs when some are able to dodge the drug target even when the community has not evolved mutations to make all cells resistant to an antibiotic. Such tolerance can result in a less-effective treatment, but the mechanisms controlling tolerance are not well understood.

In the meantime, Rosenthal will continue to research these increasingly complex bacterial communities to better understand why they do what they do.

More information: Sahand Hormoz, Probe-based bacterial single-cell RNA sequencing predicts toxin regulation, Nature Microbiology (2023). DOI: 10.1038/s41564-023-01348-4.

Journal information: Nature Microbiology

Citation: New research shows that bacteria get 'hangry' too (2023, April 3) retrieved 28 September 2023 from
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