Whyatt David, Grosveld Frank
Erasmus University, Department of Cell Biology and Genetics, Medical Genetics Centre, PO Box 1738, 3000 DR Rotterdam, The Netherlands.
EMBO Rep. 2002 Feb;3(2):130-5. doi: 10.1093/embo-reports/kvf033.
Loss of the retinoblastoma protein (pRb) induces a cell-nonautonomous defect in both erythroid and neuronal differentiation. It has previously been thought that this reflects a requirement for pRb function in cells that normally support erythropoiesis and neurogenesis, rather than in the erythrocytes or neurons themselves. However, recent studies have challenged this interpretation, and it appears that erythrocytes and neurons themselves have the intrinsic requirement for pRb function. This requirement can be bypassed by signals supplied by wild-type erythroid or neuronal cells. The existence of such a signalling mechanism has implications not only in understanding pRb function but also in the interpretation of other cell-nonautonomous phenotypes.
视网膜母细胞瘤蛋白（pRb）的缺失会在红细胞生成和神经元分化过程中引发细胞非自主性缺陷。此前人们一直认为，这反映了正常支持红细胞生成和神经发生的细胞对pRb功能的需求，而非红细胞或神经元自身的需求。然而，最近的研究对这一解释提出了质疑，似乎红细胞和神经元自身对pRb功能有内在需求。野生型红细胞或神经元细胞提供的信号可以绕过这一需求。这种信号传导机制的存在不仅对理解pRb功能有意义，也对解释其他细胞非自主性表型有意义。
