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首页> 外文期刊>Molecular and Cellular Biology >Common Partner Smad-Independent Canonical Bone Morphogenetic Protein Signaling in the Specification Process of the Anterior Rhombic Lip during Cerebellum Development
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Common Partner Smad-Independent Canonical Bone Morphogenetic Protein Signaling in the Specification Process of the Anterior Rhombic Lip during Cerebellum Development

机译：小脑发育过程中前菱形唇的规范化过程中的共同伴侣独立的Smad独立规范骨形态发生蛋白信号。

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Bone morphogenetic protein (BMP) signaling is critical for cerebellum development. However, the details of receptor regulated-Smad (R-Smad) and common partner Smad (Co-Smad, or Smad4) involvement are unclear. Here, we report that cerebellum-specific double conditional inactivation of Smad1 and Smad5 (Smad1/5) results in cerebellar hypoplasia, reduced granule cell numbers, and disorganized Purkinje neuron migration during embryonic development. However, single conditional inactivation of either Smad1 or Smad5 did not result in cerebellar abnormalities. Surprisingly, conditional inactivation of Smad4, which is considered to be the central mediator of canonical BMP-Smad signaling, resulted only in very mild cerebellar defects. Conditional inactivation of Smad1/5 led to developmental defects in the anterior rhombic lip (ARL), as shown by reduced cell proliferation and loss of Pax6 and Atoh1 expression. These defects subsequently caused the loss of the nuclear transitory zone and a region of the deep cerebellar nuclei. The normal maturation of the remaining granule cell precursors in the external granular layer (EGL) suggests Smad1/5 signaling is required for the specification process in ARL but not for the subsequent EGL development. Our results demonstrate functional redundancy for Smad1 and Smad5 but functional discrepancy between Smad1/5 and Smad4 during cerebellum development.
机译：骨形态发生蛋白（BMP）信号对于小脑发育至关重要。但是，尚不清楚受体调节的Smad（R-Smad）和共同伴侣Smad（Co-Smad或Smad4）参与的细节。在这里，我们报道 Smad1 和 Smad5 （ Smad1 / 5 ）的小脑特异性双重条件失活导致小脑发育不全，颗粒细胞数量减少，并在胚胎发育过程中紊乱的浦肯野神经元迁移。但是， Smad1 或 Smad5 的单个条件失活不会导致小脑异常。令人惊讶的是， Smad4 的条件性失活仅被认为是非常轻微的小脑缺陷，这被认为是经典BMP-Smad信号转导的主要介质。 Sem1 / 5 的条件失活导致前菱形唇（ARL）的发育缺陷，表现为细胞增殖减少以及Pax6和 Atoh1 表达减少。这些缺陷随后导致核短暂区域和小脑深核区域的丢失。外部颗粒层（EGL）中其余颗粒细胞前体的正常成熟表明ARL中的规范过程需要Smad1 / 5信号传导，但随后的EGL开发则不需要。我们的结果证明了 Smad1 和 Smad5 的功能冗余，但 Smad1 / 5 和 Smad4 在小脑发育过程中的功能差异。

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