Coordination between patterning and morphogenesis ensures robustness during mouse development

Abstract

The mammalian preimplantation embryo is a highly tractable, self-organizing developmental system in which three cell types are consistently specified without the need for maternal factors or external signals. Studies in the mouse over the past decades have greatly improved our understanding of the cues that trigger symmetry breaking in the embryo, the transcription factors that control lineage specification and commitment, and the mechanical forces that drive morphogenesis and inform cell fate decisions. These studies have also uncovered how these multiple inputs are integrated to allocate the right number of cells to each lineage despite inherent biological noise, and as a response to perturbations. In this review, we summarize our current understanding of how these processes are coordinated to ensure a robust and precise developmental outcome during early mouse development. This article is part of a discussion meeting issue ‘Contemporary morphogenesis'.

Contemporary morphogenesis

“…Symmetry breaking is another key step in axis establishment and the development of inherently asymmetric organs. Mechanistic links between symmetry breaking and morphogenesis are explored in a number of contexts, including how actin flows drive polarity formation in the Caenorhabditis elegans zygote [20], asymmetric patterning in lineage segregation during early mouse development [21], and how mechanical asymmetries promote tissue folding [22]. Finally, we review how changes in cell states from epithelial to mesenchymal (and vice versa) are controlled and coordinated to facilitate tissue morphogenesis [23].…”

An Assumption of The Regulatory Function of Nf2-Amot Complex in Early Mammalian Embryos with A Computational Model

“…On the contrary, phosphorylated Amot and Nf2 form a Nf2-Amot complex on E-cadherin in the inner cell. The Nf2-Amot complex promotes phosphorylation of Lats [Yu et al, 2013; Cockburn et al, 2013; Yin et al, 2013; Li et al, 2015; Saiz et al, 2020]. The phosphorylation of Lats also causes phosphorylation of Yap, cytoplasmic localization, and degradation of Yap [Kim et al, 2011].…”

Coordination between endoderm progression and gastruloid elongation controls endodermal morphotype choice

“…Moreover, even in the face of external perturbations (mechanical compression, cell ablation or addition), embryos demonstrate morphogenetic robustness (2,3). The processes driving the morphogenetic dynamics leading to such patterns have been extensively studied in embryos, yet it is not clear what makes them so robust (1,(4)(5)(6)(7)(8)(9)(10).…”