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本文引用的文献

1
Principles of planar polarity in animal development.动物发育中的平面极性原则。
Development. 2011 May;138(10):1877-92. doi: 10.1242/dev.054080.
2
The oriented emergence of axons from retinal ganglion cells is directed by laminin contact in vivo.视网神经节细胞的轴突定向延伸是由活体层粘连蛋白接触所引导的。
Neuron. 2011 Apr 28;70(2):266-80. doi: 10.1016/j.neuron.2011.03.013.
3
Pointing in the right direction: new developments in the field of planar cell polarity.指向正确方向:平面细胞极性领域的新发展。
Nat Rev Genet. 2011 Jun;12(6):385-91. doi: 10.1038/nrg2956. Epub 2011 Apr 19.
4
Transmembrane semaphorin signalling controls laminar stratification in the mammalian retina.跨膜信号素信号控制哺乳动物视网膜的层状结构。
Nature. 2011 Feb 10;470(7333):259-63. doi: 10.1038/nature09675.
5
Atypical protein kinase C regulates primary dendrite specification of cerebellar Purkinje cells by localizing Golgi apparatus.非典型蛋白激酶 C 通过定位高尔基器调节小脑浦肯野细胞的初级树突特化。
J Neurosci. 2010 Dec 15;30(50):16983-92. doi: 10.1523/JNEUROSCI.3352-10.2010.
6
MATH5 controls the acquisition of multiple retinal cell fates.MATH5 控制着多种视网膜细胞命运的获得。
Mol Brain. 2010 Nov 18;3:36. doi: 10.1186/1756-6606-3-36.
7
Atypical cadherins Dachsous and Fat control dynamics of noncentrosomal microtubules in planar cell polarity.非中心体微管的典型钙黏着蛋白 Dachsous 和 Fat 在平面细胞极性中的动力学控制。
Dev Cell. 2010 Sep 14;19(3):389-401. doi: 10.1016/j.devcel.2010.08.004.
8
Four-jointed modulates growth and planar polarity by reducing the affinity of dachsous for fat.四联体通过降低 dachsous 与 fat 的亲和力来调节生长和平面极性。
Curr Biol. 2010 May 11;20(9):803-10. doi: 10.1016/j.cub.2010.03.056. Epub 2010 Apr 29.
9
Modulation of fat:dachsous binding by the cadherin domain kinase four-jointed.四联体钙黏蛋白激酶对 fat:dachsous 结合的调控
Curr Biol. 2010 May 11;20(9):811-7. doi: 10.1016/j.cub.2010.04.016. Epub 2010 Apr 29.
10
Branching out: mechanisms of dendritic arborization.分支扩展:树突分支的机制。
Nat Rev Neurosci. 2010 May;11(5):316-28. doi: 10.1038/nrn2836.

非典型钙黏蛋白 Fat3 对神经元形态的控制。

Control of neuronal morphology by the atypical cadherin Fat3.

机构信息

Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.

出版信息

Neuron. 2011 Sep 8;71(5):820-32. doi: 10.1016/j.neuron.2011.06.026.

DOI:10.1016/j.neuron.2011.06.026
PMID:21903076
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3521586/
Abstract

Neurons receive signals through dendrites that vary widely in number and organization, ranging from one primary dendrite to multiple complex dendritic trees. For example, retinal amacrine cells (ACs) project primary dendrites into a discrete synaptic layer called the inner plexiform layer (IPL) and only rarely extend processes into other retinal layers. Here, we show that the atypical cadherin Fat3 ensures that ACs develop this unipolar morphology. AC precursors are initially multipolar but lose neurites as they migrate through the neuroblastic layer. In fat3 mutants, pruning is unreliable and ACs elaborate two dendritic trees: one in the IPL and a second projecting away from the IPL that stratifies to form an additional synaptic layer. Since complex nervous systems are characterized by the addition of layers, these results demonstrate that mutations in a single gene can cause fundamental changes in circuit organization that may drive nervous system evolution.

摘要

神经元通过树突接收信号,树突的数量和结构差异很大,从一个主树突到多个复杂的树突树不等。例如,视网膜无长突细胞 (ACs) 将主树突投射到一个称为内丛状层 (IPL) 的离散突触层中,很少有突起延伸到其他视网膜层。在这里,我们表明,非典型钙黏蛋白 Fat3 确保 ACs 具有这种单极形态。AC 前体最初是多极的,但在它们通过神经母细胞层迁移时会失去神经突。在 fat3 突变体中,修剪不可靠,ACs 会形成两个树突树:一个在 IPL 中,另一个从 IPL 向外投射并分层形成另一个突触层。由于复杂的神经系统的特征是增加了层,这些结果表明,单个基因突变可能导致电路组织的根本变化,从而可能推动神经系统的进化。