Li Wenjun, Gao Fen-Biao
Gladstone Institute of Neurological Disease, Neuroscience Program, University of California, San Francisco, San Francisco, California 94141-9100, USA.
J Neurosci. 2003 Jul 16;23(15):6171-5. doi: 10.1523/JNEUROSCI.23-15-06171.2003.
Dendritic arbors of different neuronal subtypes cover distinct spatial territories, known as dendritic fields, to receive specific inputs in a nervous system. How the size of dendritic fields is determined by cell-intrinsic factors during development remains primarily unknown. To address this issue, we used the Drosophila embryonic peripheral nervous system. In each hemisegment, six dorsal cluster dendritic arborization (DA) neurons elaborate stereotypic dendritic branching patterns underneath the epidermis. Here we report the identification of loss-of-function mutations in the tropomyosin II gene (TmII) that result in expanded dendritic fields of DA neurons. Mosaic analysis with a repressible cell marker demonstrated that TmII functions in a cell-autonomous manner to control the formation of dendritic fields. Furthermore, we show that TmII genetically interacted with flamingo, a gene encoding a membrane receptor-like molecule that affects dendritic growth. TmII encodes multiple isoforms of a protein that stabilizes actin filaments. Our findings suggest that tropomyosin helps control the size of dendritic fields by regulating actin cytoskeletal dynamics.
不同神经元亚型的树突分支覆盖着不同的空间区域,即所谓的树突野,以便在神经系统中接收特定的输入。在发育过程中,树突野的大小如何由细胞内在因素决定,目前仍基本未知。为了解决这个问题,我们利用了果蝇胚胎外周神经系统。在每个半体节中,六个背侧簇状树突分支化(DA)神经元在表皮下形成刻板的树突分支模式。在此,我们报告了原肌球蛋白II基因(TmII)功能丧失突变的鉴定,这些突变导致DA神经元的树突野扩大。使用可抑制细胞标记的镶嵌分析表明,TmII以细胞自主的方式发挥作用,控制树突野的形成。此外,我们表明TmII与flamingo基因发生遗传相互作用,flamingo是一个编码影响树突生长的膜受体样分子的基因。TmII编码一种稳定肌动蛋白丝的蛋白质的多种亚型。我们的研究结果表明,原肌球蛋白通过调节肌动蛋白细胞骨架动力学来帮助控制树突野的大小。