Abstract
Erythropoiesis is a process of enormous magnitude, with the average person generating two to three million red cells every second. Erythroid progenitors start as large cells with large nuclei, and over the course of three to four cell divisions they undergo a dramatic decrease in cell size accompanied by profound nuclear condensation, which culminates in enucleation. As maturing erythroblasts are undergoing these dramatic phenotypic changes, they accumulate hemoglobin and express high levels of other erythroid-specific genes, while silencing much of the non-erythroid transcriptome. These phenotypic and gene expression changes are associated with distinct changes in the chromatin landscape, and require close coordination between transcription factors and epigenetic regulators, as well as precise regulation of RNA polymerase II activity. Disruption of these processes are associated with inherited anemias and myelodysplastic syndromes. Here, we review the epigenetic mechanisms that govern terminal erythroid maturation, and their role in human disease.
Highlights
Erythropoiesis is the process of making red blood cells
This process requires the coordinated effort of epigenetic regulators and transcription factors, as well as precise regulation of RNA polymerase II activity (Figure 1)
A recent paper using novel methods to assess nascent transcription during the terminal maturation of murine erythroblasts found that transcriptional initiation is a critical regulatory step in the transcription of many erythroid genes, and they utilized elegant functional studies to demonstrate that recruitment of RNA polymerase II is an important point of transcriptional regulation for the alpha and beta globin loci.(Larke et al, 2021)
Summary
Erythropoiesis is the process of making red blood cells. At each stage of maturation, erythroblasts are both phenotypically distinct and have a unique transcriptomic profile (An et al, 2014) and chromatin landscape. Histone marks that reflect active transcription through gene bodies, such as H3K36me2/3 and H3K72me2 vary dynamically during terminal maturation, (Murphy et al, 2021), and play a critical role in the regulation of erythroid gene expression.
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