在正在發(fā)育的大腦中，會(huì)生成很多不同的神經(jīng)細(xì)胞,，其中每一種形成特定突觸連接,。每個(gè)生長(zhǎng)中的軸突或樹突會(huì)設(shè)法到達(dá)其目標(biāo),，然后停止生長(zhǎng),。
科學(xué)家對(duì)允許連接神經(jīng)元識(shí)別它們突觸伙伴的機(jī)制還不是很了解,。本期Nature上兩篇論文對(duì)這一問題進(jìn)行了研究。
Morey等人對(duì)正,、負(fù)基因轉(zhuǎn)錄調(diào)控因子之間的相互作用進(jìn)行了分析,，這種相互作用在果蠅視覺系統(tǒng)的一個(gè)組成單元——R7神經(jīng)元中調(diào)控特定光敏色素及軸突引導(dǎo)分子的合成。令人吃驚的是,，他們發(fā)現(xiàn),，R7層特定性的調(diào)控中的一個(gè)關(guān)鍵步驟是向另一層（該層由一個(gè)相關(guān)的R8光受體神經(jīng)元支配）定位的一個(gè)選擇性程序的抑制。Milan Petrovic 和 Thomas Hummel也是以果蠅視覺系統(tǒng)為模型,，他們發(fā)現(xiàn),，時(shí)間選擇對(duì)于一個(gè)神經(jīng)元找到其突觸伙伴來說是關(guān)鍵,。層特定性（layer-specific）突觸連接的形成由一個(gè)細(xì)胞內(nèi)在的時(shí)程機(jī)制控制，該機(jī)制使不同軸突在不同N-鈣粘蛋白表達(dá)層上停止,，具體情況取決于它們什么時(shí)候表達(dá)轉(zhuǎn)錄因子Sequoia以及表達(dá)時(shí)間有多長(zhǎng)。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
