Stem Cells International / 2017 / Article / Tab 2

Review Article

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.

GeneGenetic backgroundTargeted exonMouse knockout phenotypeReferences

Mtg16SvEv129 X C57BL/68(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]

Mtg8C57BL/62(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]

Mtgr1SvEv129 X C57BL/67(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]