Citi Lab

@J_Cell_Sci @Co_Biologists Well done, congratulations!👏

JCS congratulates our Editor-in-Chief Michael Way on his election as a Fellow of the Royal Society, the UK’s national academy of sciences. royalsociety.org/news/2026/05/n…

Léa Marpeaux, Claire Baudouin, Gregory Emery @GregoryEmery8 and colleagues @IRIC_umontreal identify an apical supracellular actin network in epithelial cells that acts as a long-range force transmission device. Highlight: journals.biologists.com/jcs/article/13… Article: journals.biologists.com/jcs/article/13…

New JCS snapshot - Bile canaliculi formation in primary hepatocytes requires α1β1 integrin-dependent adherens junction re-organisation Anne Müsch presents the key findings from their recent JCS paper with David Cohen and Francisco Lázaro-Diéguez. journals.biologists.com/jcs/article/13…

Is Depression a “Mental” or a “Metabolic” Disorder? For decades, depression has been framed as a disorder of neurotransmitters. Low serotonin. Faulty signalling. Chemical imbalance. But for a clinically meaningful subset of patients, the primary driver may sit upstream of neurotransmission. The 'problem' isn’t the signal. It's the energy required to generate it. Here’s how brain insulin resistance (BIR) can drive a hypometabolic depressive state 👇🧵

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Check out the latest paper by Dr. Marine Mauperin in my lab, in collaboration with the Janshoff lab. New functions for NM2B! 💪Nonmuscle Myosin-2B Regulates Apical Cortical Mechanics, ZO-1 Dynamics and Cell Size in MDCK Epithelial Cells mdpi.com/2073-4409/14/1…

@AntoniKourtidis @toothscience @MrslncRNA @ScienceAlyssa Well done !👏

Very happy to share our latest work revealing that localization of the #RNAi machinery at #adherens junctions is a universal feature of epithelial cells and tissues. Great work and team effort by Joyce Nair-Menon @toothscience @MrslncRNA @ScienceAlyssa nature.com/articles/s4159…

Paracingulin controls the junctional accumulation of nonmuscle myosin-2 in endothelial cells in vivo doi.org/10.17912/micro… Great little paper validating our insights (JCB 2023) about the role of cingulin family proteins in cytoskeleton organization at junctions!

Congratulations @SandraCiti_Lab for your latest publication! @sciences_UNIGE @MoCel_Geneva

L’hypertension artérielle est l’un des principaux facteurs de risque de maladies cardiovasculaires🫀. Des scientifiques de l’UNIGE se sont penché-es sur le rôle d’une protéine, la paracinguline, dans cette maladie. Leur récente étude🔬met en lumière sa contribution déterminante à l’apparition de l’hypertension et propose une analyse détaillée du mécanisme en jeu. @sciences_UNIGE @sandraciti Plus d’infos 👉unige.ch/medias/2025/un…

In our interview with Jennifer Lippincott-Schwartz @JLS_Lab, we discuss her research career, her advice on building collaborations and learn why she is looking forward to #biologists100. Jennifer will be speaking in our emerging technologies session. journals.biologists.com/jcs/article/13…

Hello everyone, please check out our preprint paper 🥰 I appreciate Dr. Nakamura, Dr. Otani (@tetsuotani1), Dr. Togashi, and all helping members.

The fine control of cell mechanics - Medias - UNIGE unige.ch/medias/en/2025…

Congratulations @SandraCiti_Lab for your latest publication in @NatureComms A feedback circuitry involving γ-actin, β-actin and nonmuscle myosin-2 A controls #tight #junction and apical cortex mechanics unige.ch/medias/en/2025… @MoCel_Geneva @sciences_UNIGE

The greatest team of all celebrates Marine Mauperin's publication on Nature Communications!🥇🥂🎈🎉🎊👍👍👏👏💪💪

6. Fluorescence recovery after photobleaching showed that both CGN and ZO-1 are more dynamic in gamma actin KO cells: so, actin isoforms regulate the dynamic of junctional proteins!

5. Thanks to our great collaborators in the lab of Jie Yan (Singapore) and Andreas Janshoff (Göttingen)we could also show decreased apical cortical stiffness, similar to CGN-KO cells. So, gamma-actin is required to keep the apical cortex stiff!

4. Gamma-actin KO cells showed increased TJ membrane tortuosity, and depletion of NM2A rescued this mechanical phenotype of the TJ membrane cortex. So, it's increased NM2A that makes TJ more tortuous!

3. But, in addition, Marine noted that nonmuscle myosin2A was also increased and (!!!) by depleting NM2A the increase in beta was reversed!!! A mechanosensing feedback circuitry!!!

2. It all started with the question: is the uncoupling of gamma actin from TJ involved in any of the phenotypes of CGN-KO cells? Marine made gamma actin-KO MDCK cells and saw the (expected) up regulation of beta (actin)