Knirr S, Azpiazu N, Frasch M
Department of Biochemistry and Molecular Biology, Mount Sinai School of Medicine, New York, NY 10029, USA.
Development. 1999 Oct;126(20):4525-35. doi: 10.1242/dev.126.20.4525.
In the Drosophila embryo, a distinct class of myoblasts, designated as muscle founders, prefigures the mature pattern of somatic body wall muscles. Each founder cell appears to be instrumental in generating a single larval muscle with a defined identity. The NK homeobox gene S59 was the first of a growing number of proposed 'identity genes' that have been found to be expressed in stereotyped patterns in specific subsets of muscle founders and their progenitor cells and are thought to control their developmental fates. In the present study, we describe the effects of gain- and loss-of-function experiments with S59. We find that a null mutation in the gene encoding S59, which we have named slouch (slou), disrupts the development of all muscles that are derived from S59-expressing founder cells. The observed phenotypes upon mutation and ectopic expression of slouch include transformations of founder cell fates, thus confirming that slouch (S59) functions as an identity gene in muscle development. These fate transformations occur between sibling founder cells as well as between neighboring founders that are not lineage-related. In the latter case, we show that slouch (S59) activity is required cell-autonomously to repress the expression of ladybird (lb) homeobox genes, thereby preventing specification along the lb pathway. Together, these findings provide new insights into the regulatory interactions that establish the somatic muscle pattern.
在果蝇胚胎中,一类独特的成肌细胞,即肌肉始祖细胞,预示着体壁肌肉的成熟模式。每个始祖细胞似乎对于生成具有特定身份的单个幼虫肌肉起着关键作用。NK 同源框基因 S59 是越来越多被提出的“身份基因”中的第一个,已发现它在特定肌肉始祖细胞及其祖细胞亚群中以固定模式表达,并被认为控制着它们的发育命运。在本研究中,我们描述了 S59 功能获得和功能缺失实验的效果。我们发现,编码 S59 的基因中的无效突变,我们将其命名为 slouch(slou),会破坏所有源自表达 S59 的始祖细胞的肌肉发育。slouch 突变和异位表达时观察到的表型包括始祖细胞命运的转变,从而证实 slouch(S59)在肌肉发育中作为身份基因发挥作用。这些命运转变发生在同胞始祖细胞之间以及非谱系相关的相邻始祖细胞之间。在后一种情况下,我们表明 slouch(S59)活性在细胞自主水平上是抑制瓢虫(lb)同源框基因表达所必需的,从而防止沿着 lb 途径的特化。总之,这些发现为建立体壁肌肉模式的调控相互作用提供了新的见解。