Jill A Henrich, Eleanor I Sams, Vikram R Paralkar
Hematopoiesis is governed by precisely coordinated transcriptional programs that balance hematopoietic stem cell (HSC) self-renewal with the ability to differentiate into multiple blood lineages. During normal hematopoiesis, cells maintain tight control over the level of ribosomal RNA (rRNA) transcription by RNA Polymerase I (Pol I) and over mature rRNA abundance (ribosomal subunits). Although the factors governing RNA Polymerase II (Pol II)-mediated gene expression and their roles in cell fate determination are well characterized, far less is known about the regulation of rRNA transcription and ribosome abundance. Little is known also about how ribosome numbers contribute to hematopoietic cell fate. This review summarizes current literature on the mechanisms by which hematopoietic cell types fine-tune rRNA transcription and ribosomal subunit abundance throughout cell fate trajectories, and how dysregulation of these processes contributes to acute myeloid leukemia (AML).