The function of the neurogenic genes during epithelial development in the Drosophila embryo.
The function of the neurogenic genes during epithelial development in the Drosophila embryo.
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发表时间：
1992-12
期刊：
影响因子：
4.6
通讯作者：
Amelia Y. Hartenstein;Astrid Rugendorff;Ulrich Tepass;V. Hartenstein
中科院分区：
文献类型：
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作者：
Amelia Y. Hartenstein;Astrid Rugendorff;Ulrich Tepass;V. Hartenstein
利用不同的抗体和PlacZ标记分析了Notch、mastermind、big brain、Delta、Enhancer of split和neuralized 6个神经基因突变的复杂胚胎表型，使我们能够标记大多数已知的胚胎组织。我们的研究结果表明，所有的神经原性突变体在来自所有三个胚层的许多不同器官中都表现出异常。外胚层来源组织中由神经源性突变引起的缺陷分为两类。首先，所有从外胚层剥离的细胞类型（神经母细胞、感觉神经元、周围胶质细胞和卵泡细胞）数量增加。其次，野生型形成上皮结构的外胚层组织失去上皮表型并游离（视叶、口胃神经系统）或表现出明显的分化异常（气管、马氏小管和唾液腺）。在所有六种神经源性突变中都观察到来自中胚层的组织异常。最重要的是，成肌细胞不会融合和/或形成异常的肌肉模式。成心细胞（形成胚胎心脏）数量增加并表现出分化异常；其他中胚层细胞类型（脂肪体、心包细胞）明显减少。大多数神经源性突变（Notch、Delta、分裂增强子和神经化增强子）至少在两个阶段内破坏了内胚层（中肠雏形）的发育。当内陷的中肠雏形过早地失去其上皮特征时，缺陷早在原肠形成期间就会发生。之后，中肠雏形向中肠上皮的转变不会发生。此外，从中肠雏形中分离出来的成体中肠前体细胞数量显著增加。我们认为，至少在外胚层和内胚层衍生组织中，神经源性基因功能主要参与需要获得或维持上皮表型的细胞之间的相互作用。
The complex embryonic phenotype of the six neurogenic mutations Notch, mastermind, big brain, Delta, Enhancer of split and neuralized was analyzed by using different antibodies and PlacZ markers, which allowed us to label most of the known embryonic tissues. Our results demonstrate that all of the neurogenic mutants show abnormalities in many different organs derived from all three germ layers. Defects caused by the neurogenic mutations in ectodermally derived tissues fell into two categories. First, all cell types that delaminate from the ectoderm (neuroblasts, sensory neurons, peripheral glia cells and oenocytes) are increased in number. Secondly, ectodermal tissues that in the wild type form epithelial structures lose their epithelial phenotype and dissociate (optic lobe, stomatogastric nervous system) or show significant differentiative abnormalities (trachea, Malpighian tubules and salivary gland). Abnormalities in tissues derived from the mesoderm were observed in all six neurogenic mutations. Most importantly, somatic myoblasts do not fuse and/or form an aberrant muscle pattern. Cardioblasts (which form the embryonic heart) are increased in number and show differentiative abnormalities; other mesodermal cell types (fat body, pericardial cells) are significantly decreased. The development of the endoderm (midgut rudiments) is disrupted in most of the neurogenic mutations (Notch, Delta, Enhancer of split and neuralized) during at least two stages. Defects occur as early as during gastrulation when the invaginating midgut rudiments prematurely lose their epithelial characteristics. Later, the transition of the midgut rudiments to form the midgut epithelium does not occur. In addition, the number of adult midgut precursor cells that segregate from the midgut rudiments is strongly increased. We propose that, at least in the ectodermally and endodermally derived tissues, neurogenic gene function is primarily involved in interactions among cells that need to acquire or to maintain an epithelial phenotype.