Maden M
The Randall Institute, King's College London, 26-29 Drury Lane, London WC2B 5RL, UK.
Bioessays. 1999 Oct;21(10):809-12. doi: 10.1002/(SICI)1521-1878(199910)21:10<809::AID-BIES2>3.0.CO;2-0.
A recent study (Niederreither et al. Nat Genet 1999;21:444-448 [Ref. 1]) describes the phenotype of a gene knockout for an enzyme, retinaldehyde dehydrogenase 2 (RALDH-2), that synthesizes retinoic acid (RA) in the early embryo. The effects generated by this single enzyme mutation are remarkably similar to those previously described in vitamin A-deprivation studies and compound retinoic acid receptor knockouts, which involve multiple systems of the embryo. With other data on the distribution of RA, its role in axial specification of the early embryo is considerably clarified. Surprisingly, it seems that head development is unaffected in these RALDH-2 knockout embryos; thus, the anterior of the embryo does not require RA, despite the observations that the hindbrain seems exquisitely sensitive to RA perturbation. Head development may be realised by a cytochrome P450 enzyme (CYP26), which has been described recently. Between these two opposing forces, the hindbrain develops.
最近的一项研究（尼德赖特等人，《自然遗传学》，1999年；21:444 - 448 [参考文献1]）描述了一种基因敲除的表型，该基因敲除针对的是一种酶——视黄醛脱氢酶2（RALDH - 2），它在早期胚胎中合成视黄酸（RA）。这种单一酶突变产生的效应与之前在维生素A缺乏研究和复合视黄酸受体基因敲除研究中所描述的效应非常相似，而后两项研究涉及胚胎的多个系统。结合关于视黄酸分布的其他数据，视黄酸在早期胚胎轴向特化中的作用得到了相当程度的阐明。令人惊讶的是，在这些RALDH - 2基因敲除胚胎中，头部发育似乎未受影响；因此，尽管有观察表明后脑对视黄酸扰动似乎极为敏感，但胚胎的前部并不需要视黄酸。头部发育可能是由一种最近被描述的细胞色素P450酶（CYP26）实现的。在这两种相反的力量之间，后脑得以发育。
