Emerging Roles of MTG16 in Cell-Fate Control of Hematopoietic Stem Cells and Cancer

Table 2

Mtg family knockout mice have varying but related phenotypes.

Gene	Genetic background	Targeted exon	Mouse knockout phenotype	References
Mtg16	SvEv129 X C57BL/6	8	(i) Mild anemia and reticulocytosis; (ii) Extramedullary hematopoiesis during neonatal growth; (iii) Reduced numbers of B-cells, megakaryocytes, and erythroid progenitors; (iv) Increased numbers of granulocyte/macrophage progenitors (CFU-G); (v) Highly sensitive to phenylhydrazine-induced hemolysis; (vi) Unable to undergo compensatory, stress erythropoiesis; (vii) Reduced absolute number of LSK HSPC population, relative increase in CMPs and GMPs, relative reduction in MEPs; (viii) Loss of quiescence in LSK CD150^+ CD48^− (LT-HSPCs); (ix) Cell intrinsic decrease in stem cell self-renewal; (x) Increased proliferation and apoptosis of colonic epithelial cells; (xi) Exaggerated immune response following chemically induced colitis; (xii) Increased regenerative capacity in intestinal crypt stem cells following ionizing radiation-induced colitis	[18, 19, 45, 67, 68]
Mtg8	C57BL/6	2	(i) 25% of homozygous knockouts show deletion of the midgut; (ii) Blunted colonic villi and dilated lumen; (iii) 30–50% smaller than littermate controls; (iv) Male sterility	[16]
Mtgr1	SvEv129 X C57BL/6	7	(i) 15–20% smaller than littermate controls; (ii) 50% of embryos die E18.5–P21; (iii) Progressive loss of the pansecretory lineage of colonic epithelium; (iv) Mild inflammatory infiltrate in gut	[17]