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首页> 外文期刊>The international journal of developmental biology >XSu(H)2 is an essential factor for gene expression and morphogenesis of the Xenopus gastrula embryo
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XSu(H)2 is an essential factor for gene expression and morphogenesis of the Xenopus gastrula embryo

机译：XSu（H）2是非洲爪蟾胚胎的基因表达和形态发生的重要因素

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The CSL (CBF-1, Suppressor of Hairless, Lag-1) transcriptional factor is an important mediator of Notch signal transduction. It plays a key role in cell fate determination by cell-cell interaction. CSL functions as a transcriptional repressor before the activation of Notch signaling. However, once Notch signaling is activated, CSL is converted into a transcriptional activator. It remains unclear if CSL has any function during early development before neurogenesis, while transcriptional products exist from the maternal stage. Here, we analyzed the function of Xenopus Suppressor of Hairless (XSu(H)) using morpholino antisense oligonucleotides (MO), which interfere with the translation of transcripts. In Xenopus embryos, maternal transcripts of both XSu(H) 1 and XSu(H)2 were ubiquitously observed until the blastula stage and thereafter only XSu(H)1 was zygotically transcribed. Knockdown experiments with MO demonstrated that XSu(H)2 depletion caused a decrease in the expression of the Xbrachyury, MyoD and JNK1 genes. Morphological and histological examinations indicated that XSu(H)2 depletion caused abnormal gastrulation, which resulted in severe defects of the notochord and somitic mesoderm. The effect of XSu(H)2-MO was completely rescued by co-injection of XSu(H)2 mRNAs, but not by XSu(H)1 mRNAs. XESR-1, a Notch signaling target gene, inhibited Xbrachyury expression. However, expression of the XESR-1 gene was not induced by depletion of XSu(H)2. Co-injection of the dominant-negative form of XESR-1 could not rescue the suppression of Xbrachyury expression in the XSU(H)2-depleted embryo. These results suggest that XSu(H)2 is involved in mesoderm formation and the cell movement of gastrula embryos in a different manner from the XESR-1-mediated Notch signaling pathway.
机译：CSL（CBF-1，无毛发抑制因子，Lag-1）转录因子是Notch信号转导的重要介体。它在通过细胞间相互作用确定细胞命运中起着关键作用。 CSL在激活Notch信号之前起转录抑制因子的作用。但是，一旦Notch信号被激活，CSL就被转换为转录激活因子。尚不清楚CSL是否在神经发生之前的早期发育期间具有任何功能，而转录产物从母体阶段就存在。在这里，我们使用吗啉代反义寡核苷酸（MO）分析了无脚非洲爪蟾（XSu（H））的功能，这会干扰转录物的翻译。在非洲爪蟾胚胎中，普遍观察到XSu（H）1和XSu（H）2的母本转录本，直到囊胚阶段，此后只有XSu（H）1才被合子转录。 MO的组合实验表明XSu（H）2耗竭导致Xbrachyury，MyoD和JNK1基因的表达减少。形态学和组织学检查表明，XSu（H）2耗竭导致异常胃形成，从而导致脊索和体细胞性中胚层严重缺陷。通过共注射XSu（H）2 mRNA可以完全挽救XSu（H）2-MO的作用，但不能通过XSu（H）1 mRNA共同注射。 XESR-1，Notch信号转导靶基因，抑制Xbrachyury表达。但是，XESR-1基因的表达不是由XSu（H）2的消耗诱导的。共注射XESR-1的显性负型不能拯救XSU（H）2缺失胚胎中Xbrachyury表达的抑制。这些结果表明，XSu（H）2参与中胚层形成和腹胚胚胎的细胞运动，其方式不同于XESR-1介导的Notch信号通路。

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