Oops, I did It Again: Bacteria Remixing Host Translation!
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
Oops, I did It Again: Bacteria Remixing Host Translation! Read More »
However, while we advocate for this, many people face more and more discrimination, bullying and toxic behavior. As a result, we have chosen to disengage from actively participating on this platform. Moving forward, we will limit our presence there to sharing publications, lab news and job advertisements only.
Despite moments of disillusionment and some disappointments, 2024 has been an incredibly productive year for us. One of our major accomplishments has been the establishment of a faculty-wide confocal microscopy platform, spearheaded by Üstün Lab postdoc Manuel González Fuente. The platform is already being utilized by more than 30 researchers from seven different groups across the faculty. We’re both proud and delighted to have successfully launched this initiative and look forward to growing it further in the future. We hope that other groups will follow suit, as diverse and impactful research can only thrive with access to a variety of cutting-edge platforms and facilities.
Another exciting project is Shanshuo’s postdoc paper, which uncovers how cell-type-specific autophagy responses shape plant-pathogen interactions. A sneak peek: stomata play a crucial role!
This year, our own 5-week course, “Plant Cell Biology Meets Plant-Pathogen Interactions”, organized by Manuel and Suayb, gained even more attention. We decided to expand the course, accepting 10 students instead of the usual 6. Over the five weeks, students engaged in lectures on plant-microbe interactions, fundamental plant cell biology, experiments on proteostasis and plant immunity, and a fantastic seminar that explored recent papers in the field.Although teaching was demanding and exhausting, we thoroughly enjoyed the experience, particularly the opportunity to engage with the enthusiastic and talented bachelor and master students at RUB. We observed that smaller course formats foster faster learning, as students benefit from closer interactions with their supervisors and the ability to ask questions at any time. It is part of our lab’s philosophy to have close interaction with students, taking away the distance that academic teaching can create sometimes.
Our team aims to delve deeper into how pathogens disrupt this mechanism. Through the generous support of approximately 565,000 euros from the 
Our first review that appeared in 
In our second invited review in 
Which brings us to our latest published preprint “ER-anchored protein sorting controls the fate of two proteasome activators for intracellular organelle communication during proteotoxic stress”, the SFB1101 funded PhD work of Gautier Langin. As proposed in our review about the proteasome and its role in plant immune reactions, we tried to decipher how proteotoxicity, caused by pathogens, diseases, organelle stress, and Co. is regulated. We show that the proteasome autoregulatory feedback loop acts as a gatekeeper to facilitate the communication between nucleus and chloroplast. In our study we revealed that the ER-anchored protein sorting system (ERAPS) controls the proteasomal degradation or nuclear translocation of proteasome activators NAC53 and NAC78. While both transcription factors activate the proteasome gene expression, they repress photosynthesis-associated nuclear genes during proteotoxicity. It appears that this trade-off is highly “conserved” as other stress conditions and developmental cues also lead to similar responses. We think that our findings also provide a new conceptual framework for understanding the integral role of transcription factors in managing cellular proteostasis under environmental stress, suggesting conservation of these mechanisms across kingdoms. But this is just a small summary and teaser 🙂 We promise it will be a good read over the Christmas holidays, lots of data, and possible future implications on other trade-offs between the proteasome and energy metabolism.
Full of hopes we started 2021, posting our first preprint on
Managing a lab with various lab members and different projects is already challenging. Recruiting new team members to start their new projects is always a difficult task. The pandemic doesn’t make it easier. Nevertheless, beginning 2021, we started our search, and with the help of the entire lab we found new members, Shanshuo Zhu and Shiji Hou, to kickstart the ERC project DIVERSIPHAGY. Shanshuo and Shiji have promising results in their projects so far, and we hope to continue this in 2022. We also started a completely new project on the role of “P-Bodies in bacterial infection” with Manuel Gonzalez Fuente, who joined our lab as a postdoc with his own DFG funding from the Walter Benjamin Programme. All in all, it is great to see the group growing, different projects progressing and developing, even though we had limited space in the lab (thanks to the pandemic). The new year will again bring some changes to our group: We are very happy to welcome another postdoc in the new year, Margot Raffeiner (former PhD student in the Börnke Lab), who will join our ERC team, working on the autophagy degradome. Sadly, Shiji had to leave our lab by the end of the year, and we are currently trying to find a new postdoc to study plant microbiome and its influence on degradation pathways (you can find the ad 
Regarding grants for our lab, the year was pretty much focused to get approval for our project (“Specificity of proteasome regulation during plant immunity”) in the 
Usually, in the pre-pandemic era, we would report about exciting meetings, international conferences, and networking events as well as huge social events. Especially not having any international conferences is affecting early career researchers a lot: It is crucial to present your science, to meet new people (future employees, collaborators, friends). Some of our lab members never went to international conferences. This is an essential part of building your own network and preparing yourself for your future. As much as online conferences are a great distraction, and a way to communicate your science (if you don’t present only published things), it misses the “social” part as most social interactions on Zoom or other platforms are impersonal. Our own lab meetings and journal clubs improved a lot when we started having in person meetings again. Our highlight of an in-person meeting was in November, when Yasin Dagdas, group leader at GMI Vienna, visited us, to participate in Gautier’s thesis advisory committee. We had great discussions about Gautier’s PhD project and future publication strategy that helped him a lot to focus his research. We hope for 2022 to have more in person meetings and small conferences.
My talented and super motivated PhD student Jia Xuan Leong joined our lab last year as a master student and was able to show that, in contrast to Pseudomonas, Xanthomonas blocks autophagy in an effector-dependent manner to enhance its pathogenicity. We then went on and screened a couple of effectors for their ability to block autophagy. We analysed XopJ, XopS and XopD, as they have known effects on proteolytic degradation pathways and of course included XopL, because of its ability to interact with SH3P2. Fortunately, it turned out that XopL is able to suppress autophagy which made us very confident that we have to further characterize its function. However, our major concern was that previous reports stated that XopL is not a major virulence fac
Fortunately, with the help of Mary Beth Mudgett and her amazing lab, we were able to show that XopL is one of the major virulence factors r
Meanwhile we got a bit confused, as we realized that XopL is also degraded by autophagy. XopL associates with selective autophagy receptor NBR1/Joka2 which mediates the degradation of XopL. So far NBR1/Joka2 was known to degrade aggregates (aggrephagy), viral proteins and intracellular pathogens (xenophagy) but not bacterial effector proteins. We further discovered that XopL undergoes self-ubiquitination in vitro and in planta, at Lysine 191. Although, mutation of this lysine stabilizes XopL, XopL is still ubiquitinated in plants. We assume (and have also indications) that other lysines within XopL are ubiquitinated.
