Abstract
Embryogenesis is an extraordinarily robust process, exhibiting the ability to control tissue size and repair patterning defects in the face of environmental and genetic perturbations. The size and shape of a developing tissue is a function of the number and size of its constituent cells as well as their geometric packing. How these cellular properties are coordinated at the tissue level to ensure developmental robustness remains a mystery; understanding this process requires studying multiple concurrent processes that make up morphogenesis, including the spatial patterning of cell fates and apoptosis, as well as cell intercalations. In this work, we develop a computational model that aims to understand aspects of the robust pattern repair mechanisms of the Drosophila embryonic epidermal tissues. Size control in this system has previously been shown to rely on the regulation of apoptosis rather than proliferation; however, to date little work has been done to understand the role of cellular mechanics in this process. We employ a vertex model of an embryonic segment to test hypotheses about the emergence of this size control. Comparing the model to previously published data across wild type and genetic perturbations, we show that passive mechanical forces suffice to explain the observed size control in the posterior (P) compartment of a segment. However, observed asymmetries in cell death frequencies across the segment are demonstrated to require patterning of cellular properties in the model. Finally, we show that distinct forms of mechanical regulation in the model may be distinguished by differences in cell shapes in the P compartment, as quantified through experimentally accessible summary statistics, as well as by the tissue recoil after laser ablation experiments.
Highlights
The mechanisms underlying tissue size control during embryonic development are extremely robust
Comparing the model to previously published data across wild type and genetic perturbations, we show that passive mechanical forces suffice to explain the observed size control in the posterior (P) compartment of a segment
Tissue Size Control through Passive Mechanical Forces had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
Summary
The mechanisms underlying tissue size control during embryonic development are extremely robust. In fruit fly embryos, overexpressing the maternal effect gene bicoid leads to stark overgrowth in the head region, but the excess tissue is removed during later stages of development through apoptosis (programmed cell death), leading to viable adults [2]. Upregulation of myosin II generates tension that helps to straighten compartment boundaries in the Drosophila wing imaginal disc [6], while controlled cell death provides the tension required for invagination during Drosophila leg development [7]. It has been illustrated theoretically how mechanical feedback might facilitate uniform growth in epithelia in the face of morphogen gradients [8]. Could mechanical forces play a significant role in robustly maintaining tissue size?
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