Drosophila homeodomain protein dHb9 directs neuronal fate via crossrepressive and cell-nonautonomous mechanisms
Drosophila homeodomain protein dHb9 directs neuronal fate via crossrepressive and cell-nonautonomous mechanisms
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DOI：
10.1016/s0896-6273(02)00743-2
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发表时间：
2002-07-03
期刊：
影响因子：
16.2
通讯作者：
Skeath, JB
中科院分区：
文献类型：
--
作者：
Broihier, HT;Skeath, JB
在这里，我们介绍了dHb9的鉴定和特性，dHb9是脊椎动物HB9的果蝇同源物，它编码一个运动神经元(MN)发育的中心因子。我们发现dHb9通过限制Lim3和Even-Skiped(Eve)的表达来调节神经元的命运，这两种蛋白质是发育不同神经元类别所必需的同源结构域(HD)。此外，dHb9和Lim3在几乎相同的腹侧投射MN中彼此独立激活。令人惊讶的是，dHb9在背部投射的MN的子集中非自主地抑制Lim3细胞，揭示了细胞间信号在建立果蝇神经元命运中的新角色。最后，我们提供了dHb9和Eve通过Groucho依赖的交叉抑制相互调节彼此表达的证据。这种相互拮抗的关系与形成脊椎动物神经管的HD蛋白对之间的交叉抑制关系相似。
Here we present the identification and characterization of dHb9, the Drosophila homolog of vertebrate Hb9, which encodes a factor central to motorneuron (MN) development. We show that dHb9 regulates neuronal fate by restricting expression of Lim3 and Even-skipped (Eve), two homeodomain (HD) proteins required for development of distinct neuronal classes. Also, dHb9 and Lim3 are activated independently of each other in a virtually identical population of ventrally and laterally projecting MNs. Surprisingly, dHb9 represses Lim3 cell nonautonomously in a subset of dorsally projecting MNs, revealing a novel role for intercellular signaling in the establishment of neuronal fate in Drosophila. Lastly, we provide evidence that dHb9 and Eve regulate each other's expression through Groucho-dependent crossrepression. This mutually antagonistic relationship bears similarity to the crossrepressive relationships between pairs of HD proteins that pattern the vertebrate neural tube.