April 2026

Our journey to publish our P-body paper

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Everything started maybe 9 years ago, during my postdoc in Sweden. My colleague and friend Anders Hafrén, now also a group leader working on P-bodies and stress granules during viral infection, had a couple of leftover DCP1 plants – a P-body marker, from his last experiment.

When he told me “just put your Pseudomonas on it” and “see what happens”, I was honestly a bit like—why would I do this? I was not interested in condensates storing mRNA. I was all about autophagy and proteasomal degradation and their roles in plant immunity.

But Anders insisted. He said this will become huge, and that there is an interplay between degradation machineries, P-bodies, and RNA biology in general. He already saw it back then.

Figure 1: First ever P-body quantification

Convinced, but also curious, I used some extra confocal time. This time not imaging my autophagosome “dotties” (which were always a nightmare in leaf tissues…), but bright P-body condensates. And wow – indeed, Pseudomonas actively modified them. Their number increased after 24 hpi (Figure 1).

So the question became: could bacterial pathogens hijack this pathway – and why?

At that time, still focused on degradation, I thought maybe P-bodies are recycled via the proteasome or autophagy, explaining their altered numbers. I went back to my proteomics data and realized that one component associates with ATG8. Could it be that Pseudomonas, by activating autophagy, recycles P-bodies? But I wasn’t fully convinced. The strong increase in P-body foci didn’t quite fit with what we knew about Pseudomonas-triggered autophagy. So I stepped away from the idea, keeping it only as a small side project. But that’s where it initially stalled. Apart from a few preliminary experiments, showing that P-body induction depends on bacterial effector delivery and hinting at interactions between autophagy components and DCPs, we didn’t pursue the project further, as we shifted our focus to other promising directions.

And then things changed.

When Manuel González-Fuente decided to join the lab with his own fellowship after finishing his PhD, I proposed several projects, but this one immediately caught his interest. It was novel, ambitious, and risky. After many discussions, grant writing, and nearly a year of waiting, Manuel secured his DFG fellowship and started working on P-bodies during bacterial infection. From there on, we fully committed to this fascinating but also enigmatic compartment. The beginning was not easy, many experiments didn’t work, we had setbacks, and progress was slow. Even our move to Bochum cost us almost a year of experiments.

But we didn’t give up.

Instead, we kept going analyzing -omics data, refining ideas, and this is when the link between ER stress and P-bodies started to emerge. Manuel presented his exciting project at several conferences, received prizes, awards and encouraging feedback. Eventually, all in all it felt like the first “season” of the story came together, and Manuel started writing the paper, which we preprinted more than a year ago.

Then the real gamble began.

We were excited to be reviewed in a top journal, but quickly realized how tough the process would be. We didn’t give up and eventually submitted the manuscript to Science Advances.

Figure 3: Pseudomonas does not induce stress granules.

After multiple rounds of revision (and moments where it really looked like we wouldn’t make it), the paper was finally accepted. If you wanna read it you can find it here: https://www.science.org/doi/10.1126/sciadv.aec4477#  Huge credit here to Manuel: he always believed in the story, even at times when I had doubts and felt very low (also due to another manuscript that we have been trying to publish since two years – wait for this Thursday!)

Looking back, some, but not all, reviewer feedback actually helped us improve the manuscript and led to additional insights—for example, that Pseudomonas specifically induces P-bodies without triggering stress granules (Figure 2).

So what about season 2? 🔬

There are still many open questions we are now actively working on:

Which mRNAs are selectively repressed in P-bodies? A question Manuel and I have been asked so often when presenting our work at conferences. We will soon conduct polysome profiling and Ribo-seq experiments across different genotypes during bacterial infection.

How exactly does ER stress control P-body assembly? We finally have the genetic material to address this—and a small teaser: P-body assembly depends on transcription factors that regulate ER stress – Manuel and his talented Bachelor student Nea Khalo are currently investigating this.

What defines selective autophagic turnover of P-bodies? This is a hidden gem in our manuscript. We believe we have identified the selective autophagy receptor, and likely also the E3 ligase mediating the degradation of P-body components—but this is still ongoing work that PhD candidate Wentao Luo is trying to solve.

How does HopN1 suppress translation if it is not dependent on P-bodies? For this, we already performed proteomics experiments ~4 years ago in Tübingen and identified several proteins involved in translation regulation and ribosome stalling. Manuel will now continue to follow up on this now that his paper is finally published 😊

Figure 3: Pseudomonas inhibits TOR activity.

How does Pseudomonas inhibit TOR activity? We do not know whether this is dependent on effector proteins or simply the pathogen turing source tissue into a sink (Figure 3). We have some hints that effectors can indeed interact with TOR and manipulate its “properties”. More to come in the future.

 

What is the role of P-bodies in abiotic stress, and how are they regulated by posttranslational modifications? We have become particularly interested in whether distinct or shared modification signatures control P-body dynamics under different stress conditions, something Thorben Krüger is now beginning to explore.

Final thoughts

This journey would not have been possible without the people behind it.

A very special thank you to Manuel González-Fuente, for his persistence, curiosity, and resilience. He drove this project through 5 years of challenges, setbacks, and revisions, and never lost belief in the story, even when things were not working at all. This paper is a testament to his dedication.

And of course, huge thanks to all co-authors, collaborators, and lab members who contributed along the way, this was truly a collective effort 🙌🌱

Şuayb

Original publication:

Manuel González-Fuente et al.: Bacteria Use P-body Condensates to Attenuate Host Translation During Infection, in: Science Advances, 2026, DOI: 10.1126/sciadv.aec4477

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Autophagy acts as a spatial organizer of cell-type-specific plant immunity

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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.

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