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Thorens, L.

Publications and source records attributed to Thorens, L..

2 recordsLinked to original sources

Dendritic Morphology Constrains Microtubule Dynamics and Organization

Neuronal dendrites form highly branched morphologies supported by spatially patterned microtubule arrays that are essential for intracellular transport and structural stability, yet how this organization is established and maintained remains unclear. Here we analyze microtubule behavior in Drosophila sensory neurons using live-cell imaging, deep learning-based analysis, and genetic perturbations. We find that microtubules are shorter and fewer in thin distal branches and progressively longer and more abundant in thicker proximal branches. Locally, polymerization slows in narrow branches due to soluble tubulin depletion, while catastrophe frequency increases near branch points upon cortical encounter. A physical model incorporating these morphology-dependent constraints reproduces both local microtubule dynamics and global organization. Inverting the textbook view that microtubule dynamics shape cell morphology, our results demonstrate that, on short timescales, cell morphology instead constrains microtubule dynamics, thereby determining large-scale cytoskeletal organization.

biophysics↗

Type I interferon primes the alveolar epithelium to receive reparative signals from tissue-resident macrophages

Lung repair in response to viral infection requires integrated communication between epithelial and immune compartments, yet the impact of antiviral mediators on epithelial regenerative capacity remains poorly defined. Here, we demonstrate that type I interferon (IFN-I) signaling primes the lung for alveolar renewal following viral challenge. IFN-I contributes to the induction of an interferon-stimulated gene-high (ISG)hi Sca-1Pos population of alveolar type II (ATII) epithelial cells. Sca-1Pos ATIIs exhibit enhanced proliferative capacity and increased organoid-forming efficiency compared with their Sca-1Neg counterparts. Viral challenge concurrently drives phenotypic reprogramming of tissueresident alveolar macrophages (trAMs). Sca-1Pos ATIIs display heightened responsiveness to oncostatin M (OSM) and, following viral challenge, require trAM-derived OSM for their proliferation. Together, these findings reveal that viral stimuli induce coordinated IFN-I-dependent epithelial and macrophage states that poise the lung for regeneration, positioning IFN-I not only as a central antiviral defense mechanism but as a priming signal that prepares lung tissue for renewal.

immunology↗