生物
生殖系
干细胞
细胞生物学
JAK-STAT信号通路
间质细胞
体细胞
斯达
异位表达
成体干细胞
细胞分化
信号转导
遗传学
车站3
癌症研究
细胞培养
基因
受体酪氨酸激酶
作者
Lourdes López-Onieva,Ana Fernández‐Miñán,Acaimo González‐Reyes
出处
期刊:Development
[The Company of Biologists]
日期:2008-01-03
卷期号:135 (3): 533-540
被引量:119
摘要
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 Drosophilaovarian 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.
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