If you want to hear about our latest work at @suaybuestuen.bsky.social's lab on pathogen manipulation of host translation and P-bodies at #2025ISMPMI, pass by my presentation today at 12:20 in the concurrent session "Effector interference mechanism" (Room M+N).

Honoured to receive the #YoungScientistAward from the @sebiology.bsky.social in the Cell section at the Antwerp conference. Thank you for this amazing recognition — I’m truly grateful!

It's happening now! @suaybuestuen.bsky.social is presenting now at @sebiology.bsky.social such an amazing work on how plants cope with proteotoxicity!! 🌱#proteostasis

So this is our final model: Pseudomonas induce P-body assembly via phase-separating effectors. This leads to attenuation of translation, which might be beneficial for the bacteria. Autophagy and ER stress responses are also required for this P-body-mediated attenuation of translation. 💭

🧵 (11/14)

Interestingly, Pseudomonas also requires #autophagy to induce P-bodies and to attenuate translation. This eveidences a tight interconnection between P-bodies, translation, autophagy and ER stress responses. 🍽️

🧵 (10/14)

This motivated us to have a look into different proxys of translation upon infection, and we observed that Pseudomonas seemts to attenuate the host translation, and that P-bodies are required for this. 🦠

🧵 (9/14)

To better understand the role of these effector-triggered P-bodies, we conducted several proteomic analyses and, among many interesting candidates, we found several proteins related to #translation. 💡

🧵 (8/14)

Moreover, we showed that P-body-inducing effector HopM1 is also responsible for the repression of ER stress responses, possibly by preventing the nuclear translocation of bZIP28. 🚫

🧵 (7/14)

Transcriptomic analyses upon infection showed us that #ERstress responses are deregulated in a P-body defective mutant, linking P-bodies with ER stress responses. 🥅

🧵 (6/14)

But is this P-body induction a defense response of the plant, or a virulence strategy of the bacteria? 🤔
We prove it is rather the second, as the P-body deffective mutant dcp5-1 is more tolerant to Pseudomonas without being majorly affected in canonical defense responses.

🧵 (5/14)

We identified that Pseudomonas effectors HopM1 and HopN1 were responsible for this induction of P-bodies. Moreover, we they co-localize and associate with P-body components, and they also undergo liquid-liquid phase separation. 🔬

🧵 (4/14)

We observed that bacterial pathogen Pseudomonas syringae induced the formation of these P-bodies through the translocation of its effector proteins. 🦠🌱

🧵 (3/14)

For long in the lab, we have worked on how pathogens mediate #proteostasis, focusing on protein degradation, but what about protein synthesis? For this, we had first a look into #P-bodies (biomolecular condensates containing translationally inactive transcripts).⁉️

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It is with great pleasure that I inaugurate my Bluesky account sharing our last @biorxiv-plants.bsky.social at @theustunlab.bsky.social, about pathogen-mediated modulation of host P-bodies and translation. 🆕 🎉

www.biorxiv.org/content/10.1...

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