López-Onieva Lourdes, Fernández-Miñán Ana, González-Reyes Acaimo
Centro Andaluz de Biología del Desarrollo (CABD Pablo de Olavide, Carretera de Utrera km 1, 41013 Sevilla, Spain.
Development. 2008 Feb;135(3):533-40. doi: 10.1242/dev.016121. Epub 2008 Jan 2.
The existence of specialised regulatory microenvironments or niches that sustain stable stem cell populations is well documented in many tissues. However, the specific mechanisms by which niche support (or stromal) cells govern stem cell maintenance remain largely unknown. Here we demonstrate that removal of the Jak/Stat pathway in support cells of the Drosophila ovarian niche leads to germline stem cell loss by differentiation. Conversely, ectopic Jak/Stat activation in support cells induces stem cell tumours, implying the presence of a signal relay between the stromal compartment and the stem cell population. We further show that ectopic Jak/Stat signalling in support cells augments dpp mRNA levels and increases the range of Dpp signalling, a Bmp2 orthologue known to act as a niche extrinsic factor required for female germline stem cell survival and division. Our results provide strong evidence for a model in which Jak/Stat signalling in somatic support cells regulates dpp transcription to define niche size and to maintain the adjacent germline stem cells in an undifferentiated state.
许多组织中都有充分的文献记载，存在维持稳定干细胞群体的特殊调节微环境或生态位。然而，生态位支持（或基质）细胞控制干细胞维持的具体机制在很大程度上仍不清楚。在这里，我们证明，去除果蝇卵巢生态位支持细胞中的Jak/Stat信号通路会导致生殖系干细胞因分化而丢失。相反，支持细胞中异位的Jak/Stat激活会诱导干细胞肿瘤，这意味着基质区室和干细胞群体之间存在信号传递。我们进一步表明，支持细胞中异位的Jak/Stat信号会增加dpp mRNA水平，并扩大Dpp信号的范围，Dpp是一种Bmp2直系同源物，已知是雌性生殖系干细胞存活和分裂所需的生态位外在因子。我们的结果为一个模型提供了有力证据，即体细胞支持细胞中的Jak/Stat信号调节dpp转录，以定义生态位大小，并使相邻的生殖系干细胞保持未分化状态。
