Department of Biological Science, Florida State University, Tallahassee, FL 32306-4295, USA.
Dev Cell. 2013 May 28;25(4):350-63. doi: 10.1016/j.devcel.2013.04.013. Epub 2013 May 16.
In multicellular organisms, tissue integrity and organ size are maintained through removal of aberrant or damaged cells and compensatory proliferation. Little is known, however, about this homeostasis system in postmitotic tissues, where tissue-intrinsic genetic programs constrain cell division and new cells no longer arise from stem cells. Here we show that, in postmitotic Drosophila follicular epithelia, aberrant but viable cells are eliminated through cell competition, and the resulting loss of local tissue volume triggers sporadic cellular hypertrophy to repair the tissue. This "compensatory cellular hypertrophy" is implemented by acceleration of the endocycle, a variant cell cycle composed of DNA synthesis and gap phases without mitosis, dependent on activation of the insulin/IGF-like signaling pathway. These results reveal a remarkable homeostatic mechanism in postmitotic epithelia that ensures not only elimination of aberrant cells through cell competition but also proper organ-size control that involves compensatory cellular hypertrophy induced by physical parameters.
在多细胞生物中，组织完整性和器官大小通过去除异常或受损细胞和代偿性增殖来维持。然而，对于有丝分裂后组织中的这种动态平衡系统知之甚少，在有丝分裂后组织中，组织内在的遗传程序限制了细胞分裂，并且新细胞不再由干细胞产生。在这里，我们表明，在有丝分裂后的果蝇滤泡上皮细胞中，异常但存活的细胞通过细胞竞争被清除，并且由此导致的局部组织体积损失引发散发性细胞肥大以修复组织。这种“代偿性细胞肥大”是通过内圈（endocycle）的加速来实现的，内圈是一种由 DNA 合成和间隙相组成的变体细胞周期，没有有丝分裂，依赖于胰岛素/ IGF 样信号通路的激活。这些结果揭示了有丝分裂后上皮组织中一种显著的动态平衡机制，不仅确保了通过细胞竞争清除异常细胞，而且还确保了适当的器官大小控制，其中涉及由物理参数诱导的代偿性细胞肥大。
