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Trenado-Yuste, C.

Publications and source records attributed to Trenado-Yuste, C..

2 recordsLinked to original sources

Interfacial morphodynamics of proliferating microbial communities

In microbial communities, various cell types often coexist by occupying distinct spatial domains. What determines the shape of the interface between such domains--which in turn influences the interactions between cells and overall community function? Here, we address this question by developing a continuum model of a 2D spatially-structured microbial community with two distinct cell types. We find that, depending on the balance of the different cell proliferation rates and substrate friction coefficients, the interface between domains is either stable and smooth, or unstable and develops finger-like protrusions. We establish quantitative principles describing when these different interfacial behaviors arise, and find good agreement both with the results of previous experimental reports as well as new experiments performed here. Our work thus helps to provide a biophysical basis for understanding the interfacial morphodynamics of proliferating microbial communities, as well as a broader range of proliferating active systems.

biophysics↗

Vangl facilitates mesenchymal thinning during lung sacculation independently of Celsr

The planar cell polarity (PCP) complex orients cytoskeletal and multicellular organization throughout vertebrate development. PCP is speculated to function in formation of the murine lung, where branching morphogenesis generates a complex tree of tubular epithelia whose distal tips expand dramatically during sacculation in preparation for gas exchange after birth. Here, using tissue-specific knockouts, we show that the PCP complex is dispensable in the airway epithelium for sacculation. Rather, we find a novel, Celsr1-independent role for the PCP component Vangl in the pulmonary mesenchyme: loss of Vangl1/2 inhibits mesenchymal thinning and expansion of the saccular epithelium. Further, loss of mesenchymal Wnt5a mimics the sacculation defects observed in Vangl2-mutant lungs, implicating mesenchymal Wnt5a/Vangl signaling as a key regulator of late lung morphogenesis. By mathematically modeling sacculation, we predict that the process of sacculation requires a fluid mesenchymal compartment. Finally, lineage-tracing and cell-shape analyses are consistent with the pulmonary mesenchyme acting as a fluid tissue, and suggest that loss of Vangl1/2 likely impacts the ability of mesenchymal cells to exchange neighbors. Our data thus uncover an explicit function for Vangl and the pulmonary mesenchyme during late lung morphogenesis to actively shape the saccular epithelium.

developmental biology↗