Understanding Apical Constriction Mechanisms in Epithelial Tissue Morphogenesis

Kernekoncepter

The author challenges the conventional belief that apical myosin drives cellular deformation, proposing an alternative model based on cell membrane elasticity and endocytosis to explain apical constriction.

Resumé

The content explores the mechanism of apical constriction in epithelial tissue morphogenesis. Contrary to previous beliefs, the author suggests that cell shape is determined by cell membrane elasticity and endocytosis rather than apically localized myosin. The study uses a cellular Potts model simulation to demonstrate how increased pressure inside cells can lead to tissue invagination. The findings challenge existing models of apical constriction driven by myosin contractility and highlight the importance of considering alternative mechanisms involving cell physical properties.
Key points include:

Apical constriction transforms columnar cells into wedge shapes.
Previous models attributed this process to apically localized myosin generating contractile force.
Cellular Potts model simulations suggest that increased pressure inside cells can deform tissues.
An alternative model proposes that cell shape is determined by cell membrane elasticity and endocytosis.
Supracellular myosin cables play a role in promoting invagination during tissue bending.

Statistik

"The actomyosin network is formed beneath the cell apical surface (cortical actomyosin) and lining apical-lateral cell-cell interface (circumferential actomyosin), linked with adherens junction and tight junction so that it makes a supracellular continuous structure."
"In Drosophila melanogaster mesoderm invagination, ventral cells express transcription factors Twist and Snail which then induce expression of numerous genes including regulators of the actin and myosin, such as T48, Fog, Mist, RhoGEF2, Rho, and Rock."

Citater

"The cellular Potts model simulation succeeded in reproducing the apical constriction."
"Studies suggest that too high apical surface tension may prevent tissue invagination."

Vigtigste indsigter udtrukket fra

Apical constriction requires patterned apical surface remodeling to synchronize cellular deformation

by Yamashita,S.... kl. www.biorxiv.org 12-20-2023

https://www.biorxiv.org/content/10.1101/2023.12.19.572310v1

Dybere Forespørgsler

How do variations in cell membrane elasticity impact tissue morphogenesis

Variations in cell membrane elasticity can have a significant impact on tissue morphogenesis. In the context of epithelial tissue, where apical constriction is a key mechanism for bending or invaginating the tissue, changes in cell membrane elasticity can alter how cells deform and interact with their surroundings.
In the study mentioned above, it was demonstrated that modifying the surface elasticity of cells through endocytosis regulation played a crucial role in driving the apical constriction process. By decreasing the reference value of apical surface elasticity during pulsed myosin activation, cells were able to synchronize their contraction and maintain balanced pressure among them. This led to successful tissue invagination.
The variations in cell membrane elasticity can influence how cells respond to mechanical forces during morphogenesis. Stiffer membranes may resist deformation more effectively, while more elastic membranes could facilitate shape changes required for tissue bending or folding. Therefore, understanding and manipulating cell membrane elasticity are essential for controlling tissue morphogenesis processes.

What implications do these findings have for understanding developmental processes beyond epithelial tissue

These findings have broader implications beyond epithelial tissues and provide insights into developmental processes across different biological systems. By highlighting the importance of physical properties such as cell membrane elasticity in regulating cellular behavior during morphogenesis, researchers can apply similar principles to other developmental contexts.
For example, in organ development or embryonic patterning, where complex three-dimensional structures are formed from initially simple configurations of cells, variations in cell physical properties could play a critical role. Understanding how changes in stiffness or flexibility affect cellular behaviors like migration, adhesion, and shape change can help unravel the mechanisms underlying organ formation and differentiation.
Moreover, these findings open up new avenues for studying disease processes where aberrant tissue morphogenesis occurs. Conditions such as cancer metastasis or birth defects often involve disruptions in normal developmental pathways that lead to abnormal tissue growth or organization. Investigating how alterations in cell physical properties contribute to these pathological conditions could offer novel therapeutic targets for intervention.

How might exploring different physical properties of cells lead to novel insights into morphogenetic mechanisms

Exploring different physical properties of cells offers a promising avenue for uncovering novel insights into morphogenetic mechanisms across various biological systems. By considering factors like surface tension, contractility dynamics (such as pulsed vs constant), and interactions between neighboring cells within tissues - researchers can gain a deeper understanding of how mechanical forces drive shape changes during development.
By integrating computational models like cellular Potts simulations with experimental data on subcellular components and signaling pathways involved in morphogenesis processes - scientists can create comprehensive frameworks that capture both biophysical aspects and molecular regulations governing tissue formation.
Furthermore, investigating how specific physical properties influence collective behaviors at the multicellular level opens up possibilities for designing targeted interventions aimed at modulating these properties pharmacologically or genetically to guide desired outcomes during regenerative medicine approaches or correct abnormalities seen in disease states related to faulty development.