Ruprecht Lab
@Ruprecht_Lab
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Tuning cell and tissue #dynamics by #mechanical and biochemical environment using #zebrafish 🐟 model at @CRGenomica. Tweets are from lab members.
Barcelona, Spagna
Joined November 2018
Fantastic way to start the year 🥳 Our collaboration work with @NMSBlab @ICFOnians is finally out in @NatureNano! Great job to all the authors 👏🏼🐟🔬
📝#NEWPaper: Innovative Optical Tweezers Technique Discovers Novel Disease Indicators in Aging Animals A new method, based on optical tweezers, allows to measure viscoelasticity of biological materials in a simpler and more versatile way. ICFO News 👉 https://t.co/xnoaodsCjp
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Apply for your funded early-career researcher place at our Workshop on “Mechanometabolism Unleashed: The Interface of Cell Mechanics and Metabolism” where you can listen to our recent research on mechanometabolism. Apply by 13 Dec at https://t.co/AoYlS4VWTB
#BiologistsWorkshops
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Apply for your funded early-career researcher place at our Workshop on 'Mechanometabolism Unleashed: The Interface of Cell Mechanics and Metabolism', organised by @MFoiani, @LennonLab, @VickySanzMoreno and @scita_lab Apply by 13 Dec https://t.co/Xe59YsX9Y1
#BiologistsWorkshops
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📣 PRBB-CRG Conference 📋 "Optimality for developmental robustness" 🗣️ Takashi Hiiragi @_Hubrecht 🤝Hosted by @AdelAlJord & Verena @Ruprecht_Lab 📅 September 6- 12:00 📍 Marie Curie room @the_prbb
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Congrats @valeria_ventur 🎊🎊
🏆 @valeria_ventur i @adriacanyellas han guanyat el #PremiSCB2024 al #JoveInvestigador/a per les seves tesis doctorals #NitBio2024 #PremisSCB2024
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A few #zebrafish peeps are attending this #ZebrafishMeeting including @diana__pinheiro, @J_Rodenfels, & @Ruprecht_Lab, for those finterested!
🏹 #PLM18 You have until May 31st to register to the 18th edition of the Physics of Living Matter #conference ! 📌Where: Palais du Pharo 📅When: September 16-17, 2024 More info: https://t.co/e9yl061lEr
@univamu
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Early-career researchers can now apply for a funded place at our Workshop "Immune Cell Interactions in Development, Homeostasis and Immunity" organised by @BoussoLab, @griffiths_lab, @SarrisLab & Michael Sixt @ISTAustria Find out more and apply at https://t.co/8trll8jMb9
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What doesn’t kill them makes them stronger: cancer cells under confinement. New #preLights post prepared by Teodora Piskova covers recent work from @RitobrataGhose, @fabio_pezzano, @SdelciL, @Ruprecht_Lab & team. #preprint Take a look! ⬇️ 👀
prelights.biologists.com
What doesn’t kill them makes them stronger: cancer cells under confinement.
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Our latest study on mechanical profiling of colorectal cancer organoids is out! We've uncovered a distinct phenotype in cancer stem cells (red 👇) caused by differences in membrane-to-cortex attachment. Led by @SeforaConti @IBECBarcelona #PhysicsOfCancer
https://t.co/GIjj5BCKex
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We thank all the contributors of this paper that have made this incredible collaboration a great success! We also acknowledge the support from @CRGenomica @the_prbb @CienciaGob @ERC_Research
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This nuclear ATP is critical to prevent delays in confinement-induced DNA damage, which in the long-term, impacts post-confinement cell proliferation. In essence, acute metabolic stress sensitises cells towards acquiring a mechanical stress-induced memory.
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This nuclear ATP surge regulates chromatin accessibility, which is required for timely DNA damage repair and proper S-phase progression. Without the nuclear ATP surge, the chromatin remains compacted, preventing nuclear adaptability to mechanical stress.
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Functionally, this NAM accumulation leads to an amazing nuclear ATP surge, which is abolished either by actin depolymerization, but also by inhibiting mitochondrial ATP production.
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NAM are trapped by an immobilized ER network in an actin-dependent manner, forming a mesh-like trap. Interfering with actin polymerization, but not intracellular calcium levels, prevented this accumulation of NAM, and prevented nuclear deformation.
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High resolution confocal microscopy confirmed the accumulation of mitochondria at the nuclear periphery of cancer cells (tested across 4 types), forming "nucleus-associated mitochondria" (NAM), and in turn physically deforming and indenting the nucleus.
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Acute physical confinement causes a major enrichment in mitochondrial terms within the nuclear fraction in a subcellularly-resolved proteomic analysis of mechanically confined cancer cells.
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We are super excited to share news about an amazing collaboration with the @SdelciLab: Mechanobio ♥️ Metabolism 👉“Mitochondria-derived nuclear ATP surge protects against confinement-induced proliferation defects” by @RitobrataGhose and @Fabio_Pezzano! https://t.co/tjy8y0sDcf
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Happy to see online our contribution to this amazing paper by our lab neighbours @SdelciL ! Great job @RitobrataGhose and @fabio_pezzano🐟
Very excited to share our pre-print “Adaptation to ARF6-depletion in KRAS-driven PDAC is abolished by targeting TLR2” by @RitobrataGhose, et al., which explores TLR2 and ARF6 co-knockdown as a new PDAC therapeutic strategy. https://t.co/ANUbAIPcKJ
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Apply to our lab for the #BISTMaster #MMRES program! 🐟🔬
📢 The #BISTMaster #MMRES is open for applications for the course 24-25‼️ 👉Full-time 1-year programme 👉Very hands-on #Master. Develop a research project in outstanding #research centres in #Barcelona in biology, chemistry, physics... All info ➡️ https://t.co/4VVTTsFZWg
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Are colorectal cancer stem cells mechanically distinct from the rest of the tumor? @SeforaConti addressed this question using patient-derived colorectal cancer organoids. The answer is yes and you can read it in our new preprint (LGR5+ CSCs labelled red) https://t.co/oS5dWfjt7u
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