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Bacterial Dormancy and Viral Interactions

Study reveals how bacterial dormancy provides protection against viral infections.

― 5 min read


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Dormancy is a survival method used by many types of living beings, including tiny organisms like bacteria. When bacteria go into dormancy, they slow down their activities and stop dividing. This helps them survive when faced with tough conditions. One well-known form of dormancy in bacteria is the process of forming Spores, which occurs in groups like Bacillus and Clostridia.

What is Spores Formation?

Spores are protective structures that bacteria create to survive extreme conditions such as high heat, dryness, and lack of energy. The process of forming spores is complicated and involves several steps. First, the bacterial cell duplicates its genetic material. Then, it starts to form a small area called a forespore, which eventually gets surrounded by the rest of the cell before being transformed into a protein-rich spore. These spores can last for a very long time-sometimes thousands or even millions of years-and they can hold a lot of genetic variety.

Dormancy and Viral Infection

Dormancy also helps bacteria defend themselves against viruses. Viruses can kill a significant number of bacteria. To protect themselves, bacteria have developed various methods to fight off Viral Infections. Some changes happen on the surface of bacteria, preventing viruses from attaching. Other methods happen inside the cell, where special systems can help resist the virus’s effects.

Even genetically identical bacteria can behave differently in response to viruses. For example, when bacteria are not growing fast, or when they have formed spores, they might be less likely to be infected by viruses. While these changes can help, they do not provide complete protection. Some viruses can still attack bacteria, even if they are dormant.

Dormancy and Population Dynamics

The way bacteria enter and exit dormancy can influence how they interact with viruses. For example, when viruses infect bacteria, they can trigger dormancy in certain bacterial cells. This means that as bacteria respond to an infection, some may go dormant, helping to lessen the impact of the virus on the bacterial population.

The environment also plays a role in how viruses and bacteria interact. Viruses infect bacteria in various settings, such as in the soil, on surfaces, or inside other organisms. In these situations, bacteria that are close to each other might react differently than those that are spread out. This proximity can impact how viruses spread and how bacteria respond.

Studying Interactions Between Dormancy and Viruses

To understand how dormancy affects the spread of viruses in groups of bacteria, researchers conducted experiments in a controlled environment. They looked at two types of Bacillus subtilis-a wild type that can form spores and a mutant type that cannot. They mixed these bacteria with viruses and observed how the viruses grew.

Initially, Plaques formed at similar rates in both types of bacteria, but the final sizes of the plaques were different. The plaques that formed in the wild type bacterial cultures were smaller compared to those in the mutant cultures. This suggests that the ability to form spores influences how bacteria respond to viral infections.

Experimental Setup

The researchers grew two strains of Bacillus subtilis: the wild type, which can form spores, and a mutant strain that cannot form spores. They used a special fluorescent marker to visualize the process of sporulation. By placing these bacterial cultures in a rich nutrient medium, they ensured high rates of sporulation.

In their experiments, the researchers mixed the bacteria with specific bacteriophages (viruses that infect bacteria) and used a technique to measure the growth of plaques. They also took images of the plaques over time to monitor how quickly they grew and the sizes of the plaques in both types of bacteria.

Findings from the Experiments

The results showed that plaques formed by the wild type bacteria were smaller than those formed by the mutant strain. This difference was noted consistently across various experiments, regardless of the specific conditions. The growth rate of the plaques did not differ significantly, but the size of the plaques varied based on the ability of the bacteria to form spores.

As the researchers conducted further analysis, they found that there was a notable increase in the number of spores formed around the edges of the plaques. The presence of spores was evident before they were seen in other areas of the culture. This phenomenon indicated that the bacteria were responding to the viral infection by starting the sporulation process early, particularly in areas where the virus was spreading.

Mathematical Models of Bacterial and Viral Interactions

Researchers used mathematical modeling to better understand how dormancy affects viral growth in bacterial populations. They created equations that described the interactions between bacteria, viruses, and resources. Several models were tested to see how different factors influenced plaque growth.

One model focused on resource depletion as the main trigger for dormancy, while others considered the role of viral interactions and lysis-associated molecules. These models helped explain the observed sizes and growth patterns of the plaques in the experiments.

Conclusion and Implications

The findings suggest that sporulation acts as a protective strategy for bacteria against viral infections. As viruses spread and cause damage, the bacteria in the surrounding area start forming spores, thus limiting the overall impact of the viruses. This process serves as a collective defense mechanism where bacteria can adapt and reduce the spread of infections.

Moreover, the research highlights the importance of understanding how bacterial dormancy affects their interactions with viruses. This knowledge can help inform studies on microbial dynamics in various environments and has significant implications for ecological and therapeutic applications. By recognizing the balance between dormancy and viral infections, researchers can better grasp the complex relationships between bacteria and viruses in natural systems.

Original Source

Title: Phage infection fronts trigger early sporulation and collective defense in bacterial populations

Abstract: I.Bacteriophage (phage) infect, lyse, and propagate within bacterial populations. However, physiological changes in bacterial cell state can protect against infection even within genetically susceptible populations. One such example is the generation of endospores by Bacillus and its relatives, characterized by a reversible state of reduced metabolic activity that protects cells against stressors including desiccation, energy limitation, antibiotics, and infection by phage. Here we tested how sporulation at the cellular scale impacts phage dynamics at population scales when propagating amongst B. subtilis in spatially structured environments. Initially, we found that plaques resulting from infection and lysis were approximately 3-fold smaller on lawns of sporulating wild-type bacteria vs. non-sporulating bacteria. Notably, plaque size was reduced due to an early termination of expanding phage plaques rather than the reduction of plaque growth speed. Microscopic imaging of the plaques revealed sporulation rings, i.e., spores enriched around plaque edges relative to phage-free regions. We developed a series of mathematical models of phage, bacteria, spore, and small molecules that recapitulate plaque dynamics and identify a putative mechanism: sporulation rings arise in response to lytic activity. In aggregate, sporulation rings inhibit phage from accessing susceptible cells even when sufficient resources are available for further infection and lysis. Together, our findings identify how dormancy can self-limit phage infections at population scales, opening new avenues to explore the entangled fates of phages and their bacterial hosts in environmental and therapeutic contexts.

Authors: Joshua Weitz, A. Magalie, T. Marantos, D. Schwartz, J. Marchi, J. T. Lennon

Last Update: 2024-05-22 00:00:00

Language: English

Source URL: https://www.biorxiv.org/content/10.1101/2024.05.22.595388

Source PDF: https://www.biorxiv.org/content/10.1101/2024.05.22.595388.full.pdf

Licence: https://creativecommons.org/licenses/by/4.0/

Changes: This summary was created with assistance from AI and may have inaccuracies. For accurate information, please refer to the original source documents linked here.

Thank you to biorxiv for use of its open access interoperability.

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