Development of the Drosophila entero-endocrine lineage and its specification by the Notch signaling pathway.
Development of the Drosophila entero-endocrine lineage and its specification by the Notch signaling pathway.
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果蝇肠道内分泌谱系的开发及其通过Notch信号通路的规范。
DOI：
10.1016/j.ydbio.2011.01.039
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发表时间：
2011-05-15
影响因子：
2.7
通讯作者：
Hartenstein V
中科院分区：
文献类型：
--
作者：
Takashima S;Adams KL;Ortiz PA;Ying CT;Moridzadeh R;Younossi-Hartenstein A;Hartenstein V
本文研究了黑腹果蝇从胚胎到成体肠内分泌系统的发育遗传过程。该过程开始于早期胚胎的内胚层，其中幼虫中肠的内分泌细胞和肠细胞的前体以及成虫中肠的祖细胞由Notch信号依赖性机制指定。在第二步中，发生在幼虫后期，肠上皮细胞和内分泌细胞的一个短暂的蛹中肠的成年中肠祖细胞的集群内选择。在胚胎中，Notch通路的激活触发肠上皮细胞分化，并抑制细胞进一步增殖或选择内分泌命运。肠内分泌细胞发育的第三步发生在蛹中期。在此时间点之前，注定成为成体中肠的上皮层缺乏内分泌细胞。然而，肠中肠干细胞（pISCs）的前体已经存在。在导致其自身群体大小增加的对称分裂的初始阶段之后，pISCs开始分离细胞，这些细胞成为有丝分裂后的细胞并表达内分泌命运标记物Prospero。pISC中Notch的激活迫使这些细胞进入肠上皮细胞命运。Notch功能的丧失导致pISCs的增殖活性增加，以及Prospero阳性细胞的比例更高。
In this paper we have investigated the developmental-genetic steps that shape the entero-endocrine system of Drosophila melanogaster from the embryo to the adult. The process starts in the endoderm of the early embryo where precursors of endocrine cells and enterocytes of the larval midgut, as well as progenitors of the adult midgut, are specified by a Notch signaling-dependent mechanism. In a second step that occurs during the late larval period, enterocytes and endocrine cells of a transient pupal midgut are selected from within the clusters of adult midgut progenitors. As in the embryo, activation of the Notch pathway triggers enterocyte differentiation, and inhibits cells from further proliferation or choosing the endocrine fate. The third step of entero-endocrine cell development takes place at a mid-pupal stage. Before this time point, the epithelial layer destined to become the adult midgut is devoid of endocrine cells. However, precursors of the intestinal midgut stem cells (pISCs) are already present. After an initial phase of symmetric divisions which causes an increase in their own population size, pISCs start to spin off cells that become postmitotic and express the endocrine fate marker, Prospero. Activation of Notch in pISCs forces these cells into an enterocyte fate. Loss of Notch function causes an increase in the proliferatory activity of pISCs, as well as a higher ratio of Prospero-positive cells.
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