text: The Persistent Expression of epsilony Globin in Sox6-Deficient Mice Is Due to a Defect in the epsilony-Gene-Silencing Mechanism in Definitive Erythroid Cells
  Normally, the epsilony globin gene is exclusively expressed in primitive erythrocytes and silenced in definitive erythrocytes. To determine whether the persistent expression of epsilony globin is due to residual primitive erythrocytes or is due to ectopic expression of epsilony globin in definitive erythrocytes, we examined the spatial pattern of epsilony globin transcripts in mouse embryos by in situ hybridization (Figure 5). As expected, epsilony globin is not expressed in the WT 14.5-dpc liver, the site of definitive erythropoiesis in the fetus. In contrast, abundant ectopic epsilony mRNA expression is seen in the liver of 14.5-dpc mutants (Figure 5 A-D). However, the expression of betamaj/min globin is equally abundant in both WT and p100H mutant mice (Figure 5 E and F). These data demonstrate that the persistent high levels of epsilony are due to ectopic expression in the definitive erythroid cells that mature in the fetal liver, suggesting that there is an intrinsic defect of the epsilony silencing mechanism in Sox6-null mice. 
  