Abstract

Smooth muscle is increasingly recognized as a key mechanical sculptor of epithelia during embryonic development. Smooth muscle is a mesenchymal tissue that surrounds the epithelia of organs including the gut, blood vessels, lungs, bladder, ureter, uterus, oviduct and epididymis. Smooth muscle is stiffer than its adjacent epithelium and often serves its morphogenetic function by physically constraining the growth of a proliferating epithelial layer. This constraint leads to mechanical instabilities and epithelial morphogenesis through buckling. Smooth muscle stiffness alone, without smooth muscle cell shortening, seems to be sufficient to drive epithelial morphogenesis. Fully understanding the development of organs that use smooth muscle stiffness as a driver of morphogenesis requires investigating how smooth muscle develops, a key aspect of which is distinguishing smooth muscle-like tissues from one another in vivo and in culture. This necessitates a comprehensive appreciation of the genetic, anatomical and functional markers that are used to distinguish the different subtypes of smooth muscle (for example, vascular versus visceral) from similar cell types (including myofibroblasts and myoepithelial cells). Here, we review how smooth muscle acts as a mechanical driver of morphogenesis and discuss ways of identifying smooth muscle, which is critical for understanding these morphogenetic events.This article is part of the Theo Murphy meeting issue 'Mechanics of Development'.

Highlights

  • Smooth muscle is recognized as a key contributor to the morphogenesis of branched and folded organs

  • There, they reside between the secretory epithelial layer and the basement membrane and express both epithelial and smooth muscle markers [108]

  • In each of the systems described above, it appears that the stiffness of the smooth muscle tissue rather than cell shortening is sufficient to drive the morphogenesis of an underlying proliferating epithelium or endothelium

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Summary

Introduction

Smooth muscle is recognized as a key contributor to the morphogenesis of branched and folded organs. Starting from a uniform, unbranched tube, a single buckling event can create branches throughout an epithelium by homogeneously tuning the proliferation rate of the entire epithelium relative to that of the adjacent smooth muscle [2] Creating this architecture through diffusion, would require multiple shortrange foci of high morphogen concentration to specify the location of each branch through local changes in proliferation or cell shape [3]. In smooth muscle-induced physical mechanisms of morphogenesis, there is a complex interplay of physical and biochemical mechanisms, and understanding this interplay is key to building a complete picture of the morphogenetic events. Further investigating these phenomena will require a combination of in vivo and cell and tissue culture assays to understand how the differentiation of smooth muscle is controlled. Because understanding the control of smooth muscle differentiation in each of these tissues is the step for developing a complete model of how they are constructed, we review markers and phenotypes used to distinguish amongst various smooth muscle-like cells

Definition and properties of smooth muscle
Respiratory system
Urinary and vascular systems
The next step: studying smooth muscle differentiation
Conclusion
47. Walton KD et al 2016 Villification in the mouse
48. Freddo AM et al 2016 Coordination of signaling and
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