Xu R H, Kim J, Taira M, Lin J J, Zhang C H, Sredni D, Evans T, Kung H F
Laboratory of Biochemical Physiology, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702-1201, USA.
Mol Cell Biol. 1997 Jan;17(1):436-43. doi: 10.1128/MCB.17.1.436.
Previously, we have shown that the ventralizing factor bone morphogenetic protein 4 (BMP-4) can inhibit Xenopus neurogenesis. The erythroid transcription factor GATA-1 functions downstream of the BMP-4 signaling pathway and mediates BMP-4-induced erythropoiesis. We have found that similar to BMP-4, GATA-1b inhibits neuralization of Xenopus animal cap (AC) cells. The neural inhibition is not seen with GATA-1a, although both GATA-1a and GATA-1b RNAs are translated at the same efficiency and induce globin expression equally in AC cells. GATA-1b RNA injection into AC cells neither induces expression of Xbra (a general mesoderm marker) nor affects expression of XK81 (epidermal keratin) or BMP-4 and Xvent-1 (two ventral markers). These data suggest that GATA-1b retains the epidermal fate of the AC. Intact GATA-1b protein is required for both inhibition of neurogenesis and induction of globin expression. Our findings indicate that GATA-1b can function in ectoderm to specifically regulate neural inducing mechanisms, apparently related to the expression of chordin, a neuralizing gene. Furthermore, tadpole stage embryos injected with GATA-1b are devoid of all dorsoanterior structures including neural tissue. This report provides evidence that the two transcription factors, derived from a recent genome duplication, share a common biological activity (stimulation of erythropoiesis) while also exhibiting a distinct function (inhibition of neurogenesis).
此前，我们已经表明，腹侧化因子骨形态发生蛋白4（BMP - 4）可抑制非洲爪蟾的神经发生。红系转录因子GATA - 1在BMP - 4信号通路下游发挥作用，并介导BMP - 4诱导的红细胞生成。我们发现，与BMP - 4相似，GATA - 1b可抑制非洲爪蟾动物帽（AC）细胞的神经化。而GATA - 1a则未见这种神经抑制作用，尽管GATA - 1a和GATA - 1b的RNA翻译效率相同，且在AC细胞中均能同等程度地诱导珠蛋白表达。向AC细胞中注射GATA - 1b的RNA既不会诱导Xbra（一种一般中胚层标记物）的表达，也不会影响XK81（表皮角蛋白）或BMP - 4以及Xvent - 1（两种腹侧标记物）的表达。这些数据表明，GATA - 1b维持了AC细胞的表皮命运。完整的GATA - 1b蛋白对于神经发生的抑制和珠蛋白表达的诱导均是必需的。我们的研究结果表明，GATA - 1b可在外胚层中发挥作用以特异性调节神经诱导机制，这显然与一种神经化基因脊索蛋白的表达有关。此外，注射了GATA - 1b的蝌蚪期胚胎缺乏包括神经组织在内的所有背前部结构。本报告提供了证据表明，这两种源于近期基因组复制的转录因子具有共同的生物学活性（刺激红细胞生成），同时也表现出独特的功能（抑制神经发生）。
