JAK-STAT 受到 Notch 的限制，以控制果蝇肠道干细胞的细胞增殖。
JAK-STAT is restrained by Notch to control cell proliferation of the Drosophila intestinal stem cells.
机构信息
The Mouse Cancer Genetics Program, National Cancer Institute at Frederick, National Institutes of Health, Frederick, Maryland 21702, USA.
出版信息
J Cell Biochem. 2010 Apr 1;109(5):992-9. doi: 10.1002/jcb.22482.
Abstract
The Drosophila midgut epithelium undergoes continuous regeneration that is sustained by multipotent intestinal stem cells (ISCs) underneath. Notch signaling has dual functions to control ISC behavior: it slows down the ISC proliferation and drives the activated ISCs into different differentiation pathways at a dose-dependent manner. Here we identified a molecular mechanism to unite these two contradictory functions. We found JAK-STAT signaling controls ISC proliferation and this ability is negatively regulated by Notch at least through a transcriptional control of the JAK-STAT signaling ligand, unpaired (upd). This study provides insight into how stem cells, under steady conditions, balance the processes of proliferation and differentiation to maintain the stable cellular composition of a healthy tissue.
摘要
果蝇中肠上皮细胞经历持续的再生，这一过程由位于其下方的多能肠干细胞（ISCs）维持。Notch 信号通路具有双重功能来控制 ISC 行为：它以剂量依赖的方式减缓 ISC 的增殖，并驱动激活的 ISC 进入不同的分化途径。在这里，我们确定了一个将这两个矛盾的功能统一起来的分子机制。我们发现 JAK-STAT 信号通路控制 ISC 的增殖，而 Notch 通过对 JAK-STAT 信号通路配体 unpaired（upd）的转录调控，至少在一定程度上负调控 ISC 的增殖能力。这项研究深入了解了在稳态条件下，干细胞如何平衡增殖和分化过程，以维持健康组织中稳定的细胞组成。
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