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cdx4 mutants fail to specify blood progenitors and can be rescued by multiple hox genes

机译：cdx4突变体无法指定血液祖细胞，可以被多个hox基因拯救

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摘要

Organogenesis is dependent on the formation of distinct cell types within the embryo. Important to this process are the hox genes, which are believed to confer positional identities to cells along the anteroposterior axis. Here, we have identified the caudal-related gene cdx4 as the locus mutated in kugelig (kgg), a zebrafish mutant with an early defect in haematopoiesis that is associated with abnormal anteroposterior patterning and aberrant hox gene expression. The blood deficiency in kgg embryos can be rescued by overexpressing hoxb7a or hoxa9a but not hoxb8a, indicating that the haematopoietic defect results from perturbations in specific hox genes. Furthermore, the haematopoietic defect in kgg mutants is not rescued by scl overexpression, suggesting that cdx4 and hox genes act to make the posterior mesoderm competent for blood development. Overexpression of cdx4 during zebrafish development or in mouse embryonic stem cells induces blood formation and alters hox gene expression. Taken together, these findings demonstrate that cdx4 regulates hox genes and is necessary for the specification of haematopoietic cell fate during vertebrate embryogenesis.
机译：器官发生取决于胚胎内不同细胞类型的形成。对这一过程很重要的是hox基因，其被认为可以沿前后轴赋予位置同一性。在这里，我们已经确定了与尾端相关的基因cdx4为kugelig（kgg）突变的基因座，该突变是斑马鱼突变体中具有早期造血功能缺陷的斑马鱼突变体，与异常前后模式和异常的hox基因表达相关。可以通过过表达hoxb7a或hoxa9a而不是hoxb8a来挽救kgg胚胎中的血液缺乏，这表明造血缺陷是由特定hox基因的扰动引起的。此外，kgg突变体的造血缺陷不能通过scl的过表达来挽救，这表明cdx4和hox基因的作用是使后中胚层有能力进行血液发育。斑马鱼发育过程中或小鼠胚胎干细胞中cdx4的过表达诱导血液形成并改变hox基因表达。综上所述，这些发现表明cdx4调节hox基因，并且对于脊椎动物胚胎发生过程中造血细胞命运的规范是必需的。

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