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Ibrahimi, M.

Publications and source records attributed to Ibrahimi, M..

2 recordsLinked to original sources

A non-invasive approach for understanding localized force generation in 3D tissues

The development, maintenance and repair of epithelial tissues critically rely on adhesion complexes that ensure structural integrity while enabling dynamic remodeling. Such tissue remodeling underpins both physiological morphogenesis and pathological transformation. Central to these processes are mechanical forces, which tightly couple cytoskeletal organization to adhesion dynamics. Despite extensive investigations in two-dimensional (2D) systems, how these interactions are orchestrated within polarized three-dimensional (3D) epithelia remains largely unresolved. Here, we introduce a new, non-invasive strategy to probe localized force generation within 3D epithelial tissues. We engineered elastic polyacrylamide (PAAm) microbeads with cell-mimetic size and mechanical properties, enabling their seamless integration. In contrast to conventional bead injection approaches, these PAAm microbeads were spontaneously engulfed by the tissue, thereby establishing an intrinsic interface through which bead deformation can be directly correlated with local cytoskeletal architecture and adhesion organization, as visualized through high-resolution imaging combined with quantitative 3D computational reconstruction. Using this approach, we demonstrated that localized mechanical perturbations trigger pronounced cytoskeletal remodelling while preserving global tissue polarity. We further identified the extracellular matrix composition as key determinant of bead-tissue interactions, with collagen-I coating promoting robust adhesion and efficient incorporation. At the bead-cell interface, cells assembled tension-bearing focal adhesions and organized actin stress fibers, revealing the emergence of active cortical stress. Strikingly, quantitative analysis of bead deformation revealed a previously unrecognized mechanical duality: spatially segregated regions of pulling and pushing forces coexisted at the microscale, directly correlated with local cytoskeleton dynamics. This finding challenges the prevailing view of homogenous force application and instead supports a model in which cells deploy highly coordinated and spatially patterned force-generating strategies. Altogether, this integrative and non-invasive strategy offers a comprehensive pipeline for dissecting the dynamic interplay between cellular processes and tissue mechanics during morphogenesis in 3D model systems.

cell biology↗

TRACR: an anterograde transneuronal tracing system for genetic access across synapses and longitudinal circuit analysis

Following neural signals as they converge onto and diverge from individual neurons is central to understanding circuit function and disease-related dysfunction. Existing anterograde transneuronal tracers are limited by cytotoxicity and incomplete genetic control over connected partners. To address these limitations, we adapted synthetic Notch designs to create TRanssynaptic Anterograde Circuit Readout (TRACR). Binding of the engineered ligand-receptor across synapses induces TRE-driven reporter transcription, enabling characterization of postsynaptic neurons. TRACR provides segregated genetic access to pre- and postsynaptic populations, and can be combined with markers, sensors, or effectors to expand circuit analysis. By applying TRACR at multiple synapses in the mouse visual system, we show that TRACR labels postsynaptic partners of sensory neurons, long-range projections and local inhibitory interneurons. TRACR signaling is reversible and fails to activate when synapses are absent or disrupted. Together, TRACR is an accessible, AAV-deliverable transneuronal reporting tool for longitudinal analysis of circuit assembly, degeneration, and repair. HIGHLIGHTSO_LITRACR adapts the synNotch system to signal across synapses for tracing postsynaptic targets. C_LIO_LITRACR identifies local and long-range postsynaptic targets in the mouse visual system. C_LIO_LITRACR activation requires intact synaptic connectivity rather than proximity. C_LIO_LITRACR signals are reversible, diminishing upon synapse loss and activating following assembly. C_LI

neuroscience↗