Conditional nmy-1 and nmy-2 alleles establish that non-muscle myosins are required for late C. elegans embryonic elongation.

Abstract

The elongation of C. elegans embryos allows examination of mechanical interactions between adjacent tissues. Muscle contractions during late elongation induce the remodelling of epidermal circumferential actin filaments through mechanotransduction. Force inputs from the muscles deform circumferential epidermal actin filament, which causes them to be severed, eventually reformed and shortened. This squeezing force drives embryonic elongation. We investigated the possible role of the non-muscle myosins NMY-1 and NMY-2 in this process using nmy-1 and nmy-2 thermosensitive alleles. Our findings show these myosins act redundantly in late elongation, since double nmy-2(ts); nmy-1(ts) mutants immediately stop elongation when raised to 25°C. Their inactivation does not reduce muscle activity, as measured from epidermis deformation, suggesting that they are directly involved in the multi-step process of epidermal remodeling. Furthermore, NMY-1 and NMY-2 inactivation is reversible when embryos are kept at the non-permissive temperature for a few hours. However, after longer exposure to 25°C double mutant embryos fail to resume elongation, presumable because NMY-1 was seen to form protein aggregates. We propose that the two C. elegans non-muscle myosin II act during actin remodeling either to bring severed ends or hold them.