在正在发育的大脑中，会生成很多不同的神经细胞，其中每一种形成特定突触连接。每个生长中的轴突或树突会设法到达其目标，然后停止生长。
科学家对允许连接神经元识别它们突触伙伴的机制还不是很了解。本期Nature上两篇论文对这一问题进行了研究。
Morey等人对正、负基因转录调控因子之间的相互作用进行了分析，这种相互作用在果蝇视觉系统的一个组成单元——R7神经元中调控特定光敏色素及轴突引导分子的合成。令人吃惊的是，他们发现，R7层特定性的调控中的一个关键步骤是向另一层（该层由一个相关的R8光受体神经元支配）定位的一个选择性程序的抑制。Milan Petrovic 和 Thomas Hummel也是以果蝇视觉系统为模型，他们发现，时间选择对于一个神经元找到其突触伙伴来说是关键。层特定性（layer-specific）突触连接的形成由一个细胞内在的时程机制控制，该机制使不同轴突在不同N-钙粘蛋白表达层上停止，具体情况取决于它们什么时候表达转录因子Sequoia以及表达时间有多长。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature 456, 795-799 (11 December 2008) | doi:10.1038/nature07419
Coordinate control of synaptic-layer specificity and rhodopsins in photoreceptor neurons
Marta Morey1,3, Susan K. Yee1,3, Tory Herman1,4, Aljoscha Nern1, Enrique Blanco2 & S. Lawrence Zipursky1
1 Department of Biological Chemistry, Howard Hughes Medical Institute, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California 90095, USA
2 Departament de Genètica and Institut de Biomedicina de la Universitat de Barcelona (IBUB), Universitat de Barcelona, 08028 Barcelona, Catalunya, Spain
3 These authors contributed equally to this work.
How neurons make specific synaptic connections is a central question in neurobiology. The targeting of the Drosophila R7 and R8 photoreceptor axons to different synaptic layers in the brain provides a model with which to explore the genetic programs regulating target specificity. In principle this can be accomplished by cell-type-specific molecules mediating the recognition between synaptic partners1. Alternatively, specificity could also be achieved through cell-type-specific repression of particular targeting molecules. Here we show that a key step in the targeting of the R7 neuron is the active repression of the R8 targeting program. Repression is dependent on NF-YC, a subunit of the NF-Y (nuclear factor Y) transcription factor2. In the absence of NF-YC, R7 axons terminate in the same layer as R8 axons. Genetic experiments indicate that this is due solely to the derepression of the R8-specific transcription factor Senseless3 (Sens) late in R7 differentiation. Sens is sufficient to control R8 targeting specificity and we demonstrate that Sens directly binds to an evolutionarily conserved DNA sequence upstream of the start of transcription of an R8-specific cell-surface protein, Capricious (Caps) that regulates R8 target specificity. We show that R7 targeting requires the R7-specific transcription factor Prospero4, 5 (Pros) in parallel to repression of the R8 targeting pathway by NF-YC. Previous studies demonstrated that Sens6, 7 and Pros8 directly regulate the expression of specific rhodopsins in R8 and R7. We propose that the use of the same transcription factors to promote the cell-type-specific expression of sensory receptors and cell-surface proteins regulating synaptic target specificity provides a simple and general mechanism for ensuring that transmission of sensory information is processed by the appropriate specialized neural circuits.
