An actin-based viscoplastic lock ensures progressive body-axis elongation

Area of Science:

• Developmental Biology
• Cellular Mechanics
• Molecular Biology

Background:

• Body-axis elongation is crucial for animal development, influenced by intrinsic, extrinsic, and resistance forces.
• Understanding the cellular and molecular mechanisms of mechanical forces in morphogenesis is challenging.
• Embryonic elongation in Caenorhabditis elegans involves muscle activity and epidermal mechanotransduction.

Purpose of the Study:

• To identify molecular mechanisms stabilizing cell shapes during C. elegans embryonic elongation.
• To investigate the role of p21-activating kinase homologue PAK-1 and its interacting partners in this process.

Main Methods:

• Genetic and molecular interaction searches for factors interacting with PAK-1.
• Analysis of combined PAK-1 and alpha-spectrin SPC-1 absence on embryonic axis elongation.
• Mechanical modeling to predict embryo shape stabilization processes.
• Molecular analysis of epidermal microfilament dynamics and associated proteins.

Main Results:

• Identified alpha-spectrin SPC-1 as a key factor interacting with PAK-1 in C. elegans embryos.
• Combined absence of PAK-1 and SPC-1 leads to complete axis retraction due to defective epidermal actin stress fibers.
• Mechanical modeling suggests a viscoplastic deformation process underlies embryo shape stabilization.
• Viscoplasticity arises from muscle-contraction-induced microfilament shortening, mediated by actin-severing proteins and FHOD-1 bundling.

Conclusions:

• A molecular network involving PAK-1 and SPC-1 stabilizes cell shapes during embryonic elongation.
• This network acts as a developmental ratchet, preventing axis retraction through viscoplastic deformation.
• The findings elucidate the cellular basis of mechanical force regulation in morphogenesis.