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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Ventralized dorsal telencephalic progenitors in Pax6 mutant mice generate GABA interneurons of a lateral ganglionic eminence fate
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Ventralized dorsal telencephalic progenitors in Pax6 mutant mice generate GABA interneurons of a lateral ganglionic eminence fate

机译：Pax6突变小鼠的腹侧背脑端祖细胞产生侧神经节突出命运的GABA interneurons

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摘要

The transcription factor Pax6 is expressed by progenitors in the ventricular zone (VZ) of dorsal telencephalon (dTel), which generate all cortical glutamatergic neurons, but not by progenitors in the medial ganglionic eminence (MGE), which generate cortical GABAergic interneurons (GABA INs), or the lateral ganglionic eminence (LGE), which generate GABA INs that normally migrate to the olfactory bulb. We show that perinatally, Pax6~(sey/sey) mice, which lack functional Pax6 protein, have large subpial ectopias in dTel and ventral telencephalon connected by cell streams arising from an aberrant paraventricular ectopia found throughout dTel. The subpial and paraventricular ectopias and connecting cell streams are comprised of postmitotic neurons expressing markers for GABA INs characteristic of a LGE fate. Marker analyses show that dTel VZ progenitors in Pax6 mutants are progressively ven-tralized, acquiring expression of regulatory genes normally limited to GE progenitors; by midneurogenesis, the entire dTel VZ exhibits ventralization. This ventralization of the dTel VZ is paralleled by the expression of markers for GABA INs superficial to it, suggesting that it ectopically produces GABA INs, leading to their ectopias and a thinner cortical plate due to diminished production of glutamatergic neurons. Genetic lineage tracing demonstrates that the GABA INs comprising the ectopias are from a cortical Emx1 lineage generated in the dTel VZ, definitively showing that dTel progenitors and progeny acquire a ventral, GE, fate in Pax6 mutants. Thus, Pax6 delimits the appropriate proliferative zone for GABA INs and regulates their numbers and distributions by repressing the ventral fates of dTel progenitors and progeny.
机译：转录因子Pax6由背侧脑神经元（dTel）的心室区（VZ）的祖细胞表达，该祖细胞生成所有皮质谷氨酸能神经元，但不由内神经节隆起（MGE）的祖细胞表达，后者生成皮质GABA能神经元（GABA INs）。 ）或外侧神经节隆起（LGE），这些产生通常会迁移到嗅球的GABA IN。我们发现，围产期，缺乏功能性Pax6蛋白的Pax6〜（sey / sey）小鼠在dTel和腹侧端脑中都存在较大的pipial ectopias，其通过在整个dTel中发现的异常室旁性ectopia引起的细胞流而连接。椎下和脑室旁的异视和连接的细胞流由有丝分裂后的神经元组成，这些神经元表达了LGE命运的特征性GABA INs的标记。标记分析表明，Pax6突变体中的dTel VZ祖细胞逐渐被验证，获得通常限于GE祖细胞的调节基因的表达。通过中神经发生，整个dTel VZ表现出腹侧化。 dTel VZ的这种腹侧空转与表面上的GABA INs的标志物的表达相平行，这表明它异位产生GABA INs，由于谷氨酸能神经元的产生减少，从而导致它们的扩张和皮层板变薄。遗传谱系追踪表明，构成胞外体的GABA INs来自dTel VZ中产生的皮质Emx1谱系，明确表明dTel祖细胞和后代在Pax6突变体中具有腹侧GE命运。因此，Pax6通过抑制dTel祖细胞和后代的腹侧命运，为GABA INs划定了适当的增殖区，并调节了它们的数量和分布。

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