Biology subjects

Tzipilevich, E.

Publications and source records attributed to Tzipilevich, E..

4 recordsLinked to original sources

bioRxiv2021

Phage-resistant bacteria reveal a role for potassium in root colonization

Bacteriophage predation is an important factor in bacterial community dynamics and evolution. Phage-bacteria interaction has mainly been studied in lab cultures, while dynamics in natural habitats, and especially in the plant root niche are underexplored. To better understand this process, we characterized infection of the soil bacterium B. subtilis NCBI 3610 by the lytic phage SPO1 during growth in LB medium and compared it to root colonization. Resistance in vitro was primarily through modification of the phage receptor. However, this type of resistance reduced the ability to colonize the root. From a line that survived phage infection while retaining the ability to colonize the root, we identified a plant-specific phage resistance mechanism involving potassium (K+) ion influx modulation and enhanced biofilm formation.

microbiology↗

bioRxiv2021

Plant immune system activation is necessary for efficient interaction with auxin secreting beneficial bacteria

Plants continuously monitor the presence of microorganisms through their immune system to establish an adaptive response. Unlike immune recognition of pathogenic bacteria, how beneficial bacteria interact with the plant immune system is not well understood. Analysis of colonization of Arabidopsis thaliana by auxin producing beneficial bacteria revealed that activation of the plant immune system is necessary for efficient bacterial colonization and auxin secretion. A feedback loop is established in which bacterial colonization triggers an immune reaction and production of reactive oxygen species, which, in turn, stimulate auxin production by the bacteria. Auxin promotes bacterial survival and efficient root colonization, allowing the bacteria to inhibit fungal infection and promote plant health.

plant biology↗

bioRxiv2021

Bacteria elicit a phage tolerance response subsequent to infection of their neighbors

Plaque occurrence on a bacterial lawn manifests successive rounds of bacteriophage infection. Yet, mechanisms evolved by bacteria to limit plaque spread have been hardly explored. Here we investigated the dynamics of plaque development by lytic phages infecting the bacterium Bacillus subtilis. We report that plaque expansion is followed by a constriction phase owing to bacterial growth into the plaque zone. This phenomenon is caused by an adaptive process, herein termed "phage tolerance response", elicited by non-infected bacteria located at the plaque rim upon sensing infection of their neighbors. The temporary phage-tolerance is executed by the stress response RNA polymerase sigma factor {sigma}X, primarily through activation of the dlt operon, encoding enzymes that catalyze D-alanylation of cell wall teichoic acid polymers, the major attachment sites for phages infecting Gram-positive bacteria. D-alanylation impedes phage binding and hence infection, thus enabling the uninfected bacteria to form a protective shield opposing plaque spread.

microbiology↗

bioRxiv2018

A mutant bacteriophage evolved to infect resistant bacteria gained a broader host range

Bacteriophages (phages) are the most abundant entities in nature, yet little is known about their capacity to acquire new hosts and invade new niches. By exploiting the Gram positive soil bacterium Bacillus subtilis (B. subtilis) and its lytic phage SPO1 as a model, we followed the co-evolution of bacteria and phages. After infection, phage resistant bacteria were readily isolated. These bacteria were defective in production of glycosylated wall teichoic acid (TA) polymers, served as SPO1 receptor. Subsequently, a SPO1 mutant phage that could infect the resistant bacteria evolved. The emerging phage contained mutations in two genes, encoding the baseplate and fibers required for host attachment. Remarkably, the mutant phage gained the capacity to infect non-host Bacillus species that are not infected by the wild type phage. We provide evidence that the evolved phage lost its dependency on the species specific glycosylation pattern of TA polymers. Instead, the mutant phage gained the capacity to directly adhere to the TA backbone, conserved among different species, thereby crossing the species barrier.

microbiology↗