Biology subjects

Baraban, M.

Publications and source records attributed to Baraban, M..

4 recordsLinked to original sources

bioRxiv2025

Dynamic interactions between epithelial skin cells and a sensory cavity sculpt the growing olfactory orifice

During morphogenesis and in pathological conditions, gaps can form in the plane of epithelial barriers upon cellular forces that disrupt intercellular junctions. How the size of these epithelial holes further increases over time and what sets their shape remain poorly understood. Here we analyze the formation of the olfactory orifice (the nostril) in zebrafish, which opens and grows in the skin epithelium above a rosette of olfactory placode cells, allowing the sensory neurons to directly access odor cues. Using quantitative imaging and tissue-specific perturbations, we analyzed the dynamic remodeling of skin cells allowing the expansion of the orifice edge. We identified the sensory cavity located in the center of the placodal rosette as a crucial player that sets the size of the growing epithelial hole in the skin. We further showed that fine-tuning of actomyosin contractility within each tissue (skin and sensory cavity) exerts non-autonomous effects on the neighboring tissue, thereby shaping the nostril structure. This study uncovers dynamic cell behaviors and reciprocal tissue-tissue interplay that control the growth and shape of an epithelial hole in vivo.

developmental biology↗

bioRxiv2022

Actomyosin contractility in olfactory placode neurons opens the skin epithelium to form the nostril

Despite their barrier function, epithelial layers can locally lose their integrity to create physiological openings during morphogenesis. The cellular and molecular mechanisms driving the formation of these epithelial breaks are only starting to be investigated. Here, we studied the formation of the zebrafish nostril (the olfactory orifice), which opens in the skin epithelium to expose the olfactory neurons to external odorant cues. Combining live imaging, drug treatments, laser ablation and tissue-specific functional perturbations, we demonstrate that the formation of the orifice is driven by a mechanical interplay between the olfactory placode neurons and the skin: the neurons pull on the overlying skin cells in an actomyosin-dependent manner, thus triggering the opening of the orifice. This work unravels an original mechanism to break an epithelial sheet, in which an adjacent group of cells instructs and mechanically assists the epithelium to induce its local rupture.

developmental biology↗

bioRxiv2021

Traction forces exerted by the developing optic cup mediate cell movements and axon extension in the olfactory placode

While the chemical signals guiding neuronal migration and axon elongation have been extensively studied, the influence of mechanical cues on these processes remains poorly studied in vivo. Here, we investigate how mechanical forces exerted by surrounding tissues steer neuronal movements and axon extension during the morphogenesis of the olfactory placode in zebrafish. We mainly focus on the mechanical contribution of the adjacent eye tissue, which develops underneath the placode through extensive evagination and invagination movements. Using quantitative analysis of cell movements and biomechanical manipulations, we show that the developing eye exerts lateral traction forces on the olfactory placode through extracellular matrix, mediating proper morphogenetic movements and axon extension within the placode. Our data shed new light on the key participation of intertissue mechanical interactions in the sculpting of neuronal circuits.

developmental biology↗

bioRxiv2019

Disruption to NKCC1 impairs the response of myelinating Schwann cells to neuronal activity and leads to severe peripheral nerve pathology

Myelinating Schwann cells of the peripheral nervous system (PNS) express numerous ion channels and transporters, and have the capacity to respond to neuronal activity. However, it remains unknown how the response of Schwann cells to neuronal activity affects peripheral nerve formation, health or function in vivo. Through a genetic screen in zebrafish, we identified a mutant, ue58, with severe disruption to the morphology of myelin along peripheral nerves and associated nerve oedema. Molecular analyses indicated that this phenotype was caused by the loss of function of a previously uncharacterized gene, slc12a2b, which encodes a zebrafish paralog of the solute carrier NKCC1. NKCC1 is a co-transporter of Na+, K+, and Cl- ions and water, typically from the extracellular space into cells. Upon impairing slc12a2b function, constitutively, or specifically in neurons or myelinating Schwann cells, we observed disruption to myelin and nerve oedema. Strikingly, we found that treatment of slc12a2b mutants with TTX completely prevented the emergence of these pathologies. Furthermore, TTX treatment rescued pathology in animals with cell-type specific loss of slc12a2b from myelinating Schwann cells. Together our data indicate that NKCC1 regulates ion homeostasis following neuronal activity and that this is required to maintain myelinated axon and peripheral nerve integrity.

neuroscience↗