The striated body wall muscles of Caenorhabditis elegans are a simple model for sarcomere assembly. Previously, we observed deletion mutants for two formin genes, fhod‐1 and cyk‐1, develop thin muscles with abnormal dense bodies (the sarcomere Z‐line analogs). However, this work left in question whether these formins work in a muscle cell autonomous manner, particularly since cyk‐1(∆) deletion has pleiotropic effects on development. Using a fast acting temperature‐sensitive cyk‐1(ts) mutant, we show here that neither postembryonic loss nor acute loss of CYK‐1 during embryonic sarcomerogenesis cause lasting muscle defects. Furthermore, mosaic expression of CYK‐1 in cyk‐1(∆) mutants is unable to rescue muscle defects in a cell autonomous manner, suggesting muscle phenotypes caused by cyk‐1(∆) are likely indirect. Conversely, mosaic expression of FHOD‐1 in fhod‐1(Δ) mutants promotes muscle cell growth and proper dense body organization in a muscle cell autonomous manner. As we observe no effect of loss of any other formin on muscle development, we conclude FHOD‐1 is the only worm formin that directly promotes striated muscle development, and the effects on formin loss in C. elegans are surprisingly modest compared to other systems.

中文翻译：

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FHOD-1 是秀丽隐杆线虫中唯一一种以细胞自主方式促进横纹肌生长和 Z 线组织的形式

秀丽隐杆线虫的横纹体壁肌肉是肌节组装的简单模型。以前，我们观察到两个 formin 基因fhod-1和cyk-1 的缺失突变体会产生具有异常致密体（肌节 Z 线类似物）的瘦肌肉。然而，这项工作对这些形式是否以肌肉细胞自主方式起作用存在疑问，特别是因为cyk-1(∆)缺失对发育具有多效性影响。使用快速作用的温度敏感cyk-1(ts)突变体，我们在这里表明，在胚胎肌瘤发生过程中，CYK-1 的胚胎后丢失和急性丢失都不会导致持久的肌肉缺陷。此外，CYK-1 在cyk-1(∆)中的嵌合表达突变体无法以细胞自主方式修复肌肉缺陷，表明由cyk-1 (Δ)引起的肌肉表型可能是间接的。相反，fhod-1(Δ)突变体中FHOD-1 的镶嵌表达以肌肉细胞自主方式促进肌肉细胞生长和适当的致密身体组织。由于我们没有观察到任何其他福明损失对肌肉发育的影响，因此我们得出结论，FHOD-1 是唯一直接促进横纹肌发育的蠕虫福明，以及对C 中福明损失的影响。与其他系统相比，elegans出奇地温和。