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During thrombopoiesis, the promegakaryocyte matures into the form of a megakaryocyte. From the megakaryocyte, platelets are formed. [1] The megakaryoblast is the beginning of the thrombocytic series or platelet forming series. Megakaryoblasts typically have a large oval-shaped nucleus or a nucleus that is lobed with many nuclei. [2]
Once the cell has completed differentiation and become a mature megakaryocyte, it begins the process of producing platelets. The maturation process occurs via endomitotic synchronous replication whereby the cytoplasmic volume enlarges as the number of chromosomes multiplies without cellular division.
Acute megakaryoblastic leukemia (AMKL) is life-threatening leukemia in which malignant megakaryoblasts proliferate abnormally and injure various tissues. Megakaryoblasts are the most immature precursor cells in a platelet-forming lineage; they mature to promegakaryocytes and, ultimately, megakaryocytes which cells shed membrane-enclosed particles, i.e. platelets, into the circulation.
When the megakaryoblast matures into the promegakaryocyte, it undergoes endoreduplication [5] and forms a promegakaryocyte which has multiple nuclei, azurophilic granules, and a basophilic cytoplasm. [6] The promegakaryocyte has rotary motion, but no forward migration. [7]
CFU-S divides into two lineages: the lymphoid precursor (CFU-LSC) and the myeloid precursor (CFU-GEMM). The CFU-GEMM cell is capable of differentiating into white blood cells, red blood cells, and platelets, all of which are normally found in circulating blood.
Megakaryoblasts are hematological precursor cells which mature to megakaryocytes. Megakaryocytes release platelets into the bloodstream. Platelets are critical for normal blood clotting. [3] In consequence of this mutation, megkaryoblasts fail to mature properly, accumulate in multiple organs, may damage these organs, and may become cancerous.
This maturation involves the stimulation of megakaryoblasts to mature ultimately to megakaryocytes which cells shed membrane-enclosed fragments of their cytoplasm, i.e. platelets, into the blood. GATA1-inactivating mutations may thereby result in reduced levels of and/or dysfunctional blood platelets.
For example, "blast" forms of erythrocytes, leukocytes, and megakaryocytes start with an N:C ratio of 4:1, which decreases as they mature to 2:1 or even 1:1 (with exceptions for mature thrombocytes and erythrocytes, which are anuclear cells, and mature lymphocytes, which only decrease to a 3:1 ratio and often retain the original 4:1 ratio). [1]