Agenda

Aurélien Roux (Université de Genève) will give a short external seminar, hosted by Thomas Lecuit (IBDM).

This seminar will take place in the Hexagone Auditorium.
CENTURI is also providing for off-campus participants only a zoom link to attend the seminar: https://us02web.zoom.us/j/85941690095?pwd=Nm5NVGhESGlUbG1FMnZ2dU5vSlkxUT09

Meeting ID: 859 4169 0095
Secret Code: 002024

Title: Topological defects in the orientational order of cells are stress organizers of tissue morphogenesis.

Abstract:
Most tissues are made of elongated cells, that organize into an orientational order, as cells locally align to their neighbors. This order of cells dictates the orientation of actin contractile fibers within cells, setting the collective active contractility of the cells. Thus, orientational order of cells and actin creates specific stress fields. This is most evidenced around topological defects within the nematic field of cells, which are punctual structures where the orientational order is lost. Around the defects, as the cells have a specific pattern of orientation that depends on the topological charge of the defect, specific stress patterns appear. These stress fields can create sufficient force gradients to deform tissues, participating in morphogenesis. I will review published and unpublished work from the lab that will show how topological defects control the formation of multi-cellular tornado-like structures and the regeneration of heads in the cnidarian Hydra I will expand on recent results to show how topology and geometry of the initial tissue organization sets the position and the charge of defects, therefore directing the sequence of morphogenetic events.

Emilie Franceschini (LMA) will give a short internal seminar.

This seminar will take place at the Hexagone Auditorium.
CENTURI is also providing for off-campus participants only a zoom link to attend the seminar: https://us02web.zoom.us/j/85941690095?pwd=Nm5NVGhESGlUbG1FMnZ2dU5vSlkxUT09

Meeting ID: 859 4169 0095
Secret Code: 002024

Title: Ultrasound as a Tool for Inferring Blood Cell Mechanics and Neurostimulation

Abstract:
This talk explores how ultrasound can be harnessed to probe blood microstructure and stimulate sensory neurons.

In the first part, we use quantitative ultrasound to investigate the anisotropic microstructure of blood under flow, which depends on red blood cell deformability. The spatial organization of cells then reveals clear distinctions between healthy and artificially rigidified red blood cells. This approach offers new possibilities for studying blood pathologies (e.g., sickle cell disease, spherocytosis) and could deepen our understanding of hemorheological dysfunction.

The second part dives into ultrasound neurostimulation. We demonstrate in vitro that focused ultrasound can activate dorsal root ganglion (DRG) neurons, with a preferential activation in the DRG neurons expressing the G_αi-interacting protein (GINIP). High-speed imaging shows that this activation is driven by ultrasound-induced membrane deformation, revealing key molecular and physical mechanisms underlying ultrasound neurostimulation.

Jay Groves (UC Berkeley) will give a short external seminar, hosted by Kheya Sengupta (CINaM) and Pierre-Henri Puech (CINaM).

This seminar will take place in the Hexagone Auditorium.
CENTURI is also providing for off-campus participants only a zoom link to attend the seminar: https://us02web.zoom.us/j/85941690095?pwd=Nm5NVGhESGlUbG1FMnZ2dU5vSlkxUT09

Meeting ID: 859 4169 0095
Secret Code: 002024

Title: Phase transitions, mechanics, and stochastic timing in signal transmission form single T cell receptors

 

Abstract: The T cell receptor (TCR) signaling system is on the front line of the adaptive immune system’s ability to recognize foreign antigens.  At the same time, TCR signaling mechanisms are a gold mine of interesting physics in molecular signaling processes.  It has long been known that TCRs discriminate foreign from self antigen based on  a kinetic proofreading process.  More recent work has revealed that T cells are single molecule sensors and that the entire signaling process operates deep in the stochastic limit of molecular discreteness.  My lab has been broadly focused on using imaging experiments to directly resolve the TCR signaling process–down to the single receptor level–and build a quantitative understanding of its mechanisms from this.  These efforts have revealed an important role for a type of protein condensation phase transition to provide noise suppression and signal amplification.  Perhaps most surprisingly, we have recently determined that these LAT condensates (as we and some others call them) consist of complete, yet entirely isolated, signaling systems.  Individual LAT condensates form in response to single antigen-TCR binding events, and each condensate faithfully translates a successful TCR activation event into a single, cell-wide calcium spike.  I will discuss these observations and our interpretation of how they provide a signaling mechanism with unique capabilities to suppress noise while achieving single molecule sensitivity.  I will also discuss even newer results from our efforts to track the process of condensate nucleation by activated TCR–essentially watching the cellular decision to activate in real time.