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首页> 外文期刊>Development >LSox5 regulates RhoB expression in the neural tube and promotes generation of the neural crest.
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LSox5 regulates RhoB expression in the neural tube and promotes generation of the neural crest.

机译：LSox5调节神经管中RhoB的表达并促进神经rest的生成。

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摘要

Members of the Sox family of transcription factors are involved in a number of crucial developmental processes, including sex determination, neurogenesis and skeletal development. LSox5 is a member of the group D Sox factors that, in conjunction with Sox6 and Sox9, promotes chondrogenesis by activating the expression of cartilage-specific extracellular matrix molecules. We have cloned the chicken homologue of LSox5 and found that it is initially expressed in the premigratory and migratory neural crest after Slug and FoxD3. Subsequently, the expression of LSox5 is maintained in cephalic crest derivatives, and it appears to be required for the development of the glial lineage, the Schwann cells and satellite glia in cranial ganglia. Misexpression of LSox5 in the cephalic neural tube activated RhoB expression throughout the dorsoventral axis. Furthermore, the prolonged forced expression of LSox5 enlarged the dorsal territory in which the neural crest is generated, extended the 'temporal window' of neural crest segregation, and led to an overproduction of neural crest cells in cephalic regions. In addition to HNK-1, the additional neural crest cells expressed putative upstream markers (Slug, FoxD3) indicating that a regulatory feedback mechanism may operate during neural crest generation. Thus, our data show that in addition to the SoxE genes (Sox9 and Sox10) a SoxD gene (Sox5) also participates in neural crest development and that a cooperative interaction may operate during neural crest generation, as seen during the formation of cartilage.
机译：Sox转录因子家族的成员参与许多关键的发育过程，包括性别确定，神经发生和骨骼发育。 LSox5是D类Sox因子的成员，该因子与Sox6和Sox9一起通过激活软骨特异性细胞外基质分子的表达来促进软骨形成。我们已经克隆了LSox5的鸡同源物，发现它最初在Slug和FoxD3之后在迁移前和迁徙的神经rest中表达。随后，LSox5的表达在头顶畸形中得以维持，似乎是神经节中神经胶质谱系，雪旺氏细胞和附属神经胶质细胞发育所必需的。头神经管中LSox5的错误表达激活了整个背腹轴的RhoB表达。此外，长期强迫表达的LSox5扩大了产生神经c的背侧区域，延长了神经c分离的“时间窗口”，并导致了头部区域神经c细胞的过度生产。除HNK-1外，其他神经c细胞还表达了假定的上游标记（Slug，FoxD3），表明在神经c生成过程中可能存在调节反馈机制。因此，我们的数据表明，除了SoxE基因（Sox9和Sox10）外，SoxD基因（Sox5）也参与神经c的发育，并且在软骨形成过程中可以看到，在神经c的产生过程中可能发生了协同作用。

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