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突触可塑性结构和功能成分的遗传学剖析。I. 成束蛋白II控制突触稳定和生长。

Genetic dissection of structural and functional components of synaptic plasticity. I. Fasciclin II controls synaptic stabilization and growth.

作者信息

Schuster C M, Davis G W, Fetter R D, Goodman C S

机构信息

Howard Hughes Medical Institute, Department of Molecular and Cell Biology, University of California, Berkeley 94720, USA.

出版信息

Neuron. 1996 Oct;17(4):641-54. doi: 10.1016/s0896-6273(00)80197-x.

DOI:10.1016/s0896-6273(00)80197-x
PMID:8893022
Abstract

The glutamatergic neuromuscular synapse in Drosophila forms and differentiates into distinct boutons in the embryo and grows by sprouting new boutons throughout larval life. We demonstrate that two axons form approximately 18 boutons on muscles 7 and 6 by hatching and grow to approximately 180 boutons by third instar. We further show that, after synapse formation, the homophilic cell adhesion molecule Fasciclin II (Fas II) is localized both pre- and postsynaptically where it controls synapse stabilization. In FasII null mutants, synapse formation is normal, but boutons then retract during larval development. Synapse elimination and resulting lethality are rescued by transgenes that drive Fas II expression both pre- and postsynaptically; driving Fas II expression on either side alone is insufficient. Fas II can also control synaptic growth; various FasII alleles lead to either an increase or decrease in sprouting, depending upon the level of Fas II.

摘要

果蝇中的谷氨酸能神经肌肉突触在胚胎中形成并分化为不同的突触小体,在幼虫期通过长出新的突触小体而生长。我们证明,两条轴突在孵化时在肌肉7和6上形成约18个突触小体,并在三龄幼虫时生长到约180个突触小体。我们进一步表明,在突触形成后,同嗜性细胞粘附分子Fasciclin II(Fas II)定位于突触前和突触后,在那里它控制突触稳定。在FasII基因敲除突变体中,突触形成正常,但突触小体在幼虫发育过程中会回缩。通过在突触前和突触后驱动Fas II表达的转基因可以挽救突触消除和由此导致的致死性;仅在一侧驱动Fas II表达是不够的。Fas II还可以控制突触生长;各种FasII等位基因根据Fas II的水平导致突触小体生长增加或减少。

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