Autophagy acts as a spatial organizer of cell-type-specific plant immunity
To prevent frequent outbreak of diseases, plants have acquired a complex and multi-layered immune system. Cell surface immune receptors recognize conserved pathogen-associated molecular patterns (PAMPs) and initiate basal defences, known as PAMP-triggered immunity (PTI), while intracellular receptors activate effector-triggered immunity (ETI). Over the past years, this view has evolved toward a model of mutual potentiation, where PTI and ETI reinforce each other to generate robust defence. Yet one fundamental question has remained unresolved: how are these immune responses coordinated across the highly heterogeneous cellular landscape of a leaf?

Our study (you can find it now on the biorxiv server: https://www.biorxiv.org/content/10.64898/2026.04.06.716646v1) led by our amazing postdoc Shanshuo Zhu provides a compelling answer by positioning autophagy, not simply as a degradation pathway, but as a spatial organizer of immunity across cell types. Our findings try to decipher the long-standing controversial role of autophagy as a pro- or anti-immunity factor: autophagy partitions immune responses between cell-types, aligning defence outputs with cellular context.
Resolving a long-standing paradox
Autophagy has been implicated in contrasting roles during plant-microbe interactions, promoting susceptibility in some contexts while enhancing resistance in others or restricting cell death. This ambiguity has persisted for over a decade, largely because most studies treated the leaf as a homogeneous tissue. Advances in single-cell RNA sequencing have opened new avenues to resolve cell-type-specific responses, an essential step for understanding Pseudomonas infections that enter through stomata and establish within the mesophyll.
By combining single-cell transcriptomics with cell-type-specific complementation approaches, we reveal that this paradox dissolves when spatial context is considered. Autophagy exerts distinct, even opposing functions in different cell-types, likely explaining conflicting observations in the literature.
Guard cells: facilitating pathogen entry
At the leaf surface, guard cells form the first line of defence by closing stomata to prevent bacterial invasion. Intriguingly, our study shows that autophagy actively promotes early stomatal re-opening during infection, thereby facilitating pathogen entry.
Mechanistically, this process is linked to the vacuolar recycling of the ABA receptor PYL4. By targeting PYL4 for degradation, autophagy dampens ABA signalling, which would otherwise maintain stomatal closure. In autophagy-deficient plants, elevated ABA signalling prevents re-opening, restricting bacterial entry.
This finding reframes autophagy as a pathway that pathogens may exploit early during infection – not by directly suppressing immunity, but by modulating physiological gatekeeping at the tissue interface.
Mesophyll: restraining and enabling immunity
Once bacteria bypass the stomatal barrier, the battleground shifts to the mesophyll. Here, autophagy plays a fundamentally different role. We initially hypothesized a mesophyll-specific role, as autophagy-deficient mutants exhibited severe phenotypes, such as chlorosis and tissue collapse upon syringe infiltration, likely originating from mesophyll cells.
Our scRNAseq analysis revealed that loss of autophagy leads to a pre-activated immune state, characterized by elevated expression of key regulators such as the EDS1–PAD4–ADR1 node. At first glance, this might suggest enhanced resistance, possibly also explaining the severe phenotype after infection. However, our investigation reveals a striking uncoupling: despite elevated immune signalling, canonical PTI outputs, such as ROS production and transcriptional responses, are impaired.
This disconnect leads to a central conceptual advance:
immune activation alone is not sufficient for effective defence.
Instead, autophagy appears to maintain the functional integrity and spatial organization of immune signalling networks, ensuring that activation translates into execution. Without it, signalling becomes misregulated, amplified yet ineffective.
We are currently trying to deliver the final evidence that this is indeed driven by the cell-type specific role of autophagy.
A spatial model of immune coordination
Taken together, our work supports a model in which autophagy orchestrates immunity across different cell-types:
- Guard cells: autophagy promotes pathogen entry by enabling stomatal re-opening
- Mesophyll cells: autophagy constrains and organizes immune signalling to ensure effective defence response
This dual role transforms autophagy into a spatial coordinator, aligning immune strategies with tissue-specific demands.
Implications for PTI-ETI potentiation
The findings also offer a fresh perspective on PTI-ETI interplay. The impaired PTI outputs observed in autophagy mutants provide a plausible explanation for previously reported defects in ETI-associated responses, including EDS1-dependent hypersensitive cell death. Here, we are also looking into final experiments to validate a cell-type specific role for autophagy in this process.
Our current working model suggests that autophagy may be required but for maintaining the conditions under which PTI and ETI can effectively potentiate each other. EDS1 may play a central role in it, since it has been shown to be an autophagy target, being essential to constrain immune signalling (Clavel et al., 2024).
Beyond degradation: toward proteostasis-driven immunity
In summary, our study reinforces an emerging view of proteostasis pathways as central regulators of immunity explaining why pathogens love to hijack it – see also our recent review article “Every step you take: How pathogens hijack host proteostasis“.
Our findings raise several intriguing questions:
- How is autophagy itself spatially regulated during infection?
- Do pathogens actively manipulate autophagy in a cell-type-specific manner?
- Would this explain contrasting functions of effectors from the same pathogen inhibiting or activcating autophagy?
- Can spatial control of proteostasis be engineered to enhance crop resistance?
By integrating single-cell resolution with genetics and cell biology, we established a unifying framework:
Plant immunity is not only multilayered but also spatially partitioned-a concept recognized for decades—and autophagy emerges as a key organizer of this architecture.
Autophagy acts as a spatial organizer of cell-type-specific plant immunity Read More »

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
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.


