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.

Animals, Cell Differentiation/physiology, Erythropoiesis, Humans, Neurons/physiology, Research Support, Non-U.S. Gov't, Retinoblastoma Protein/*physiology, Signal Transduction/physiology, Tumor Suppressor Proteins/*physiology
dx.doi.org/10.1093/embo-reports/kvf033, hdl.handle.net/1765/13018
E M B O Reports
Erasmus MC: University Medical Center Rotterdam

Whyatt, D, & Grosveld, F.G. (2002). Cell-nonautonomous function of the retinoblastoma tumour suppressor protein: new interpretations of old phenotypes. E M B O Reports, 3(2), 130–135. doi:10.1093/embo-reports/kvf033