Moreno Eduardo, Basler Konrad, Morata Ginés
Institut für Molekularbiologie, Universität Zürich, Winterthurerstrasse 190, 8057 Zürich, Switzerland.
Nature. 2002 Apr 18;416(6882):755-9. doi: 10.1038/416755a.
During the growth of Drosophila imaginal discs a process called 'cell competition' eliminates slow-proliferating but otherwise viable cells. We report here that cell competition requires the function of the brinker (brk) gene, whose expression is normally repressed by Decapentaplegic (Dpp) signalling but is upregulated in slow-growing Minute/+ cells. Excess brk expression activates the c-Jun amino-terminal kinase pathway, which in turn triggers apoptosis in these cells. We propose that slow-proliferating cells upregulate Brk levels owing to a disadvantage in competing for, or in transducing, the Dpp survival signal. This sequence of events might represent a general mechanism by which weaker cells are eliminated from a growing population, and might serve as a method of controlling cell number and optimizing tissue fitness and hence organ function.
在果蝇成虫盘生长过程中，一个名为“细胞竞争”的过程会消除增殖缓慢但其他方面仍具活力的细胞。我们在此报告，细胞竞争需要brinker（brk）基因发挥作用，该基因的表达通常受到Decapentaplegic（Dpp）信号通路的抑制，但在生长缓慢的Minute/+细胞中会上调。过量的brk表达会激活c-Jun氨基末端激酶通路，进而引发这些细胞的凋亡。我们提出，增殖缓慢的细胞由于在竞争或转导Dpp存活信号方面处于劣势而上调Brk水平。这一系列事件可能代表了一种普遍机制，通过该机制较弱的细胞会从生长的群体中被清除，并且可能作为一种控制细胞数量以及优化组织适应性从而优化器官功能的方法。
