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首页> 外文期刊>Current Biology: CB >Notch-dependent induction of left/right asymmetry in C. elegans interneurons and motoneurons.
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Notch-dependent induction of left/right asymmetry in C. elegans interneurons and motoneurons.

机译：Notch引起的C中左右不对称性的诱导。线虫间神经元和运动神经元。

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摘要

Although nervous systems are largely bilaterally symmetric on a structural level, they display striking degrees of functional left/right (L/R) asymmetry. In Caenorhabditis elegans, two structurally symmetric pairs of sensory neurons, ASE and AWC, display two distinctly controlled types of functional L/R asymmetries (stereotyped versus stochastic asymmetry) [[1], [2] and [3]]. Beyond these two cases, the extent of neuronal asymmetry in the C. elegans nervous system was unclear. Here, we report that the Beta3/Olig-type bHLH transcription factor hlh-16 is L/R asymmetrically expressed in several distinct, otherwise bilaterally symmetric interneuron and motoneuron pairs that are part of a known navigation circuit. We find that hlh-16 asymmetry is generated during gastrulation by an asymmetric LAG-2/Delta signal originating from the mesoderm that promotes hlh-16 expression in neurons on the left side through direct binding of the Notch effector LAG-1/Su(H)/CBF to a cis-regulatory element in the hlh-16 locus. Removal of hlh-16 reveals an unanticipated asymmetry in the ability of the axons of the AIY interneurons to extend into the nerve ring, with the left AIY axon requiring elevated hlh-16 expression for correct extension. Our study suggests that the extent of molecular L/R asymmetry in the C. elegans nervous system is broader than previously anticipated, establishes a novel signaling mechanism that crosses germ layers to diversify bilaterally symmetric neuronal lineages, and reveals L/R asymmetric control of axonal outgrowth of bilaterally symmetric neurons.
机译：尽管神经系统在结构上基本上是双向对称的，但它们显示出功能性左右（L / R）不对称的惊人程度。在秀丽隐杆线虫中，感觉神经元的两个结构对称对，ASE和AWC，显示两种明显受控制的功能性L / R不对称类型（定型与随机性不对称）[[1]，[2]和[ 3]]。除了这两种情况外， C中神经元的不对称程度。线虫的神经系统不清楚。在这里，我们报道Beta3 / Olig型bHLH转录因子 hlh-16 在几个不同的，左右对称的中间神经元和运动神经元对中以L / R不对称表达，它们是已知导航电路的一部分。我们发现 hlh-16 的不对称是由中胚层产生的，在左侧神经元中促进 hlh-16 表达的不对称LAG-2 / Delta信号引起的。通过将Notch效应子LAG-1 / Su（H）/ CBF直接结合到 hlh-16 基因座中的顺式调节元件上。去除 hlh-16 揭示了AIY中神经元轴突伸入神经环的能力出乎意料的不对称，而左AIY轴突则需要升高 hlh-16 正确扩展的表达式。我们的研究表明，在C中分子L / R不对称的程度。线虫的神经系统比以前预期的更广泛，建立了一种跨胚层的新信号传导机制，以使双侧对称神经元谱系多样化，并揭示了双侧对称神经元轴突生长的L / R不对称控制。

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