The BMP homolog Gbb provides a retrograde signal that regulates synaptic growth at the Drosophila neuromuscular junction
The BMP homolog Gbb provides a retrograde signal that regulates synaptic growth at the Drosophila neuromuscular junction
复制标题
DOI：
10.1016/s0896-6273(03)00426-4
复制
发表时间：
2003-07-17
期刊：
影响因子：
16.2
通讯作者：
O'Connor, MB
中科院分区：
文献类型：
--
作者：
McCabe, BD;Marqués, G;O'Connor, MB
我们发现，BMP的直系同源物GBB可以通过逆行机制来调节果蝇神经肌肉接头（NMJ）的突触生长。gbb突变体具有减小的NMJ突触大小、减少的神经递质释放和异常的突触前超微结构。这些缺陷与我们在BMP受体和Smad转录因子突变体中观察到的缺陷相似。然而，而这些BMP受体和信号传导组件所需的突触前运动神经元，GBB的表达是需要在很大程度上在突触后肌肉; GBB在肌肉中的表达拯救关键方面的GBB突变体表型。与此一致的是，我们发现通过过度表达显性负性p150/Glued阻断逆行轴突运输可以抑制运动神经元中的BMP信号。这些实验表明，肌肉来源的BMP逆行信号参与协调神经肌肉突触的发育和生长。
We show that the BMP ortholog Gbb can signal by a retrograde mechanism to regulate synapse growth of the Drosophila neuromuscular junction (NMJ). gbb mutants have a reduced NMJ synapse size, decreased neurotransmitter release, and aberrant presynaptic ultrastructure. These defects are similar to those we observe in mutants of BMP receptors and Smad transcription factors. However, whereas these BMP receptors and signaling components are required in the presynaptic motoneuron, Gbb expression is required in large part in postsynaptic muscles; gbb expression in muscle rescues key aspects of the gbb mutant phenotype. Consistent with this notion, we find that blocking retrograde axonal transport by overexpression of dominant-negative p150/Glued in neurons inhibits BMP signaling in motoneurons. These experiments reveal that a muscle-derived BMP retrograde signal participates in coordinating neuromuscular synapse development and growth.