Reynolds-Kenneally Jessica, Mlodzik Marek
Brookdale Department of Molecular, Cell and Developmental Biology, Mt. Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.
Dev Biol. 2005 Sep 1;285(1):38-48. doi: 10.1016/j.ydbio.2005.05.038.
During Drosophila eye development, localized Notch signaling at the dorsal ventral (DV)-midline promotes growth of the entire eye field. This long-range action of Notch signaling may be mediated through the diffusible ligand of the Jak/STAT pathway, Unpaired (Upd), which was recently identified as a downstream target of Notch. However, Notch activity has not been shown to be cell-autonomously required for Upd expression and therefore yet another diffusible signal may be required for Notch activation of Upd. Our results clarify the Notch requirement, demonstrating that Notch activity at the DV-midline leads to cell-autonomous expression of Upd as monitored in loss and gain-of-function Notch clones. In addition, mutations in the Jak/STAT pathway interact genetically with the Notch pathway by suppressing Notch mediated overgrowth. N(act) clones show non-autonomous effects on the cell cycle anterior to the furrow, indicating function of the Jak/STAT pathway. However, cell-autonomous effects of Notch within and posterior to the furrow are independent of Upd. Here, Notch autonomously maintains cells in a proliferative state and blocks photoreceptor differentiation.
在果蝇眼睛发育过程中，背腹（DV）中线处的局部Notch信号传导促进整个眼场的生长。Notch信号传导的这种远程作用可能是通过Jak/STAT途径的可扩散配体Unpaired（Upd）介导的，Upd最近被确定为Notch的下游靶点。然而，尚未证明Notch活性对于Upd表达是细胞自主必需的，因此可能还需要另一种可扩散信号来激活Notch对Upd的作用。我们的结果阐明了Notch的需求，表明在DV中线处的Notch活性导致Upd的细胞自主表达，这在功能丧失和功能获得的Notch克隆中得到监测。此外，Jak/STAT途径中的突变通过抑制Notch介导的过度生长与Notch途径发生遗传相互作用。N（act）克隆对沟前的细胞周期显示非自主效应，表明Jak/STAT途径的功能。然而，沟内和沟后的Notch细胞自主效应独立于Upd。在这里，Notch自主地将细胞维持在增殖状态并阻止光感受器分化。
