In the ongoing battle between pathogens and their hosts, an intriguing dynamic unfolds at the cellular level, revealing how bacteria can subtly undermine host defenses. Recent research conducted by #theustunlab postdoc Manuel González-Fuente and colleagues at Ruhr-University Bochum sheds light on the sophisticated strategies employed by the bacterium Pseudomonas syringae to manipulate host translation during infection, providing a novel perspective on plant immunity. You can find our preprint ” Bacteria use processing bodies condensates to attenuate host translation during infection” on bioRxiv.
A Dual Attack on Translation
Our study demonstrates that Pseudomonas syringae (Pst), utilizes two bacterial effectors that exhibit liquid-like properties to induce the formation of plant processing bodies (P-bodies), ribonucleoprotein condensates integral to the regulation of RNA metabolism and translation. This manipulation serves to attenuate the host’s protein synthesis at a critical juncture when the plant needs to mount an adequate defense.
By targeting ribonucleoprotein condensates, Pst effectively disrupts the delicate balance of protein homeostasis within the plant. We uncovered that Pst’s repression of the endoplasmic reticulum (ER) stress response is a prerequisite for P-body assembly, a finding that highlights the intricate connection between stress responses and translation regulation.
P-Bodies and Autophagy: A New Intersection
A groundbreaking element of Manuel‘s work is the identification of a novel intersection between P-bodies and autophagy. Autophagic processes, typically known for their role in degrading cellular components, emerge as crucial players in managing P-body dynamics. We found that the clearance of P-bodies via autophagy is essential for maintaining a balance between active and inactive mRNAs. This presents a compelling narrative of how pathogens may exploit fundamental cellular pathways to subvert host responses.
Implications for Plant Immunity
The findings carry significant implications for understanding plant immunity and the ongoing arms race between pathogens and their hosts. By demonstrating that specific P-body-inducing effectors (such as HopM1 and HopN1) can suppress translation, our study emphasizes the potential for these bacterial effectors to be exploited as tools for further research into immune regulation. It raises pertinent questions about which mRNAs are affected in translation efficiency and how these components potentially contribute to the host’s susceptibility or resistance to infection. Our results show that P-bodies are involved in the posttranscriptional control of gene expression of certain immune components, indicating that Pst attenuates plant translation as a virulence strategy to dampen plant immunity.
Looking Ahead: Future Research Directions
As the field of plant pathology advances, Manuel‘s work sets the stage for future explorations into bacterial manipulation strategies. It opens new avenues for investigating how other pathogens may employ similar tactics to compromise host translation and immune responses. Additionally, understanding the mechanisms governing P-body assembly and their role in RNA metabolism could pave the way for novel strategies targeting bacterial infections in crops. In conclusion, our research not only unveils a sophisticated bacterial strategy to dampen plant immunity but also enriches our understanding of the complex interplay between translation, stress responses, and autophagy in cell biology.
References: González-Fuente et al., “Bacteria use processing body condensates to attenuate host translation during infection“, 2025