Soldati Lab

@soldatilab.bsky.social

Studying phagocytosis and cell-autonomous defences against mycobacteria

Last week, the remaining members of the Soldati lab got together for one last fun day, with indoor mini-golf, laughter and friendly competition! ⛳ The lab is now closing its doors, but the story is not quite over yet: stay tuned, a few stories are still cooking behind the scenes. 👀

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🥳 Very happy to see this collaborative work now published in @emboreports.org ! From T cells to Dictyostelium, it reveals a conserved pathway controlling amoeboid migration speed. Many thanks to @pdehio.bsky.social , Christoph and colleagues for involving our lab! doi.org/10.1038/s443...

A conserved VPS34-PIKfyve-TRPML1-myosin II axis regulates the speed of amoeboid cell migration - EMBO Reports

Amoeboid cell migration is key to efficient T cell immunity. Spatial polarization of organelles within cells, including endo-lysosomes, is a prerequisite of migration. However, how ultrastructural polarization is linked to the signaling requirements governing T cell migration remains unknown. Here we show that signaling molecules generated by endo-lysosome-localized kinases regulate velocity of amoeboid migration. Specifically, imaging of T cells identifies accumulation of endo-lysosomes decorated with the lipid kinases VPS34–PIKfyve at the uropod of polarized cells. Activity of VPS34 and PIKfyve regulates speed, but not directedness, of migrating T cells. Mechanistically, PI(3,5)P2 generated by the sequential action of VPS34 and PIKfyve, mediates Ca2+ efflux from lysosomes via the mucolipin TRP cation channel 1 (TRPML1), thus controlling activity of myosin IIA and hence the generation of propulsive force through retrograde actin flow. The VPS34–PIKfyve kinases also regulate velocity of myeloid cells, as well as of the amoeba Dictyostelium discoideum – establishing the axis as an evolutionarily conserved speed control system of amoeboid cell migration.

doi.org

How does the mycobacterial vacuole go from damage that can still be repaired to full rupture? 👀 Our new preprint shows that EsxA and PDIM act sequentially: EsxA initiates repairable lesions, and PDIM helps push them past host repair capacity toward cytosolic escape. doi.org/10.64898/202...

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📣 After 5 years, the last paper from my PhD is finally out in #ScienceTranslationalMedicine! We show that sustained tissue inflammation drives disease progression in #Buruliulcer. And targeting it alongside antibiotics can accelerate healing. www.science.org/doi/10.1126/...

The orphan receptor GPR84 drives inflammation in Buruli ulcer development

The GPR84 orphan receptor is a regulator of inflammation and a candidate therapeutic target in Buruli ulcer.

science.org

🚨 Want to know how we demonstrated the importance of sterol-rich membrane microdomains for M. marinum infection? Check out our latest paper published in Science Advances 👇 www.science.org/doi/10.1126/... ✨ Big thanks to everyone, especially Cristina Boehm-Bosmani, @soldatilab.bsky.social ! ✨

Membrane microdomains are crucial for Mycobacterium marinum EsxA-dependent membrane damage, escape to the cytosol, and infection

Sterol-rich microdomain accumulation at the MCV is crucial for Mm-induced damage and infection in D. discoideum and BV-2 cells.

science.org

🏆 It's a double win for the Soldati Lab! Last Friday, our former PhD students @angieprrt.bsky.social and Jahn Nitschke each received an award for their doctoral work: the Laemmli Prize for Angélique and Best Thesis in Life Sciences for Jahn. So proud of both for these well-deserved honors! 🤩

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Excited to share Wendy Le Mouëllic’s PhD work, now published in @pnas.org! It reveals that M. tuberculosis depends on inorganic sulfate import to survive inside host cells—fueling essential processes such as redox balance and stress resistance. Huge congrats to Wendy & colleagues! shorturl.at/WbFQC

Inorganic sulfate is critical for Mycobacterium tuberculosis lung tissue colonization and redox balance | PNAS

Tuberculosis remains the deadliest infectious disease caused by a single pathogen, highlighting the urgent need for novel therapies. A deeper under...

pnas.org

🦠 Mycobacteria aren't just tough, they're interior designers! 🦠 Check out our latest #preprint 🚨, led by our PhD student @camimille.bsky.social , where we show that #Mycobacterium tuberculosis builds secret cytoplasmic membranes to adapt its metabolism and sneak past immunity 🤫 Thread coming soon!

bioRxiv Microbiology@biorxiv-microbiol.bsky.social · 11mo ago

Nitrate-responsive Mycobacterial Intracytoplasmic Membranes dampen Inflammation during Mycobacterium tuberculosis Infection https://www.biorxiv.org/content/10.1101/2025.09.17.676823v1