The Molecular Network of YAP/Yorkie at the Cell Cortex and their Role in Ocular Morphogenesis

Abstract

During development, the precise control of tissue morphogenesis requires changes in the cell number, size, shape, position, and gene expression, which are driven by both chemical and mechanical cues from the surrounding microenvironment. Such physical and architectural features inform cells about their proliferative and migratory capacity, enabling the formation and maintenance of complex tissue architecture. In polarised epithelia, the apical cell cortex, a thin actomyosin network that lies directly underneath the apical plasma membrane, functions as a platform to facilitate signal transmission between the external environment and downstream signalling pathways. One such signalling pathway culminates in the regulation of YES-associated protein (YAP) and TAZ transcriptional co-activators and their sole Drosophila homolog, Yorkie, to drive proliferation and differentiation. Recent studies have demonstrated that YAP/Yorkie exhibit a distinct function at the apical cell cortex. Here, we review recent efforts to understand the mechanisms that regulate YAP/Yki at the apical cell cortex of epithelial cells and how normal and disturbed YAP–actomyosin networks are involved in eye development and disease.

Interplay between cell height variations and planar pulsations in epithelial monolayers

“…Therefore, the contractile stress of the cells combined with cell-cell junction height diminishes away from the pulsation centre. In this specific context, the link between junction height and the contractile molecules is an interesting question to be explored, since the accumulation of myosin could be due to intercellular flows [40] or due to transcriptional activity [41]. Finally, it would be interesting to analyse the height variations with varying cell density at plating, since cell density was reported to have direct effects on cell velocities [28] and cell extrusion [31].…”