Skeath J B, Doe C Q
Department of Cell and Structural Biology, Howard Hughes Medical Institute, University of Illinois, Urbana, Illinois 61801, USA.
Development. 1998 May;125(10):1857-65. doi: 10.1242/dev.125.10.1857.
In Drosophila, most neuronal siblings have different fates ('A/B'). Here we demonstrate that mutations in sanpodo, a tropomodulin actin-binding protein homologue, equalize a diverse array of sibling neuron fates ('B/B'). Loss of Notch signaling gives the same phenotype, whereas loss of numb gives the opposite phenotype ('A/A'). The identical effect of removing either sanpodo or Notch function on the fates of sibling CNS neurons indicates that sanpodo may act in the Notch signaling pathway. In addition, sanpodo and numb show dosage-sensitive interactions and epistasis experiments indicate that sanpodo acts downstream of numb. Taken together, these results show that interactions between sanpodo, the Notch signaling pathway and numb enable CNS sibling neurons to acquire different fates.
在果蝇中，大多数神经细胞的兄弟姐妹具有不同的命运（“A/B”）。在这里，我们证明了sanpodo（一种原肌球蛋白肌动蛋白结合蛋白同源物）的突变会使多种不同的神经细胞兄弟姐妹命运变得相同（“B/B”）。Notch信号通路的缺失会产生相同的表型，而numb的缺失则会产生相反的表型（“A/A”）。去除sanpodo或Notch功能对中枢神经系统神经细胞兄弟姐妹命运的相同影响表明，sanpodo可能在Notch信号通路中起作用。此外，sanpodo和numb表现出剂量敏感的相互作用，上位性实验表明sanpodo在numb的下游起作用。综上所述，这些结果表明，sanpodo、Notch信号通路和numb之间的相互作用使中枢神经系统的神经细胞兄弟姐妹能够获得不同的命运。
