Figure 8.
Models for GATA-1 actions in MEPs. (A) The classic model for hematopoiesis in which MEPs derive from the CMP. Loss of GATA-1 generates recognizable, developmentally arrested megakaryocytes and committed erythroid precursors. Therefore, the earlier stage block to differentiation of Gata1- MEPs must be partial, because some downstream progeny are produced. GATA-1 is also required for eosinophil and mast-cell development (not shown). (B) Newer models for hematopoiesis indicate that alternate pathways may exist for MEP production. If multiple pathways exist simultaneously, then loss of GATA-1 may cause a complete block to one of these pathways with mutant erythroblasts and megakaryocytes generated through coexisting ones. HSC indicates hematopoietic stem cell; BFU-E, erythroid burst-forming unit; Pro-E, proerythroblast; meg, megakaryocyte; and CLP, common lymphoid progenitor.

Models for GATA-1 actions in MEPs. (A) The classic model for hematopoiesis in which MEPs derive from the CMP. Loss of GATA-1 generates recognizable, developmentally arrested megakaryocytes and committed erythroid precursors. Therefore, the earlier stage block to differentiation of Gata1- MEPs must be partial, because some downstream progeny are produced. GATA-1 is also required for eosinophil and mast-cell development (not shown). (B) Newer models for hematopoiesis indicate that alternate pathways may exist for MEP production. If multiple pathways exist simultaneously, then loss of GATA-1 may cause a complete block to one of these pathways with mutant erythroblasts and megakaryocytes generated through coexisting ones. HSC indicates hematopoietic stem cell; BFU-E, erythroid burst-forming unit; Pro-E, proerythroblast; meg, megakaryocyte; and CLP, common lymphoid progenitor.

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