RSY-1 is a local inhibitor of presynaptic assembly in C. elegans.

RSY-1 is a local inhibitor of presynaptic assembly in C. elegans.
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DOI:
10.1126/science.1169025
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发表时间:
2009-03-13
期刊:
Science (New York, N.Y.)
影响因子:
--
通讯作者:
Shen K
Shen K
中科院分区:
其他
文献类型:
--
作者:
Patel MR;Shen K

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作为神经元通讯的基本单位,化学突触由突触前和突触后特化组成,它们在特定位置形成,具有确定的形状和大小。突触组装必须受到严格调节,以防止突触大小和数量过度生长,但抑制突触组装的分子机制尚不清楚。我们发现突触发生调节因子-1 (RSY-1) 是一种进化上保守的分子,可局部拮抗突触前组装。秀丽隐杆线虫中 RSY-1 的缺失导致额外突触的形成,并将过量的突触物质募集到突触前位点。 RSY-1 直接与 SYD-2/liprin-alpha 相互作用并负向调节,SYD-2/liprin-alpha 是一种主组装分子,可将大量突触成分招募到突触前位点。 RSY-1 还结合并调节 SYD-1,SYD-1 是 SYD-2 正常发挥功能所需的突触蛋白。因此,局部抑制机制控制突触的形成。
As fundamental units of neuronal communication, chemical synapses are composed of presynaptic and postsynaptic specializations that form at specific locations with defined shape and size. Synaptic assembly must be tightly regulated to prevent overgrowth of the synapse size and number, but the molecular mechanisms that inhibit synapse assembly are poorly understood. We identified regulator of synaptogenesis–1 (RSY-1) as an evolutionarily conserved molecule that locally antagonized presynaptic assembly. The loss of RSY-1 in Caenorhabditis elegans led to formation of extra synapses and recruitment of excessive synaptic material to presynaptic sites. RSY-1 directly interacted with and negatively regulated SYD-2/liprin-alpha, a master assembly molecule that recruits numerous synaptic components to presynaptic sites. RSY-1 also bound and regulated SYD-1, a synaptic protein required for proper functioning of SYD-2. Thus, local inhibitory mechanisms govern synapse formation.
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