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裂和受体氨酸酶69D通过DSCAM1赋予了轴子分支的空间特异性

Dan Dascenco¹, Maria-Luise Erfurth², Azadeh Izadifar¹

¹Neuronal Wiring Laboratory, VIB, Herestraat 49, 3000 Leuven, Belgium; Department of Oncology, School of Medicine, University of Leuven, Herestraat 49, 3000 Leuven, Belgium.

|August 29, 2015

概括

受体氨酸酶69D (RPTP69D) 和Slit调节Drosophila中的特定轴突分支. 它们调节Dscam1活动,通过控制轴突附带形成来影响神经元电路的复杂性.

科学领域:

神经科学
发育生物学
分子生物学

背景情况:

轴突分支对于神经元电路的复杂性至关重要.
Dscam1受体的多样性对于Drosophila机械感应神经元的轴突分支是必不可少的.

研究的目的:

研究RPTP69D和Slit在轴突分支中的作用.
阐明Slit和RPTP69D调节Dscam1活动以控制特定的轴突附带形成的分子机制.

主要方法:

在Drosophila中进行基因分析.
研究蛋白相互作用的生物化学测试.
轴突发育的单个生长成像.

主要成果:

RPTP69D或Slit的损失抑制了特定的轴突附带形成.
裂结合Dscam1增强了Dscam1与RPTP69D的相互作用,促进了Dscam1的脱.
裂/RPTP69D是专门用于扩展轴突抵押,而不是一般的分支启动.

结论:

通过在不同的生长区调节Dscam1酸化,Slit和RPTP69D控制了轴突附带形成的空间特异性.
虽然内在的DSCAM1相互作用对所有分支至关重要,但联体诱导的信号改进了附带准.

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