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Certain concepts concerning EPO/EPOR action modes have been challenged by in vivo studies:  Bcl-x  levels are elevated in maturing erythroblasts, but not in their progenitors; truncated EPOR alleles that lack a major p85/PI3K recruitment site nonetheless promote polycythemia; and  Erk1  disruption unexpectedly bolsters erythropoiesis. To discover novel EPO/EPOR action routes, global transcriptome analyses presently are applied to interrogate EPO/EPOR effects on primary bone marrow-derived CFUe-like progenitors. Overall, 160 EPO/EPOR target transcripts were significantly modulated 2-to 21.8-fold. A unique set of EPO-regulated survival factors included  Lyl1, Gas5, Pim3 ,  Pim1 ,  Bim ,  Trib3  and  Serpina 3g . EPO/EPOR-modulated cell cycle mediators included  Cdc25a ,  Btg3, Cyclin-d2 ,  p27-kip1 ,  Cyclin-g2  and  CyclinB1-IP-1 . EPO regulation of signal transduction factors was also interestingly complex. For example, not only  Socs3  plus  Socs2  but also  Spred2, Spred1  and  Eaf1  were EPO-induced as negative-feedback components.  Socs2 , plus five additional targets, further proved to comprise new EPOR/Jak2/Stat5 response genes (which are important for erythropoiesis during anemia). Among receptors, an atypical TNF-receptor  Tnfr-sf13c  was up-modulated >5-fold by EPO. Functionally, Tnfr-sf13c ligation proved to both promote proerythroblast survival, and substantially enhance erythroblast formation. The EPOR therefore engages a sophisticated set of transcriptome response circuits, with Tnfr-sf13c deployed as one novel positive regulator of proerythroblast formation.

Defining an EPOR- Regulated Transcriptome for Primary Progenitors, including Tnfr-sf13c as a Novel Mediator of EPO- Dependent Erythroblast Formation