PubMed · 435408
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B Jaksić, B Vitale. 1979. Call for a more precise terminology.. https://doi.org/10.1111/j.1365-2141.1979.tb05898.x
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Hematopoiesis relies on precisely coordinated transcriptional programs that balance stem cell self-renewal, lineage commitment, and terminal differentiation. Central to this regulation is the Mediator complex, a large multi-subunit transcriptional co-regulator that integrates signals from transcription factors and chromatin regulators to control RNA polymerase Ⅱ (Pol Ⅱ) activity. The dynamic and modular composition of Mediator enables context-dependent transcriptional outputs, while individual subunits can exert specialized regulatory functions during hematopoietic lineage specification, thereby contributing to cell-fate-specific transcriptional outputs. Recent advances further reveal that transcriptional regulation is shaped by the spatial organization of regulatory machinery with biomolecular condensates formed through liquid-liquid phase separation (LLPS), particularly at super-enhancers. In this emerging framework, Mediator functions not only as a transcriptional integrator but also as a key coordinator of transcriptional machinery within condensates at cell-fate-related gene loci. In this chapter, we summarize how distinct Mediator subunits confer specific modes of transcriptional regulation and discuss how the interplay between Mediator and phase-separated condensates shapes transcriptional control during hematopoiesis. We highlight how specific subunits, including MED1 and MED26, participate in distinct regulatory modes in erythropoiesis, spanning super-enhancer-driven transcriptional activation, progenitor expansion, and condensate-associated mechanisms that influence Pol Ⅱ pausing and global transcription repression during terminal differentiation. Together, these findings support a model in which Mediator integrates transcriptional regulation with nuclear organization through condensate-mediated mechanisms, providing a conceptual framework for understanding hematopoietic cell fate decisions and transcriptional dysregulation in hematological diseases.
Results of a mathematical analysis of models of hematopoietic systems introduced by Mackey and Glass are given. The models include a constant time lag, and it is shown that this lag has a critical value above which oscillations in blood cell concentration occur. To reduce the likelihood of disease associated with such oscillations, physiologists should seek to learn how to increase this critical value of the lag.
Sequential hematologic studies were performed in four infants with malignant osteopetrosis who received prednisone. Prednisone therapy resulted in decreased liver and spleen size, decreased numbers of circulating immature blood cells, and increased hemoglobin concentration and platelet counts in all infants. The quantity and quality of hematopoietic tissue in bone marrow biopsies improved during prednisone therapy but showed no significant improvement without therapy. Sequential indium 111 chloride scans in one infant showed increased uptake in long bones and pelvis and decreased uptake in liver and spleen during therapy. We conclude that prednisone therapy of infantile osteopetrosis results in increased bone marrow hematopoiesis and decreased extramedullary hematopoiesis.