From their abstract:
"Emerging evidence suggests that understanding of #timescales may be important in resolving this issue, but that further work is needed to understand the role of adhesive strengthening across scales."
Same the conclusion as in our theory paper https://doi.org/10.1371/journal.pcbi.1009812 : the interplay of #cadherin #adhesion & cortical #actomyosin timescales triggers emergent phenomena in terms of #tissue mechanics. If one adds #mechanotransduction on top of that then expect awesome effects.

Adhesion-regulated junction slippage controls cell intercalation dynamics in an Apposed-Cortex Adhesion Model
Author summary During development tissues undergo dramatic shape changes to build and reshape organs. In many instances, these tissue-level deformations are driven by the active reorganisation of the constituent cells. This intercalation process involves multiple cell neighbour exchanges, where an interface shared between two cells is removed and a new interface is grown. The key molecular players involved in neighbour exchanges, such as contractile motors proteins and adhesion complexes, are now well-known. However, how their physical properties facilitate the process remains poorly understood. For example, how do cells maintain sufficient adhesive contact while actively uncoupling from one another? Then, how does a new interface grow in a contractile environment? Many existing biophysical models cannot answer such questions, due to representing shared cell interfaces as discrete elements that cannot uncouple. In this paper, we develop a model that represents cell cortices as contractile rope-loops coupled by adhesions. We outline the conditions required for successful neighbour exchanges, in terms of the properties of the known molecules that drive the process. The model predicts that tissue dynamics depend strongly on the ability of neighbouring cortices to slip relative to one another, which is regulated by adhesion turnover.