Bhat K M, van Beers E H, Bhat P
Department of Cell Biology, Emory University School of Medicine, Emory University, Atlanta, GA 30322, USA.
Development. 2000 Feb;127(3):655-65. doi: 10.1242/dev.127.3.655.
Wingless (Wg) and other Wnt proteins play a crucial role in a number of developmental decisions in a variety of organisms. In the ventral nerve cord of the Drosophila embryo, Wg is non-autonomously required for the formation and specification of a neuronal precursor cell, NB4-2. NB4-2 gives rise to a well-studied neuronal lineage, the RP2/sib lineage. While the various components of the Wg-signaling pathway are also required for generating NB4-2, the target gene(s) of this pathway in the signal-receiving cell is not known. In this paper, we show that sloppy paired 1 and sloppy paired 2 function as the downstream targets of the Wg signaling to generate the NB4-2 cell. Thus, while the loss-of-function mutations in wg and slp have the same NB4-2 formation and specification defects, these defects in wg mutants can be rescued by expressing slp genes from a heterologous promoter. That slp genes function downstream of the Wg signaling is also indicated by the result that expression of slp genes is lost from the neuroectoderm in wg mutants and that ectopic expression of wg induces ectopic expression of slp. Finally, previous results show that Gooseberry (Gsb) prevents Wg from specifying NB4-2 identity to the wg-expressing NB5-3. In this paper, we also show that gsb interacts with slp and prevents Slp from specifying NB4-2 identity. Overexpression of slp overcomes this antagonistic interaction and respecifies NB5-3 as NB4-2. This respecification, however, can be suppressed by a simultaneous overexpression of gsb at high levels. This mechanism appears to be responsible for specifying NB5-3 identity to a row 5 neuroblast and preventing Wg from specifying NB4-2 identity to that cell.
无翅(Wg)及其他Wnt蛋白在多种生物体的许多发育决策中起着关键作用。在果蝇胚胎的腹侧神经索中,神经元前体细胞NB4-2的形成和特化非自主地需要Wg。NB4-2产生了一个研究充分的神经元谱系,即RP2/姐妹谱系。虽然Wg信号通路的各种组分对于产生NB4-2也是必需的,但该通路在信号接收细胞中的靶基因尚不清楚。在本文中,我们表明稀配对1和稀配对2作为Wg信号的下游靶标发挥作用以产生NB4-2细胞。因此,虽然wg和slp中的功能丧失突变具有相同的NB4-2形成和特化缺陷,但通过从异源启动子表达slp基因可以挽救wg突变体中的这些缺陷。wg突变体的神经外胚层中slp基因的表达缺失以及wg的异位表达诱导slp的异位表达这一结果也表明slp基因在Wg信号下游发挥作用。最后,先前的结果表明醋栗(Gsb)可阻止Wg将NB4-2身份赋予表达wg的NB5-3。在本文中,我们还表明gsb与slp相互作用并阻止Slp赋予NB4-2身份。slp的过表达克服了这种拮抗作用并将NB5-3重新指定为NB4-2。然而,这种重新指定可被高水平同时过表达gsb所抑制。这种机制似乎负责将NB5-3身份赋予第5排神经母细胞,并阻止Wg将NB4-2身份赋予该细胞。