Interneurons navigate along multiple tangential paths to settle into appropriate cortical layers. They undergo a saltatory migration paced by intermittent nuclear jumps whose regulation relies on interplay between extracellular cues and genetic-encoded information. It remains unclear how cycles of pause and movement are coordinated at the molecular level. Post-translational modification of proteins contributes to cell migration regulation. The present study uncovers that carboxypeptidase 1, which promotes post-translational protein deglutamylation, controls the pausing of migrating cortical interneurons. Moreover, we demonstrate that pausing during migration attenuates movement simultaneity at the population level, thereby controlling the flow of interneurons invading the cortex. Interfering with the regulation of pausing not only affects the size of the cortical interneuron cohort but also impairs the generation of age-matched projection neurons of the upper layers.

中文翻译：

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内部神经元迁移的细胞本征控制驱动皮质形态发生。

中间神经元沿着多条切线路径导航，以沉降到适当的皮质层中。它们经历了间歇性核跳跃的盐迁移，其跳跃的调控依赖于细胞外信号与遗传编码信息之间的相互作用。尚不清楚暂停和移动的周期如何在分子水平上协调。蛋白质的翻译后修饰有助于细胞迁移的调控。本研究发现，羧肽酶1促进翻译后蛋白质的脱谷氨酰化，控制着皮层中枢神经元的迁移暂停。此外，我们证明了在迁移过程中暂停会降低群体水平上的运动同时性，从而控制侵入皮层的中间神经元的流动。