Abstract
The striated body wall muscles of Caenorhabditis elegans are a simple model system with well-characterized sarcomeres that have many vertebrate protein homologs. Previously, we observed deletion mutants for two formin genes, fhod-1 and cyk-1, developed thin muscles with abnormal dense bodies/sarcomere Z-lines. However, the nature of the cyk-1 mutation necessitated maternal CYK-1 expression for viability of the examined animals. Here, we tested the effects of complete loss of CYK-1 using a fast acting temperature-sensitive cyk-1(ts) mutant. Surprisingly, neither post-embryonic loss of CYK-1 nor acute loss of CYK-1 during embryonic sarcomerogenesis caused muscle defects, suggesting CYK-1 might not play a direct role in muscle development. Consistent with this, examination of cyk-1(Δ) mutants re-expressing CYK-1 in a mosaic pattern showed CYK-1 cannot rescue muscle defects in a muscle cell autonomous manner, suggesting muscle phenotypes caused by cyk-1 deletion are likely indirect. Conversely, mosaic re-expression of FHOD-1 in fhod-1(Δ) mutants promoted muscle cell growth, as well as proper Z-line organization, in a muscle cell autonomous manner. As we can observe no effect of loss of any other worm formin on muscle development, we conclude that FHOD-1 is the only formin that directly promotes striated muscle development in C. elegans.
Competing Interest Statement
The authors have declared no competing interest.
