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Thermoresponsive C22 phage stiffness modulates the phage infectivity

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AbstractBacteriophages offer a sustainable alternative for controlling crop disease. However, the lack of knowledge on phage infection mechanisms makes phage-based biological control varying and ineffective. In this work, we interrogated the temperature dependence of the infection and thermo-responsive behavior of the C22 phage. This soilborne podovirus is capable of lysing Ralstonia solanacearum, causing bacterial wilt disease. We revealed that the C22 phage could better infect the pathogenic host cell when incubated at low temperatures (25, 30 °C) than at high temperatures (35, 40 °C). Measurement of the C22 phage stiffness revealed that the phage stiffness at low temperatures was 2–3 times larger than at high temperatures. In addition, the imaging results showed that more C22 phage particles were attached to the cell surface at low temperatures than at high temperatures, associating the phage stiffness and the phage attachment. The result suggests that the structure and stiffness modulation in response to temperature change improve infection, providing mechanistic insight into the C22 phage lytic cycle. Our study signifies the need to understand phage responses to the fluctuating environment for effective phage-based biocontrol implementation.
Title: Thermoresponsive C22 phage stiffness modulates the phage infectivity
Description:
AbstractBacteriophages offer a sustainable alternative for controlling crop disease.
However, the lack of knowledge on phage infection mechanisms makes phage-based biological control varying and ineffective.
In this work, we interrogated the temperature dependence of the infection and thermo-responsive behavior of the C22 phage.
This soilborne podovirus is capable of lysing Ralstonia solanacearum, causing bacterial wilt disease.
We revealed that the C22 phage could better infect the pathogenic host cell when incubated at low temperatures (25, 30 °C) than at high temperatures (35, 40 °C).
Measurement of the C22 phage stiffness revealed that the phage stiffness at low temperatures was 2–3 times larger than at high temperatures.
In addition, the imaging results showed that more C22 phage particles were attached to the cell surface at low temperatures than at high temperatures, associating the phage stiffness and the phage attachment.
The result suggests that the structure and stiffness modulation in response to temperature change improve infection, providing mechanistic insight into the C22 phage lytic cycle.
Our study signifies the need to understand phage responses to the fluctuating environment for effective phage-based biocontrol implementation.

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