Andoniadou Cynthia L, Signore Massimo, Sajedi Ezat, Gaston-Massuet Carles, Kelberman Daniel, Burns Alan J, Itasaki Nobue, Dattani Mehul, Martinez-Barbera Juan Pedro
Neural Development Unit, UCL-Institute of Child Health, 30 Guilford Street, WC1N 1EH, London, UK.
Development. 2007 Apr;134(8):1499-508. doi: 10.1242/dev.02829. Epub 2007 Mar 14.
The homeobox gene Hesx1 is an essential repressor that is required within the anterior neural plate for normal forebrain development in mouse and humans. Combining genetic cell labelling and marker analyses, we demonstrate that the absence of Hesx1 leads to a posterior transformation of the anterior forebrain (AFB) during mouse development. Our data suggest that the mechanism underlying this transformation is the ectopic activation of Wnt/beta-catenin signalling within the Hesx1 expression domain in the AFB. When ectopically expressed in the developing mouse embryo, Hesx1 alone cannot alter the normal fate of posterior neural tissue. However, conditional expression of Hesx1 within the AFB can rescue the forebrain defects observed in the Hesx1 mutants. The results presented here provide new insights into the function of Hesx1 in forebrain formation.
同源框基因Hesx1是一种重要的抑制因子，在小鼠和人类中，前神经板内正常的前脑发育需要该基因。通过结合基因细胞标记和标记分析，我们证明在小鼠发育过程中，Hesx1的缺失会导致前脑前部（AFB）向后脑转变。我们的数据表明，这种转变的潜在机制是AFB中Hesx1表达域内Wnt/β-连环蛋白信号的异位激活。当在发育中的小鼠胚胎中异位表达时，单独的Hesx1不能改变后脑组织的正常命运。然而，在AFB中条件性表达Hesx1可以挽救在Hesx1突变体中观察到的前脑缺陷。本文给出的结果为Hesx1在前脑形成中的功能提供了新的见解。
