A neuronal identity code for the odorant receptor-specific and activity-dependent axon sorting
A neuronal identity code for the odorant receptor-specific and activity-dependent axon sorting
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DOI：
10.1016/j.cell.2006.10.031
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发表时间：
2006-12-01
期刊：
影响因子：
64.5
通讯作者：
Sakano, Hitoshi
中科院分区：
文献类型：
--
作者：
Serizawa, Shou;Miyamichi, Kazunari;Sakano, Hitoshi
在小鼠中，表达相同气味受体（OR）的嗅觉感觉神经元（OSN）将其轴突汇聚到嗅球中的一组特定肾小球。为了研究 OR 指示的轴突束颤是如何控制的，我们搜索了表达谱与表达的 OR 相关的基因。使用大多数 OSN 表达特定 OR 的转基因小鼠，我们鉴定了编码同质粘附分子 Kirrel2/Kirrel3 和排斥分子 ephrin-A5/EphA5 的基因。在 CNGA2 敲除小鼠中，气味引起的阳离子流入被破坏，Kirrel2 和 EphA5 下调，而 Kirrel3 和 ephrin-A5 上调，表明这些基因以活性依赖性方式转录。镶嵌分析表明，这些基因的功能获得会产生重复的肾小球。我们提出，一组特定的粘附/排斥分子（其表达水平由 OR 分子决定）在肾小球图形成过程中调节 OSN 的轴突束。
In the mouse, olfactory sensory neurons (OSNs) expressing the same odorant receptor (OR) converge their axons to a specific set of glomeruli in the olfactory bulb. To study how OR-instructed axonal fasciculation is controlled, we searched for genes whose expression profiles are correlated with the expressed ORs. Using the transgenic mouse in which the majority of OSNs express a particular OR, we identified such genes coding for the homophilic adhesive molecules Kirrel2/Kirrel3 and repulsive molecules ephrin-A5/EphA5. In the CNGA2 knockout mouse, where the odor-evoked cation influx is disrupted, Kirrel2 and EphA5 were downregulated, while Kirrel3 and ephrin-A5 were upregulated, indicating that these genes are transcribed in an activity-dependent manner. Mosaic analysis demonstrated that gain of function of these genes generates duplicated glomeruli. We propose that a specific set of adhesive/repulsive molecules, whose expression levels are determined by OR molecules, regulate the axonal fasciculation of OSNs during the process of glomerular map formation.